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Journal articles on the topic 'Insuline resistance'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 April 2022

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1

Onusyko, O. V. "Perinatal consequences in women with the Polycystic Ovarу Syndrome on a background insuline resistance in anamnesis." HEALTH OF WOMAN, no. 10(116) (December 29, 2016): 107–9. http://dx.doi.org/10.15574/hw.2016.116.107.

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In this article features of perinatal consequences in women, pregnancy, which became after the treatment of the Polycystic Ovarу Syndrome on a background of insuline resistance are considered. The clinical and static retrospective analysis of 102 of childbirth histories in women with the Polycystic Ovarу Syndrome in anamnesis is conducted for period from 2009th to 2012th on the base of maternity hospital in Uzhorod. It was found that insuline resistance has negative influence on the state of new-born. The objective: to study the effect of insulin resistance in pregnant women on neonatal status. Patients and methods. Retrospective clinico-statistical analysis of 100 individual cards and stories of labor in patients with polycystic ovary syndrome on the background of insulin resistance and 100 stories of newborns. And the first study group were children of women with PCOS on the background of IR. This is the primary group. And II group (control) took the children of healthy women, whose number was 115. Pregnant women, who were executed in vitro fertilization, the study has not been included. Resalts. The influence of insulin resistance in pregnant women on neonatal status. Established negative its effects on infants, namely an increase in the incidence of perinatal complications. Conclusion. The state of hyperandrogenism and insulin resistance in women with PCOS in history, of course, adversely affects the condition of the newborn: increased risk of asphyxia of the newborn, hypoxic-ischemic encephalopathy, respiratory insufficiency I, II and III degrees, reduced muscle tone. Also increased risk of hypoxic cardiopathy, cardio-respiratory depression and the courts. Key words: pregnancy, polycystic ovary syndrome, insulin resistance, newborn.

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2

COLINO, E., L. Pe??a, J. C. Ramos, P. Saavedra, and M. Quintana. "P0053 PP INSULINE RESISTANCE SYNDROME IN OBESE CHILDREN." Journal of Pediatric Gastroenterology and Nutrition 39, Supplement 1 (June 2004): S76—S77. http://dx.doi.org/10.1097/00005176-200406001-00177.

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3

Vigil, L., R. Garcia Carretero, C. Rodriguez Castro, A. Colas, B. Vargas, M. Lopez Jimenez, and M. Varela. "INSULINE RESISTANCE AND CHRONIC RENAL DISEASE IN A HYPERTENSIVE POPULATION." Journal of Hypertension 36, Supplement 1 (June 2018): e274. http://dx.doi.org/10.1097/01.hjh.0000539794.87223.5f.

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4

ARMASHERNANDEZ, M. "D16 Lacidipine on platelet malondialdehyde production and insuline resistance in hypertensive patients." American Journal of Hypertension 10, no. 4 (April 1997): 108A. http://dx.doi.org/10.1016/s0895-7061(97)89044-9.

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5

Conterato, Elisabete Vieira, Tania Diniz Machado, Carlos Alberto Nogueira-de-Almeida, and Elza Daniel Mello. "Leptin Levels, Basal Metabolic Rates, and Insulin Resistance in Obese Pubertal Children." International Journal of Nutrology 13, no. 01 (July 2020): 017–23. http://dx.doi.org/10.1055/s-0040-1713796.

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Abstract Introduction Obesity in children and adolescents is considered a serious public health problem. The consequences of overweight can last for life. It is extremely important to have formulas to calculate the basal metabolic rate (BMR) that are truly reliable in relation to the individual caloric expenditure. Objectives To investigate the association of serum levels of leptin, lipid profile, and insulin resistance (insuline resistance by Homeostatic Model Assessment [HOMA] index) with the body mass index (BMI) z-score of pubertal obese children. In addition, to compare the basal metabolic rate (BMR) evaluation carried out using bioimpedance (BIA) with the Food and Agricultural Organization/World Health Organization (FAO/WHO) equation. Methods Cross-sectional study including 37 pubertal obese children (aged 7 to 12 years old) seen for the first time in the outpatient care unit specialized in child obesity between June 2013 and April 2014. The participants were assessed regarding anthropometric data, body composition (fat mass) by BIA 310 bioimpedance analyzer (Biodynamic Body Composition Analyser, model 310 - Biodynamics Corporation, Seattle, EUA), and blood pressure. Blood samples were collected to measure glucose, insulin, lipid profile, triglycerides, and leptin. The stage of sexual maturity was determined by self-assessment according to the Tanner scale. Results Higher leptin levels were found in the severe obesity group (p = 0.007) and, as expected, higher BMI (p < 0.001), and fat mass (p = 0.029). The groups did not differ in relation to insulin, insulin resistance (HOMA-IR), triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), and blood pressure. The BMR measured by bioimpedance was lower as compared to the measure by the FAO/WHO equation (p < 0.001). Conclusions These results suggest that severely obese children may present leptin resistance in this early stage of life, (since this hormone is higher in these children). It is suggested that health professionals prioritize the calculation of BMR by bioimpedance, since the FAO/WHO equation seems to overestimate the caloric values.

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6

Afandi, Muhammad Rafli, and Ferdy Royland Marpaung. "CORRELATION BETWEEN APOPROTEIN B/APOPROTEIN A-I RATIO WITH HOMA IR VALUE (HOMEOSTATIC MODEL ASSESMENT INSULIN RESISTANCE) IN TYPE 2 DIABETES MELLITUS." Journal of Vocational Health Studies 3, no. 2 (December 21, 2019): 78. http://dx.doi.org/10.20473/jvhs.v3.i2.2019.78-82.

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Background: Diabetes mellitus (DM) is the seventh leading cause of death in the world (the occuring rate has reached 400 million people). Type2 DM is caused by the body cells’ inability to respond normally to insulin (insulin resistance). Homeostatic Model Assessment-Insuline Resistance (HOMA-IR) is a calculation method which function is to measure the body insulin resistance. Diabetes mellitus can cause lipid metabolism disorders (dyslipidemia) resulting in an increased level of LDL cholesterol and decreased HDL cholesterol. The apoprotein B/apoprotein A-I ratio is the result of comparisons of apoprotein B (LDL protein constituent) and apoprotein A-I (HDL protein constituent). The apo B/apo A-I ratio represents a balance between LDL cholesterol (atherogenic) and HDL (anti-atherogenic). It is astrong signifier in predicting heart disease. Purpose: This study aim to determine the correlation between the apoprotein B/apoprotein A-I ratio with HOMA-IR in patients with type 2 diabetes mellitus. Methods: Observasional, consecutive, 100 people with type 2 diabetes mellitus who is examined in apoprotein B, apoprotein A-I test that calculating the ratio in which ratio are calculated, as well as HOMA-IR in Parahita Clinical Laboratory Surabaya. This study uses Pearson correlation test method with SPSS 22.0 for Windows program. Results: The result of Pearson correlation test between apoprotein B/apoprotein A-I ratio with HOMA-IR in 100 samples is a strong and significant correlation value (r=0,610, p<0,05).Conclusion: There is a strong correlation between the apoprotein B/apoprotein A-I ratio with HOMA-IR in patients with type 2 diabetes mellitus.

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7

Mouly, S., J. F. Bergmann, and P. J. Guillausseau. "Psychological Insuline Resistance. Descriptive Observational Study in 123 Patients with Type 2 Diabetes Mellitus Not Taking Insulin in Paris Area, France." Clinical Therapeutics 39, no. 8 (August 2017): e16. http://dx.doi.org/10.1016/j.clinthera.2017.05.050.

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8

A.Taher, Mohammed, Waleed R. Sulaiman, and Hillal Y. Al-Khairi. "Rosiglitazone , Metformin or both for Treatment of Polycystic Ovary Syndrome." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 17, no. 2 (March 30, 2017): 80–86. http://dx.doi.org/10.31351/vol17iss2pp80-86.

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This study was designed to show the advantages of using the combination of metformin and rosiglitazone over using each drug alone in treatment of women with polycystic ovary syndrome (PCOS).Forty four women with PCOS were classified into 3 groups , group 1 received rosiglitazone (4mg/day) for 3 months , group Î™Î™ received metformin ( 1500 mg/day)for three months and groupÎ™Î™Î™ received the combination ( rosiglitazone 4mg/day + metformin 1500 mg/day) for the same period of treatment . The blood samples were drawn before treatment and after 3 months of treatment . The fasting serum glucose , insulin , progesterone , testosterone , leutinizing hormone were measured before and after treatment. The reduction of serum insulin , glucose ,homostasis model assessment of insuline resistance ( HOMA-IR) , LH and testosterone levels were greater in the group received the combination of rosiglitazone with metformin than that those taken each one alone. Testosterone levels decreased significantly (P<0.05) from baseline level 1Â±0.04ng/ml to 0.073Â±0.32ng/ml after treatment with combination.The rate of ovulation is 29.4%,36.4% , 62.5% in rosiglitazone , metformin and combination of both, respectively.The combination of rosiglitazone with metformin has more beneficial effect on ovulation rate. Key words: polycystic ovary syndrome, rosiglitazone, metformin, ovulation rate .

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9

Kumar, Sinha Ritesh, and Chandra Satish. "Insulin resistance." Asian Pacific Journal of Health Sciences, Supplimentary 2014 (2014): 71–78. http://dx.doi.org/10.21276/apjhs.2014.1.1s.15.

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10

Wiedemann, Jean Yves, Laurent Jacquemin, Olivier Roth, Ronan Le Bouar, Mahmoud Moussaoui, Jacques Levy, and Jean Pierre Monassier. "048 Unlike hyperglycemia, insulin deficiency and insuline resistance index are not associated with ST-segment resolution after primary percutaneous coronary intervention for acute myocardial infarction." Archives of Cardiovascular Diseases Supplements 3, no. 1 (January 2011): 15–16. http://dx.doi.org/10.1016/s1878-6480(11)70050-7.

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11

Ley, Christopher J., Jonathan Swan, Ian F. Godsland, Christopher Walton, David Crook, and John C. Stevenson. "Insuline resistance, lipoproteins, body fat and hemostasis in nonobese men with angina and a normal or abnormal coronary angiogram." Journal of the American College of Cardiology 23, no. 2 (February 1994): 377–83. http://dx.doi.org/10.1016/0735-1097(94)90423-5.

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12

Huranych, S. P., N. M. Voronych-Semchenko, and T. V. Huranych. "Prooxidant-Antioxidant Status of Dental Pulp and Lining of Oral Cavity of Rats with Experimental Iodine Deficiency and Insuline Resistance." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 2, no. 2 (May 24, 2017): 16–20. http://dx.doi.org/10.26693/jmbs02.02.016.

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13

Finocchiaro, G., F. Cappuzzo, E. Rossi, L. Toschi, P. A. Janne, M. Roncalli, C. Ligorio, L. Rimassa, A. Santoro, and M. Varella-Garcia. "Insuline like growth factor receptor-1 (IGFR-1), MET, and BRAF and primary resistance to cetuximab therapy in colorectal cancer patients." Journal of Clinical Oncology 26, no. 15_suppl (May 20, 2008): 4135. http://dx.doi.org/10.1200/jco.2008.26.15_suppl.4135.

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14

Perez-Ruiz, F. "OP0312 Association of Insuline Resistance and Hypertension with Renal Clearance of Uric Acid in Males with Gout and Normal Renal Function." Annals of the Rheumatic Diseases 72, Suppl 3 (June 2013): A160.1—A160. http://dx.doi.org/10.1136/annrheumdis-2013-eular.517.

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15

İlbay, Vasfiye, Mesrure Köseoğlu Bitnel, Oya Öztürk, Nermin Görkem Şirin İnan, Yeşim Kaykı, Mehmet İlbay, Hayrunisa Dilek Ataklı, and Aysun Soysal. "The Investigation of the Effect of Continuous Positive Airway Pressure Treatment on Metabolic Syndrome and Insuline Resistance in Obstructive Sleep Apnea Syndrome Patients." Journal of Turkish Sleep Medicine 4, no. 2 (December 21, 2017): 54–58. http://dx.doi.org/10.4274/jtsm.09797.

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16

Adiga, Usha, Kathyayani P, and Nandith P.B. "Association of Insulin Based Insulin Resistance with Liver Biomarkers in Type 2 Diabetes mellitus." Journal of Pure and Applied Microbiology 13, no. 2 (June 30, 2019): 1199–205. http://dx.doi.org/10.22207/jpam.13.2.60.

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17

Choi, Cheol S., Young-Bum Kim, Felix N. Lee, Janice M. Zabolotny, Barbara B. Kahn, and Jang H. Youn. "Lactate induces insulin resistance in skeletal muscle by suppressing glycolysis and impairing insulin signaling." American Journal of Physiology-Endocrinology and Metabolism 283, no. 2 (August 1, 2002): E233—E240. http://dx.doi.org/10.1152/ajpendo.00557.2001.

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Elevation of plasma lactate levels induces peripheral insulin resistance, but the underlying mechanisms are unclear. We examined whether lactate infusion in rats suppresses glycolysis preceding insulin resistance and whether lactate-induced insulin resistance is accompanied by altered insulin signaling and/or insulin-stimulated glucose transport in skeletal muscle. Hyperinsulinemic euglycemic clamps were conducted for 6 h in conscious, overnight-fasted rats with or without lactate infusion (120 μmol · kg−1 · min−1) during the final 3.5 h. Lactate infusion increased plasma lactate levels about fourfold. The elevation of plasma lactate had rapid effects to suppress insulin-stimulated glycolysis, which clearly preceded its effect to decrease insulin-stimulated glucose uptake. Both submaximal and maximal insulin-stimulated glucose transport decreased 25–30% ( P < 0.05) in soleus but not in epitrochlearis muscles of lactate-infused rats. Lactate infusion did not alter insulin's ability to phosphorylate the insulin receptor, the insulin receptor substrate (IRS)-1, or IRS-2 but decreased insulin's ability to stimulate IRS-1- and IRS-2-associated phosphatidylinositol 3-kinase activities and Akt/protein kinase B activity by 47, 75, and 55%, respectively ( P < 0.05 for all). In conclusion, elevation of plasma lactate suppressed glycolysis before its effect on insulin-stimulated glucose uptake, consistent with the hypothesis that suppression of glucose metabolism could precede and cause insulin resistance. In addition, lactate-induced insulin resistance was associated with impaired insulin signaling and decreased insulin-stimulated glucose transport in skeletal muscle.

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18

Barrett, Eugene J., Hong Wang, Charles T. Upchurch, and Zhenqi Liu. "Insulin regulates its own delivery to skeletal muscle by feed-forward actions on the vasculature." American Journal of Physiology-Endocrinology and Metabolism 301, no. 2 (August 2011): E252—E263. http://dx.doi.org/10.1152/ajpendo.00186.2011.

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Insulin, at physiological concentrations, regulates the volume of microvasculature perfused within skeletal and cardiac muscle. It can also, by relaxing the larger resistance vessels, increase total muscle blood flow. Both of these effects require endothelial cell nitric oxide generation and smooth muscle cell relaxation, and each could increase delivery of insulin and nutrients to muscle. The capillary microvasculature possesses the greatest endothelial surface area of the body. Yet, whether insulin acts on the capillary endothelial cell is not known. Here, we review insulin's actions at each of three levels of the arterial vasculature as well as recent data suggesting that insulin can regulate a vesicular transport system within the endothelial cell. This latter action, if it occurs at the capillary level, could enhance insulin delivery to muscle interstitium and thereby complement insulin's actions on arteriolar endothelium to increase insulin delivery. We also review work that suggests that this action of insulin on vesicle transport depends on endothelial cell nitric oxide generation and that insulin's ability to regulate this vesicular transport system is impaired by inflammatory cytokines that provoke insulin resistance.

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19

Coghlan, M. P., and D. M. Smith. "Introduction to the Kinases in Diabetes Biochemical Society focused meeting: are protein kinases good targets for antidiabetic drugs?" Biochemical Society Transactions 33, no. 2 (April 1, 2005): 339–42. http://dx.doi.org/10.1042/bst0330339.

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Insulin regulates whole-body glucose homoeostasis by modulating the activities of protein kinases in its target tissues: muscle, liver and fat. Defects in insulin's ability to modulate protein kinase activity lead to ‘insulin resistance’ or impaired insulin action. Insulin resistance in combination with defective insulin secretion from the pancreas results in the elevated blood glucose levels that are characteristic of diabetes mellitus. Pharmacological agents that selectively modulate protein kinase activities in insulin-resistant tissues may act either as insulin-sensitizing or insulin-mimetic drugs. Consistent with this, small molecule modulators of a number of protein kinases have demonstrated efficacy in animal models of insulin resistance and diabetes. Moreover, emerging data in humans suggest that marketed anti-diabetic agents may also act in part through modulating protein kinase activities. This meeting was convened to consider the potential to treat insulin resistance and Type II diabetes by modulating protein kinase activity.

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20

Beń-Skowronek, Iwona, Monika Fieluba, Beata Szyndler, and Marcin Lewicki. "Insulin resistance during growth hormone therapy in girls with Turner syndrome." Pediatric Endocrinology 13, no. 3 (2014): 17–24. http://dx.doi.org/10.18544/ep-01.13.03.1491.

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21

Baron, A. D. "Hemodynamic actions of insulin." American Journal of Physiology-Endocrinology and Metabolism 267, no. 2 (August 1, 1994): E187—E202. http://dx.doi.org/10.1152/ajpendo.1994.267.2.e187.

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There is accumulating evidence that insulin has a physiological role to vasodilate skeletal muscle vasculature in humans. This effect occurs in a dose-dependent fashion within a half-maximal response of approximately 40 microU/ml. This vasodilating action is impaired in states of insulin resistance such as obesity, non-insulin-dependent diabetes, and elevated blood pressure. The precise physiological role of insulin-mediated vasodilation is not known. Data indicate that the degree of skeletal muscle perfusion can be an important determinant of insulin-mediated glucose uptake. Therefore, it is possible that insulin-mediated vasodilation is an integral aspect of insulin's overall action to stimulate glucose uptake; thus defective vasodilation could potentially contribute to insulin resistance. In addition, insulin-mediated vasodilation may play a role in the regulation of vascular tone. Data are provided to indicate that the pressor response to systemic norepinephrine infusions is increased in obese insulin-resistant subjects. Moreover, the normal effect of insulin to shift the norepinephrine pressor dose-response curve to the right is impaired in these patients. Therefore, impaired insulin-mediated vasodilation could further contribute to the increased prevalence of hypertension observed in states of insulin resistance. Finally, data are presented to indicate that, via a yet unknown interaction with the endothelium, insulin is able to increase nitric oxide synthesis and release and through this mechanism vasodilate. It is interesting to speculate that states of insulin resistance might also be associated with a defect in insulin's action to modulate the nitric oxide system.(ABSTRACT TRUNCATED AT 250 WORDS)

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22

Wang, Nasui, Weidong Chai, Lina Zhao, Lijian Tao, Wenhong Cao, and Zhenqi Liu. "Losartan increases muscle insulin delivery and rescues insulin's metabolic action during lipid infusion via microvascular recruitment." American Journal of Physiology-Endocrinology and Metabolism 304, no. 5 (March 1, 2013): E538—E545. http://dx.doi.org/10.1152/ajpendo.00537.2012.

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Insulin delivery and transendothelial insulin transport are two discrete steps that limit muscle insulin action. Angiotensin II type 1 receptor (AT1R) blockade recruits microvasculature and increases glucose use in muscle. Increased muscle microvascular perfusion is associated with increased muscle delivery and action of insulin. To examine the effect of acute AT1R blockade on muscle insulin uptake and action, rats were studied after an overnight fast to examine the effects of losartan on muscle insulin uptake ( protocol 1), microvascular perfusion ( protocol 2), and insulin's microvascular and metabolic actions in the state of insulin resistance ( protocol 3). Endothelial cell insulin uptake was assessed, using 125I-insulin as tracer. Systemic lipid infusion was used to induce insulin resistance. Losartan significantly increased muscle insulin uptake (∼60%, P < 0.03), which was associated with a two- to threefold increase in muscle microvascular blood volume (MBV; P = 0.002) and flow (MBF; P = 0.002). Losartan ± angiotensin II had no effect on insulin internalization in cultured endothelial cells. Lipid infusion abolished insulin-mediated increases in muscle MBV and MBF and lowered insulin-stimulated whole body glucose disposal ( P = 0.0001), which were reversed by losartan administration. Inhibition of nitric oxide synthase abolished losartan-induced muscle insulin uptake and reversal of lipid-induced metabolic insulin resistance. We conclude that AT1R blockade increases muscle insulin uptake mainly via microvascular recruitment and rescues insulin's metabolic action in the insulin-resistant state. This may contribute to the clinical findings of decreased cardiovascular events and new onset of diabetes in patients receiving AT1R blockers.

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23

Davis, T. A., and I. E. Karl. "Resistance of protein and glucose metabolism to insulin in denervated rat muscle." Biochemical Journal 254, no. 3 (September 15, 1988): 667–75. http://dx.doi.org/10.1042/bj2540667.

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Denervated (1-10 days) rat epitrochlearis muscles were isolated, and basal and insulin-stimulated protein and glucose metabolism were studied. Although basal rates of glycolysis and glucose transport were increased in 1-10-day-denervated muscles, basal glycogen-synthesis rates were unaltered and glycogen concentrations were decreased. Basal rates of protein degradation and synthesis were increased in 1-10-day-denervated muscles. The increase in degradation was greater than that in synthesis, resulting in muscle atrophy. Increased rates of proteolysis and glycolysis were accompanied by elevated release rates of leucine, alanine, glutamate, pyruvate and lactate from 3-10-day-denervated muscles. ATP and phosphocreatine were decreased in 3-10-day-denervated muscles. Insulin resistance of glycogen synthesis occurred in 1-10-day denervated muscles. Insulin-stimulated glycolysis and glucose transport were inhibited by day 3 of denervation, and recovered by day 10. Inhibition of insulin-stimulated protein synthesis was observed only in 3-day-denervated muscles, whereas regulation by insulin of net proteolysis was unaffected in 1-10-day-denervated muscles. Thus the results demonstrate enhanced glycolysis, proteolysis and protein synthesis, and decreased energy stores, in denervated muscle. They further suggest a defect in insulin's action on protein synthesis in denervated muscles as well as on glucose metabolism. However, the lack of concurrent changes in all insulin-sensitive pathways and the absence of insulin-resistance for proteolysis suggest multiple and specific cellular defects in insulin's action in denervated muscle.

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24

Yeryomenko, G. "Peculiarities of Asthma and Insulin Resistance Depending on the Types of Obesity." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 3, no. 4 (May 18, 2018): 73–77. http://dx.doi.org/10.26693/jmbs03.04.073.

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25

Sowjanya, Dr B. "Vitamin D Status, Insulin Resistance and Arterial Stiffness in Normal Healthy Subjects." Journal of Medical Science And clinical Research 05, no. 01 (January 29, 2017): 17145–49. http://dx.doi.org/10.18535/jmscr/v5i1.145.

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26

Spyridopoulos, Themistoklis, Nick Dessypris, Antonis Antoniadis, Spyros Gialamas, Constantine Antonopoulos, Konstantina Katsifoti, Hans-Olov Adami, George Chrousos, and Eleni Petridou. "Insulin resistance and risk of renal cell cancer: a case-control study." HORMONES 11, no. 3 (July 15, 2012): 308–15. http://dx.doi.org/10.14310/horm.2002.1359.

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27

Johnson, Julia A., Susan K. Fried, F. Xavier Pi-Sunyer, and Jeanine B. Albu. "Impaired insulin action in subcutaneous adipocytes from women with visceral obesity." American Journal of Physiology-Endocrinology and Metabolism 280, no. 1 (January 1, 2001): E40—E49. http://dx.doi.org/10.1152/ajpendo.2001.280.1.e40.

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Visceral obesity is associated with resistance to the antilipolytic effect of insulin in vivo. We investigated whether subcutaneous abdominal and gluteal adipocytes from viscerally obese women exhibit insulin resistance in vitro. Subjects were obese black and white premenopausal nondiabetic women matched for visceral adipose tissue (VAT), total adiposity, and age. Independently of race and adipocyte size, increased VAT was associated with decreased sensitivity to insulin's antilipolytic effect in subcutaneous abdominal and gluteal adipocytes. Absolute lipolytic rates at physiologically relevant concentrations of insulin or the adenosine receptor agonist N 6-(phenylisopropyl)adenosine were higher in subjects with the highest vs. lowest VAT area. Independently of cell size, abdominal adipocytes were less sensitive to the antilipolytic effect of insulin than gluteal adipocytes, which may partly explain increased nonesterified fatty acid fluxes in upper vs. lower body obese women. Moreover, increased VAT was associated with decreased responsiveness, but not decreased sensitivity, to insulin's stimulatory effect on glucose transport in abdominal adipocytes. These data suggest that insulin resistance of subcutaneous abdominal and, to a lesser extent, gluteal adipocytes may contribute to increased systemic lipolysis in both black and white viscerally obese women.

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Townsend, Jeremy R., Jay R. Hoffman, Adam M. Gonzalez, Adam R. Jajtner, Carleigh H. Boone, Edward H. Robinson, Gerald T. Mangine, et al. "Effects ofβ-Hydroxy-β-methylbutyrate Free Acid Ingestion and Resistance Exercise on the Acute Endocrine Response." International Journal of Endocrinology 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/856708.

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Objective. To examine the endocrine response to a bout of heavy resistance exercise following acuteβ-hydroxy-β-methylbutyrate free acid (HMB-FA) ingestion.Design. Twenty resistance trained men were randomized and consumed either 1 g of HMB-FA (BetaTor) or placebo (PL) 30 min prior to performing an acute heavy resistance exercise protocol. Blood was obtained before (PRE), immediately after (IP), and 30 min after exercise (30P). Circulating concentrations of testosterone, growth hormone (GH), insulin-like growth factor (IGF-1), and insulin were assayed. Data were analyzed with a repeated measures ANOVA and area under the curve (AUC) was analyzed by the trapezoidal rule.Results. The resistance exercise protocol resulted in significant elevations from PRE in testosteroneP<0.01, GHP<0.01, and insulinP=0.05at IP, with GHP<0.01and insulinP<0.01remaining elevated at 30P. A significant interaction was noted between groups in the plasma GH response at IP, which was significantly higher following HMB-FA compared to PLP<0.01. AUC analysis revealed an elevated GH and IGF-1 response in the HMB-FA group compared to PL.Conclusion. HMB-FA prior to resistance exercise augments the GH response to high volume resistance exercise compared to PL. These findings provide further support for the potential anabolic benefits associated with HMB supplementation.

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Clark, Michael G. "Impaired microvascular perfusion: a consequence of vascular dysfunction and a potential cause of insulin resistance in muscle." American Journal of Physiology-Endocrinology and Metabolism 295, no. 4 (October 2008): E732—E750. http://dx.doi.org/10.1152/ajpendo.90477.2008.

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Insulin has an exercise-like action to increase microvascular perfusion of skeletal muscle and thereby enhance delivery of hormone and nutrient to the myocytes. With insulin resistance, insulin's action to increase microvascular perfusion is markedly impaired. This review examines the present status of these observations and techniques available to measure such changes as well as the possible underpinning mechanisms. Low physiological doses of insulin and light exercise have been shown to increase microvascular perfusion without increasing bulk blood flow. In these circumstances, blood flow is proposed to be redirected from the nonnutritive route to the nutritive route with flow becoming dominant in the nonnutritive route when insulin resistance has developed. Increased vasomotion controlled by vascular smooth muscle may be part of the explanation by which insulin mediates an increase in microvascular perfusion, as seen from the effects of insulin on both muscle and skin microvascular blood flow. In addition, vascular dysfunction appears to be an early development in the onset of insulin resistance, with the consequence that impaired glucose delivery, more so than insulin delivery, accounts for the diminished glucose uptake by insulin-resistant muscle. Regular exercise may prevent and ameliorate insulin resistance by increasing “vascular fitness” and thereby recovering insulin-mediated capillary recruitment.

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Taniguchi, Cullen M., José O. Aleman, Kohjiro Ueki, Ji Luo, Tomoichiro Asano, Hideaki Kaneto, Gregory Stephanopoulos, Lewis C. Cantley, and C. Ronald Kahn. "The p85α Regulatory Subunit of Phosphoinositide 3-Kinase Potentiates c-Jun N-Terminal Kinase-Mediated Insulin Resistance." Molecular and Cellular Biology 27, no. 8 (February 5, 2007): 2830–40. http://dx.doi.org/10.1128/mcb.00079-07.

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ABSTRACT Insulin resistance is a defining feature of type 2 diabetes and the metabolic syndrome. While the molecular mechanisms of insulin resistance are multiple, recent evidence suggests that attenuation of insulin signaling by c-Jun N-terminal kinase (JNK) may be a central part of the pathobiology of insulin resistance. Here we demonstrate that the p85α regulatory subunit of phosphoinositide 3-kinase (PI3K), a key mediator of insulin's metabolic actions, is also required for the activation of JNK in states of insulin resistance, including high-fat diet-induced obesity and JNK1 overexpression. The requirement of the p85α regulatory subunit for JNK occurs independently of its role as a component of the PI3K heterodimer and occurs only in response to specific stimuli, namely, insulin and tunicamycin, a chemical that induces endoplasmic reticulum stress. We further show that insulin and p85 activate JNK by via cdc42 and MKK4. The activation of this cdc42/JNK pathway requires both an intact N terminus and functional SH2 domains within the C terminus of the p85α regulatory subunit. Thus, p85α plays a dual role in regulating insulin sensitivity and may mediate cross talk between the PI3K and stress kinase pathways.

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Nagano, Nobuhiko, Tatsuhiko Urakami, Kazumasa Fuwa, Kazunori Kayama, Ryota Kato, Yousuke Taguchi, Kayo Yoshikawa, et al. "Association between Perinatal Status and Insulin Resistance in Neonates during the Birth Period." Journal of Nihon University Medical Association 75, no. 5 (2016): 211–18. http://dx.doi.org/10.4264/numa.75.5_211.

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Dziuba, O. S. "Blood coagulation and aortic wall integrity in rats with obesity-induced insulin resistance." Ukrainian Biochemical Journal 90, no. 2 (April 10, 2018): 14–23. http://dx.doi.org/10.15407/ubj90.02.014.

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33

Gamal. E. Abdelhameed, Gamal E. Abdelhameed, Sherif Y. Saleh, Mohamed E. Rashad Mohamed. E. Rashad, and Ibrahim A. Ibrahim Ibrahim. A. Ibrahim. "The Biochemical Efficacy of Insulin Resistance on Sex Hormones in Obese Male Rats." Indian Journal of Applied Research 3, no. 6 (October 1, 2011): 66–70. http://dx.doi.org/10.15373/2249555x/june2013/23.

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34

Diamanti-Kandarakis, Evanthia, Evangelia Zapanti, Maria-Helen Peridis, Panayiotis Ntavos, and George Mastorakos. "Insulin resistance in pheochromocytoma improves more by surgical rather than by medical treatment." HORMONES 2, no. 1 (January 15, 2003): 61–66. http://dx.doi.org/10.14310/horm.2002.1184.

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Talaei, Afsaneh, Masoud Amini, Mansour Siavash, and Maryam Zare. "The effect of Dehydroepiandrosterone on insulin resistance in patients with impaired glucose tolerance." HORMONES 9, no. 4 (October 15, 2010): 326–31. http://dx.doi.org/10.14310/horm.2002.1284.

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36

köroğlu, Mehmet, nilgün akalın, selçuk Sezikli, yıldız okuturlar, and özlem harmankaya. "Impacts of Dialysis Replacement Therapies on Insulin Resistance and Assessment of Atherosclerotic Parameters." Turkish Nephrology Dialysis Transplantation 25, no. 01 (January 22, 2016): 59–64. http://dx.doi.org/10.5262/tndt.2016.1001.06.

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37

Petersen, Max C., and Gerald I. Shulman. "Mechanisms of Insulin Action and Insulin Resistance." Physiological Reviews 98, no. 4 (October 1, 2018): 2133–223. http://dx.doi.org/10.1152/physrev.00063.2017.

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The 1921 discovery of insulin was a Big Bang from which a vast and expanding universe of research into insulin action and resistance has issued. In the intervening century, some discoveries have matured, coalescing into solid and fertile ground for clinical application; others remain incompletely investigated and scientifically controversial. Here, we attempt to synthesize this work to guide further mechanistic investigation and to inform the development of novel therapies for type 2 diabetes (T2D). The rational development of such therapies necessitates detailed knowledge of one of the key pathophysiological processes involved in T2D: insulin resistance. Understanding insulin resistance, in turn, requires knowledge of normal insulin action. In this review, both the physiology of insulin action and the pathophysiology of insulin resistance are described, focusing on three key insulin target tissues: skeletal muscle, liver, and white adipose tissue. We aim to develop an integrated physiological perspective, placing the intricate signaling effectors that carry out the cell-autonomous response to insulin in the context of the tissue-specific functions that generate the coordinated organismal response. First, in section II, the effectors and effects of direct, cell-autonomous insulin action in muscle, liver, and white adipose tissue are reviewed, beginning at the insulin receptor and working downstream. Section III considers the critical and underappreciated role of tissue crosstalk in whole body insulin action, especially the essential interaction between adipose lipolysis and hepatic gluconeogenesis. The pathophysiology of insulin resistance is then described in section IV. Special attention is given to which signaling pathways and functions become insulin resistant in the setting of chronic overnutrition, and an alternative explanation for the phenomenon of ‟selective hepatic insulin resistanceˮ is presented. Sections V, VI, and VII critically examine the evidence for and against several putative mediators of insulin resistance. Section V reviews work linking the bioactive lipids diacylglycerol, ceramide, and acylcarnitine to insulin resistance; section VI considers the impact of nutrient stresses in the endoplasmic reticulum and mitochondria on insulin resistance; and section VII discusses non-cell autonomous factors proposed to induce insulin resistance, including inflammatory mediators, branched-chain amino acids, adipokines, and hepatokines. Finally, in section VIII, we propose an integrated model of insulin resistance that links these mediators to final common pathways of metabolite-driven gluconeogenesis and ectopic lipid accumulation.

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38

Miricescu, Daniela, Alexandra Totan, Ana Maria Alexandra Stănescu, Iulia-Ioana Stănescu, Constantin Ștefani, and Maria Greabu. "Vitamin D deficiency and insulin resistance." Romanian Journal of Medical Practice 14, no. 3 (September 30, 2019): 231–36. http://dx.doi.org/10.37897/rjmp.2019.3.4.

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39

Buchanan, T. A., G. F. Sipos, N. Madrilejo, C. Liu, and V. M. Campese. "Hypertension without peripheral insulin resistance in spontaneously hypertensive rats." American Journal of Physiology-Endocrinology and Metabolism 262, no. 1 (January 1, 1992): E14—E19. http://dx.doi.org/10.1152/ajpendo.1992.262.1.e14.

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We performed euglycemic clamp studies with labeled glucose to measure insulin's effect on hepatic glucose output (HGO) and peripheral glucose clearance in eight conscious mobile spontaneously hypertensive rats (SHR) and eleven normotensive Wistar-Kyoto (WKY) rats age 9-10 wk. Systolic blood pressure was elevated in the SHR (P less than 0.001), whereas means of 12-h-fasted plasma insulin (P greater than 0.4), glucose (P greater than 0.07), HGO (P greater than 0.25), and glucose clearance (P greater than 0.2) did not differ significantly between groups. Infusions of human insulin into SHR and WKY rats (1 and 1.5 mU.min-1.kg-1, respectively) during concomitant somatostatin administration reestablished basal insulinemia in both groups. Neither HGO (P greater than 0.15) nor glucose clearance (P greater than 0.3) differed significantly between SHR and WKY rats under those conditions. Somatostatin plus higher-dose insulin infusions (4 mU.min-1.kg-1 in SHR and 3 or 6 mU.min-1.kg-1 in WKY rats) resulted in physiological hyperinsulinemia in all rats. Insulin sensitivity, calculated as the increase in glucose clearance effected by an increase in circulating insulin during higher-dose insulin infusions, did not differ significantly between SHR and WKY groups (P greater than 0.3). HGO was completely suppressed in SHR and WKY rats during the higher-dose insulin infusions. Our data indicate that hypertension is present in SHR at an age when insulin-mediated glucose disposal is not different from age-matched WKY rats. These findings do not support a role for peripheral insulin resistance in the genesis of hypertension in SHR.

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Sowers, James R., and Edward D. Frohlich. "Insulin and insulin resistance:." Medical Clinics of North America 88, no. 1 (January 2004): 63–82. http://dx.doi.org/10.1016/s0025-7125(03)00128-7.

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41

Baron, A. D., and G. Brechtel. "Insulin differentially regulates systemic and skeletal muscle vascular resistance." American Journal of Physiology-Endocrinology and Metabolism 265, no. 1 (July 1, 1993): E61—E67. http://dx.doi.org/10.1152/ajpendo.1993.265.1.e61.

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To explore the relationships among insulin action, vascular resistance, and insulin sensitivity, we studied three groups of lean (Ln) and one group of obese (Ob) men. Glucose uptake was measured in whole body (WBGU) and in leg muscle (LGU) under basal and hyperinsulinemic euglycemic conditions. Mean arterial pressure (MAP), cardiac output (CO), leg blood flow (LBF), and systemic (SVR) and leg (LVR) vascular resistance were also ascertained. Ln groups were studied during insulin infusion rates of 20, 40, and 600 mU.m-2.min-1 and the Ob group at 40 mU.m-2.min-1. In Ob vs. Ln groups, WBGU and LGU were reduced by 51 (P < 0.01) and 42% (P < 0.05), respectively. In response to insulin, LBF increased > 60% (P < 0.01) in Ln groups but only approximately 20% in the Ob group, P = not significant (NS). CO was unchanged in Ob compared with a 15% increase (P < 0.05) in Ln groups, LBF was highly correlated with CO, r 0.70, P < 0.001. During hyperinsulinemia, MAP and LVR decreased in Ln (P < 0.001) but not in the Ob group (P = NS). In Ln groups, SVR decreased by 26 vs. 9% in the Ob group, P < 0.01. In summary, 1) insulin decreases LVR more than SVR and via this mechanism redistributes CO to insulin-sensitive tissues, 2) this insulin effect is blunted in Ob humans, and 3) insulin decreases MAP and vascular resistance more effectively in insulin-sensitive than in insulin-resistant subjects. In conclusion, insulin resistance to carbohydrate metabolism is associated with resistance to insulin's effect to decrease skeletal muscle vascular resistance and as such could act as a risk factor for the development of hypertension.

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Leng, Sanhua, Wenshuo Zhang, Yanbin Zheng, Ziva Liberman, Christopher J. Rhodes, Hagit Eldar-Finkelman, and Xiao Jian Sun. "Glycogen synthase kinase 3β mediates high glucose-induced ubiquitination and proteasome degradation of insulin receptor substrate 1." Journal of Endocrinology 206, no. 2 (May 12, 2010): 171–81. http://dx.doi.org/10.1677/joe-09-0456.

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High glucose (HG) has been shown to induce insulin resistance in both type 1 and type 2 diabetes. However, the molecular mechanism behind this phenomenon is unknown. Insulin receptor substrate (IRS) proteins are the key signaling molecules that mediate insulin's intracellular actions. Genetic and biological studies have shown that reductions in IRS1 and/or IRS2 protein levels are associated with insulin resistance. In this study we have shown that proteasome degradation of IRS1, but not of IRS2, is involved in HG-induced insulin resistance in Chinese hamster ovary (CHO) cells as well as in primary hepatocytes. To further investigate the molecular mechanism by which HG induces insulin resistance, we examined various molecular candidates with respect to their involvement in the reduction in IRS1 protein levels. In contrast to the insulin-induced degradation of IRS1, HG-induced degradation of IRS1 did not require IR signaling or phosphatidylinositol 3-kinase/Akt activity. We have identified glycogen synthase kinase 3β (GSK3β or GSK3B as listed in the MGI Database) as a kinase required for HG-induced serine332 phosphorylation, ubiquitination, and degradation of IRS1. Overexpression of IRS1 with mutation of serine332 to alanine partially prevents HG-induced IRS1 degradation. Furthermore, overexpression of constitutively active GSK3β was sufficient to induce IRS1 degradation. Our data reveal the molecular mechanism of HG-induced insulin resistance, and support the notion that activation of GSK3β contributes to the induction of insulin resistance via phosphorylation of IRS1, triggering the ubiquitination and degradation of IRS1.

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43

Davidson, M. B., and D. Garvey. "Studies on mechanisms of hepatic insulin resistance in cafeteria-fed rats." American Journal of Physiology-Endocrinology and Metabolism 264, no. 1 (January 1, 1993): E18—E23. http://dx.doi.org/10.1152/ajpendo.1993.264.1.e18.

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Whether hyperinsulinemia causes insulin resistance or vice versa is controversial. The development of hyperinsulinemia and insulin resistance was tracked in the cafeteria-fed rat to determine which occurred first. After 3 days of cafeteria feeding the rats were obese, manifested a small but significant decrease in fasting glucose levels, and showed no change in fasting insulin levels, basal hepatic glucose production (HGP), insulin binding to hepatic membranes, and glucose utilization during a euglycemic hyperinsulinemic clamp, but the rats did demonstrate an increased glucose disappearance rate associated with an enhanced insulin response to intra-arterial glucose and hepatic insulin resistance during the clamp. After 7 days of cafeteria feeding, the results were similar except that fasting hyperglycemia and hyperinsulinemia, an enhanced basal HGP, and decreased insulin binding developed. After 6 wk of cafeteria feeding, both hepatic and peripheral insulin resistances were present. After 7 days of cafeteria feeding in rats given streptozotocin or etomoxir, an inhibitor of free fatty acid (FFA) oxidation, hepatic insulin resistance persisted despite elimination of hyperinsulinemia and reduction of FFA oxidation. These data do not support a causal role for either hyperinsulinemia or enhanced lipolysis of hypertrophied fat stores and subsequent FFA oxidation in the liver in the development of hepatic insulin resistance in this animal model of obesity.

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44

Carroll, P. B., and R. C. Eastman. "Insulin Resistance." Endocrinologist 1, no. 2 (April 1991): 89–97. http://dx.doi.org/10.1097/00019616-199104000-00005.

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45

Jeffery, Alison. "Insulin resistance." Nursing Standard 17, no. 32 (April 23, 2003): 47–53. http://dx.doi.org/10.7748/ns2003.04.17.32.47.c3381.

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Jeffery, Alison. "Insulin resistance." Nursing Standard 17, no. 32 (April 23, 2003): 47–55. http://dx.doi.org/10.7748/ns.17.32.47.s62.

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47

Park, Kyong Soo. "Insulin Resistance." Journal of the Korean Medical Association 44, no. 3 (2001): 302. http://dx.doi.org/10.5124/jkma.2001.44.3.302.

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48

Tomono, Syouichi. "Insulin Resistance :." Kitakanto Medical Journal 62, no. 1 (2012): 73–74. http://dx.doi.org/10.2974/kmj.62.73.

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Nesbitt, Alexander. "Insulin Resistance." Journal of Advanced Nursing 44, no. 3 (October 20, 2003): 327–28. http://dx.doi.org/10.1046/j.1365-2648.2003.02826_3.x.

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50

Sinaiko, Alan R., and Sonia Caprio. "Insulin Resistance." Journal of Pediatrics 161, no. 1 (July 2012): 11–15. http://dx.doi.org/10.1016/j.jpeds.2012.01.012.

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