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Journal articles on the topic 'Insulin secretory defects'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Otani, Kenichi, Rohit N. Kulkarni, Aaron C. Baldwin та ін. "Reduced β-cell mass and altered glucose sensing impair insulin-secretory function in βIRKO mice". American Journal of Physiology-Endocrinology and Metabolism 286, № 1 (2004): E41—E49. http://dx.doi.org/10.1152/ajpendo.00533.2001.

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Pancreatic β-cell-restricted knockout of the insulin receptor results in hyperglycemia due to impaired insulin secretion, suggesting that this cell is an important target of insulin action. The present studies were undertaken in β-cell insulin receptor knockout (βIRKO) mice to define the mechanisms underlying the defect in insulin secretion. On the basis of responses to intraperitoneal glucose, ∼7-mo-old βIRKO mice were either diabetic (25%) or normally glucose tolerant (75%). Total insulin content was profoundly reduced in pancreata of mutant mice compared with controls. Both groups also exhi

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2

Norris, Nicholas, Belinda Yau, and Melkam Alamerew Kebede. "Isolation and Proteomics of the Insulin Secretory Granule." Metabolites 11, no. 5 (2021): 288. http://dx.doi.org/10.3390/metabo11050288.

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Insulin, a vital hormone for glucose homeostasis is produced by pancreatic beta-cells and when secreted, stimulates the uptake and storage of glucose from the blood. In the pancreas, insulin is stored in vesicles termed insulin secretory granules (ISGs). In Type 2 diabetes (T2D), defects in insulin action results in peripheral insulin resistance and beta-cell compensation, ultimately leading to dysfunctional ISG production and secretion. ISGs are functionally dynamic and many proteins present either on the membrane or in the lumen of the ISG may modulate and affect different stages of ISG traf

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3

Byrne, M. M., J. Sturis, R. J. Sobel, and K. S. Polonsky. "Elevated plasma glucose 2 h postchallenge predicts defects in beta-cell function." American Journal of Physiology-Endocrinology and Metabolism 270, no. 4 (1996): E572—E579. http://dx.doi.org/10.1152/ajpendo.1996.270.4.e572.

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Studies were performed in subjects with no known family history of diabetes, normoglycemic subjects who have first-degree relatives with non-insulin-dependent diabetes mellitus (NIDDM), and subjects with nondiagnostic oral glucose tolerance tests (NDX) or impaired glucose tolerance (IGT). Insulin sensitivity index (SI) was similar in all four groups. However, a number of defects in insulin secretion were seen in the NDX and IGT groups, including reduced first-phase insulin secretory responses in intravenous glucose in relation to the degree of insulin resistance, and reduced normalized spectra

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4

Flatt, P. R., та B. D. Green. "Nutrient regulation of pancreatic β-cell function in diabetes: problems and potential solutions". Biochemical Society Transactions 34, № 5 (2006): 774–78. http://dx.doi.org/10.1042/bst0340774.

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Increasing prevalence of obesity combined with longevity will produce an epidemic of Type 2 (non-insulin-dependent) diabetes in the next 20 years. This disease is associated with defects in insulin secretion, specifically abnormalities of insulin secretory kinetics and pancreatic β-cell glucose responsiveness. Mechanisms underlying β-cell dysfunction include glucose toxicity, lipotoxicity and β-cell hyperactivity. Defects at various sites in β-cell signal transduction pathways contribute, but no single lesion can account for the common form of Type 2 diabetes. Recent studies highlight diverse

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5

Sturis, J., W. L. Pugh, J. Tang, and K. S. Polonsky. "Prevention of diabetes does not completely prevent insulin secretory defects in the ZDF rat." American Journal of Physiology-Endocrinology and Metabolism 269, no. 4 (1995): E786—E792. http://dx.doi.org/10.1152/ajpendo.1995.269.4.e786.

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The rapid insulin secretory pulses that occur in the perfused rat pancreas can be entrained by an oscillatory glucose concentration in pancreata from nondiabetic rats but not from X diabetic Zucker diabetic fatty (ZDF) rats. To investigate whether this defect is present in prediabetic ZDF rats and whether treatment with either pioglitazone or acarbose can prevent or reverse this defect, 39 ZDF and 5 lean ZDF control rats were studied. The ZDF rats were divided into six groups depending on age, form of therapy used, and the time at which pioglitazone was started in relation to the onset of diab

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6

Okura, Tsuyoshi, Etsuko Ueta, Risa Nakamura, et al. "High Serum Advanced Glycation End Products Are Associated with Decreased Insulin Secretion in Patients with Type 2 Diabetes: A Brief Report." Journal of Diabetes Research 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/5139750.

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Objective. Advanced glycation end products (AGEs) are important in the pathophysiology of type 2 diabetes mellitus (T2DM). They directly cause insulin secretory defects in animal and cell culture models and may promote insulin resistance in nondiabetic subjects. We have developed a highly sensitive liquid chromatography-tandem mass spectrometry method for measuring AGEs in human serum. Here, we use this method to investigate the relationship between AGEs and insulin secretion and resistance in patients with T2DM. Methods. Our study involved 15 participants with T2DM not on medication and 20 no

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7

Gerich, John E. "Contributions of Insulin-Resistance and Insulin-Secretory Defects to the Pathogenesis of Type 2 Diabetes Mellitus." Mayo Clinic Proceedings 78, no. 4 (2003): 447–56. http://dx.doi.org/10.4065/78.4.447.

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8

Štrbák, Vladimír. "Pancreatic Thyrotropin Releasing Hormone and Mechanism of Insulin Secretion." Cellular Physiology and Biochemistry 50, no. 1 (2018): 378–84. http://dx.doi.org/10.1159/000494013.

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Thyrotropin releasing hormone (TRH; pGlu-His-ProNH2) is expressed also in pancreatic β cells where it is colocalized in secretory granules with insulin. High perinatal changes of the TRH gene expression and TRH concentrations in rat pancreatic islets coincide with the perinatal maturation of the adequate insulin secretory responsiveness to glucose and other nutrient secretagogues. TRH secretion from pancreatic islets is stimulated by glucose and inhibited by insulin. Disruption of the TRH gene in knockout mice results in hyperglycemia accompanied by impaired insulin secretory response to gluco

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9

Nguyen, Tuyet Thi, Xianglan Quan, Kyu-Hee Hwang, et al. "Mitochondrial oxidative stress mediates high-phosphate-induced secretory defects and apoptosis in insulin-secreting cells." American Journal of Physiology-Endocrinology and Metabolism 308, no. 11 (2015): E933—E941. http://dx.doi.org/10.1152/ajpendo.00009.2015.

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Inorganic phosphate (P i) plays an important role in cell signaling and energy metabolism. In insulin-releasing cells, P i transport into mitochondria is essential for the generation of ATP, a signaling factor in metabolism-secretion coupling. Elevated P i concentrations, however, can have toxic effects in various cell types. The underlying molecular mechanisms are poorly understood. Here, we have investigated the effect of P i on secretory function and apoptosis in INS-1E clonal β-cells and rat pancreatic islets. Elevated extracellular P i (1∼5 mM) increased the mitochondrial membrane potenti

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10

Alcarraz‐Vizán, Gema, Paola Casini, Lisa Cadavez та ін. "Inhibition of BACE2 counteracts hIAPP‐induced insulin secretory defects in pancreatic β‐cells". FASEB Journal 29, № 1 (2014): 95–104. http://dx.doi.org/10.1096/fj.14-255489.

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11

Colombo, Carla, Gianfranco Alicandro, Simone Gambazza, et al. "Ventilation inhomogeneity is associated with OGTT-derived insulin secretory defects in cystic fibrosis." Pediatric Pulmonology 54, no. 2 (2018): 141–49. http://dx.doi.org/10.1002/ppul.24212.

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12

Ehrmann, D. A., J. Sturis, M. M. Byrne, T. Karrison, R. L. Rosenfield, and K. S. Polonsky. "Insulin secretory defects in polycystic ovary syndrome. Relationship to insulin sensitivity and family history of non-insulin-dependent diabetes mellitus." Journal of Clinical Investigation 96, no. 1 (1995): 520–27. http://dx.doi.org/10.1172/jci118064.

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13

Battezzati, A., A. Mari, L. Zazzeron, et al. "Identification of insulin secretory defects and insulin resistance during oral glucose tolerance test in a cohort of cystic fibrosis patients." European Journal of Endocrinology 165, no. 1 (2011): 69–76. http://dx.doi.org/10.1530/eje-10-1003.

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BackgroundCystic fibrosis (CF)-related diabetes is a leading complication of CF and is associated with pulmonary and nutritional deterioration, years before an evident hyperglycemia, possibly because of insulin deficiency and resistance.AimTo evaluate glucose tolerance, insulin secretion, and insulin sensitivity by a widely applicable method suitable for accurate and prospective measurements in a CF population.MethodsA total of 165 CF subjects (80 females) aged 17±5 years and 18 age- and sex-matched healthy controls (CON) received an oral glucose tolerance test with glucose, insulin and C-pept

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14

Chang, Annette M., and Jeffrey B. Halter. "Aging and insulin secretion." American Journal of Physiology-Endocrinology and Metabolism 284, no. 1 (2003): E7—E12. http://dx.doi.org/10.1152/ajpendo.00366.2002.

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Glucose tolerance progressively declines with age, and there is a high prevalence of type 2 diabetes and postchallenge hyperglycemia in the older population. Age-related glucose intolerance in humans is often accompanied by insulin resistance, but circulating insulin levels are similar to those of younger people. Under some conditions of hyperglycemic challenge, insulin levels are lower in older people, suggesting β-cell dysfunction. When insulin sensitivity is controlled for, insulin secretory defects have been consistently demonstrated in aging humans. In addition, β-cell sensitivity to incr

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15

Dieterle, C., M. Veitenhansl, B. Gutt, et al. "Impaired Glucose Tolerance in Pancreas Grafted Diabetic Patients is Due to Insulin Secretory Defects." Experimental and Clinical Endocrinology & Diabetes 115, no. 10 (2007): 647–53. http://dx.doi.org/10.1055/s-2007-982501.

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16

Perreault, Leigh, Bryan C. Bergman, Mary C. Playdon, Chiara Dalla Man, Claudio Cobelli, and Robert H. Eckel. "Impaired fasting glucose with or without impaired glucose tolerance: progressive or parallel states of prediabetes?" American Journal of Physiology-Endocrinology and Metabolism 295, no. 2 (2008): E428—E435. http://dx.doi.org/10.1152/ajpendo.90354.2008.

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Our objective was to determine whether defects underlying impaired fasting glucose (IFG) are maintained and additive when combined with impaired glucose tolerance (IGT) (representing a progressive form of prediabetes) or are distinct in IFG/IGT (reflecting a parallel form of prediabetes). Volunteers with IFG ( n = 10), IFG/IGT ( n = 14), or normal glucose tolerance (NGT; n = 15) were matched for demographics and anthropometry. Insulin secretion was assessed using the glucose step-up protocol and insulin action through the use of a two-stage hyperinsulinemic euglycemic clamp with infusion of [6

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17

Axen, K. V., X. Li, K. Fung, and A. Sclafani. "The VMH-dietary obese rat: a new model of non-insulin-dependent diabetes mellitus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 3 (1994): R921—R928. http://dx.doi.org/10.1152/ajpregu.1994.266.3.r921.

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A model of non-insulin-dependent diabetes mellitus (NIDDM) has been developed in adult rats by combining bilateral electrolytic lesions of the ventromedial hypothalamus (VMH) and high fat-high sucrose diets. VMH-dietary obese rats showed fasting hyperinsulinemia (> or = 540 pM) and hypertriglyceridemia (> or = 180 mg/dl) generally within 3 wk on the protocol. Fasting hyperglycemia (> or = 10 mM) was observed in the majority of animals in seven consecutive experiments. Hyperglycemic animals showed impaired glucose tolerance despite high prevailing insulin levels. Pancreatic islets isol

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18

Gorogawa, Shin-ichi, Yoshio Fujitani, Hideaki Kaneto та ін. "Insulin secretory defects and impaired islet architecture in pancreatic β-cell-specific STAT3 knockout mice". Biochemical and Biophysical Research Communications 319, № 4 (2004): 1159–70. http://dx.doi.org/10.1016/j.bbrc.2004.05.095.

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19

Hasnin, K., F. Jebunnesa, L. Ali, and Rezaul Karim. "Insulin Secretory Defects and Determinants of Attending at a Tertiary Hospital in Northern Region of Bangladesh." Anwer Khan Modern Medical College Journal 10, no. 2 (2019): 131–37. http://dx.doi.org/10.3329/akmmcj.v10i2.44125.

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Background: Bangladesh has one of the largest diabetic populations in the world and its Rajshahi region has distinct geographical and cultural identity. Determinants and basic defects of the disorder which vary substantially among populations due to racial and environmental heterogeneity. Materials & Methods: This study was conducted to characterize the new patients attending the Rajshahi Diabetic Center which gives an idea about the proportion and risk indicators of DM among people in the Rajshahi region. It was a hospital based observational analytic study with a hybrid research st

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20

Roe, M. W., J. F. Worley, Y. Tokuyama, et al. "NIDDM is associated with loss of pancreatic beta-cell L-type Ca2+ channel activity." American Journal of Physiology-Endocrinology and Metabolism 270, no. 1 (1996): E133—E140. http://dx.doi.org/10.1152/ajpendo.1996.270.1.e133.

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Development of non-insulin-dependent diabetes mellitus (NIDDM) is associated with defects in glucose-stimulated insulin secretion. We have investigated Zucker diabetic fatty rats (ZDF), an animal model of NIDDM, and found that, compared with control islets, the expression of mRNA encoding C- and D-isoforms of alpha 1-subunits of beta-cell L-type voltage-dependent Ca2+ channels (VDCC) was significantly reduced in islets isolated from ZDF rats. This correlated with a substantial reduction of L-type Ca2+ currents (ICa) in ZDF beta-cells. Intracellular Ca2+ concentration responses in ZDF islets af

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21

Rutter, G. A., A. Varadi, T. Tsuboi, L. Parton, and M. Ravier. "Insulin secretion in health and disease: genomics, proteomics and single vesicle dynamics." Biochemical Society Transactions 34, no. 2 (2006): 247–50. http://dx.doi.org/10.1042/bst0340247.

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Defective insulin secretion from pancreatic islet β-cells is a sine qua non of Type II (non-insulin-dependent) diabetes. Digital imaging analysis of the nanomechanics of individual exocytotic events, achieved using total internal reflection fluorescence microscopy, has allowed us to demonstrate that insulin is released via transient or ‘cavicapture’ events whereby the vesicle and plasma membranes fuse transiently and reversibly. Such studies reveal that an increase in the number of abortive fusion events contributes to defective insulin secretion in in vitro models of Type II diabetes. Complem

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22

Rutter, Guy A., and Elaine V. Hill. "Insulin Vesicle Release: Walk, Kiss, Pause … Then Run." Physiology 21, no. 3 (2006): 189–96. http://dx.doi.org/10.1152/physiol.00002.2006.

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The mechanisms by which insulin-containing dense core secretory vesicles approach and finally fuse with the plasma membrane are of considerable current interest: defects in these processes may be one of the contributing factors to Type 2 diabetes. In this review, we discuss the molecular mechanisms involved in vesicle trafficking within the pancreatic β-cell and the mechanisms whereby these may be regulated. We then go on to describe recent evidence that suggests that vesicle fusion at the plasma membrane is a partly reversible process (“kiss and run” or “cavity recapture”). We propose that ve

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23

Salehi, Marzieh, Benedikt A. Aulinger та David A. D'Alessio. "Targeting β-Cell Mass in Type 2 Diabetes: Promise and Limitations of New Drugs Based on Incretins". Endocrine Reviews 29, № 3 (2008): 367–79. http://dx.doi.org/10.1210/er.2007-0031.

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Abstract Progressive insulin secretory defects, due to either functional abnormalities of the pancreatic β-cells or a reduction in β-cell mass, are the cornerstone of type 2 diabetes. Incretin-based drugs hold the potential to improve glucose tolerance by immediate favorable effect on β-cell physiology as well as by expanding or at least maintaining β-cell mass, which may delay the progression of the disease. Long-term studies in humans are needed to elaborate on these effects.

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24

Pørksen, Niels, Claus Juhl, Malene Hollingdal, et al. "Concordant induction of rapid in vivo pulsatile insulin secretion by recurrent punctuated glucose infusions." American Journal of Physiology-Endocrinology and Metabolism 278, no. 1 (2000): E162—E170. http://dx.doi.org/10.1152/ajpendo.2000.278.1.e162.

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Insulin is largely secreted as serial secretory bursts superimposed on basal release, insulin secretion is regulated through changes of pulse mass and frequency, and the insulin release pattern affects insulin action. Coordinate insulin release is preserved in the isolated perfused pancreas, suggesting intrapancreatic coordination. However, occurrence of glucose concentration oscillations may influence the process in vivo, as it does for ultradian oscillations. To determine if rapid pulsatile insulin release may be induced by minimal glucose infusions and to define the necessary glucose quanti

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25

Mohtarin, Sabreena, Md Matiur Rahman, Subrata Kumar Biswas, Forhadul Hoque Mollah, and M. Iqbal Arslan. "Study of phases of insulin secretion in pre-diabetes and newly diagnosed type 2 diabetes mellitus." Bangabandhu Sheikh Mujib Medical University Journal 8, no. 2 (2016): 85. http://dx.doi.org/10.3329/bsmmuj.v8i2.28927.

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<p><strong>Background:</strong> Insulin is released from the pancreas in a biphasic manner in response to arterial glucose concentration. The assumption has been generally made that the 30-minute response reflected first-phase insulin release, whereas the 120-minute response reflected second-phase insulin release.</p><p><strong>Objectives:</strong> The aim of this study was to identify the defect in first and second phases of insulin secretion in pre-diabetes and newly diagnosed T2DM.</p><p><strong>Methods:</strong> This case-co

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26

Eva, Sohely Nazneen, Rahelee Zinnat, Golam Morshed Molla, et al. "Type 2 Diabetes Mellitus is Associated with Lower Serum Adiponectin Level in Bangladeshi Population." Anwer Khan Modern Medical College Journal 6, no. 1 (2015): 10–13. http://dx.doi.org/10.3329/akmmcj.v6i1.24978.

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Background: The physiological role of adiponectin is not yet fully clear, but it is now generally accepted that it has a protective role against the development of lifestyle disorders, related to insulin resistance and atherosclerosis. Insulin resistance is one of the basic defects of type 2 diabetes (T2DM) and adiponectin is inversely associated with T2DM. As serum adiponectin level has not yet been investigated in Bangladeshi T2DM subjects,so that the present study has been under taken to find out the association of T2DM with serum adiponectin level in Bangladeshi population.Methodology: In

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27

Kabir, Md Golam, Mosaraf Hossain, Md Omar Faruque, Mohammad Alauddin, and Liaquat Ali. "Association of serum free IGF-1 and IGFBP-1 with insulin sensitivity and insulin secretory defects in Bangladeshi type 2 diabetes mellitus." Journal of Taibah University Medical Sciences 9, no. 2 (2014): 132–38. http://dx.doi.org/10.1016/j.jtumed.2013.11.006.

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28

Swisa, Avital, Zvi Granot, Natalia Tamarina, et al. "Loss of Liver Kinase B1 (LKB1) in Beta Cells Enhances Glucose-stimulated Insulin Secretion Despite Profound Mitochondrial Defects." Journal of Biological Chemistry 290, no. 34 (2015): 20934–46. http://dx.doi.org/10.1074/jbc.m115.639237.

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The tumor suppressor liver kinase B1 (LKB1) is an important regulator of pancreatic β cell biology. LKB1-dependent phosphorylation of distinct AMPK (adenosine monophosphate-activated protein kinase) family members determines proper β cell polarity and restricts β cell size, total β cell mass, and glucose-stimulated insulin secretion (GSIS). However, the full spectrum of LKB1 effects and the mechanisms involved in the secretory phenotype remain incompletely understood. We report here that in the absence of LKB1 in β cells, GSIS is dramatically and persistently improved. The enhancement is seen

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29

Kulkarni, R. N. "Receptors for insulin and insulin-like growth factor-1 and insulin receptor substrate-1 mediate pathways that regulate islet function." Biochemical Society Transactions 30, no. 2 (2002): 317–22. http://dx.doi.org/10.1042/bst0300317.

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The insulin/insulin-like growth factor-1 (IGF-1) signalling pathways are present in most mammalian cells and play important roles in the growth and metabolism of tissues. Most proteins in these pathways have also been identified in the β-cells of the pancreatic islets. Tissue-specific knockout of the insulin receptor (βIRKO) or IGF-1 receptor (βIGFRKO) in pancreatic β-cells leads to altered glucose-sensing and glucose intolerance in adult mice, and βIRKO mice show an age-dependent decrease in islet size and β-cell mass. These data indicate that these receptors are important for differentiated

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30

Fakruddin, Md. "Genetics of Type 2 Diabetes: A Review." Journal of Current and Advance Medical Research 6, no. 1 (2019): 59–63. http://dx.doi.org/10.3329/jcamr.v6i1.40787.

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Diabetes Mellitus (DM), one of the most non-communicable diseases, is increasing day by day in an alarming way. More than 140 million people are suffering from diabetes throughout the world. It is not a single disease entity, but rather a group of metabolic disorders sharing the common underlying feature of hyperglycemia. Hyperglycemia in diabetes results from defects in insulin secretion, insulin action, or, most commonly, both. The chronic hyperglycemia and attendant metabolic deregulation may be associated with secondary damage in multiple organ systems, especially the kidneys, eyes, nerves

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31

Mari, Andrea, Amalia Gastaldelli, Andrea Natali, Torben Ostergard, Ole Schmitz та Ele Ferrannini. "Characterization of β-cell function impairment in first-degree relatives of type 2 diabetic subjects: modeling analysis of 24-h triple-meal tests". American Journal of Physiology-Endocrinology and Metabolism 288, № 3 (2005): E541—E546. http://dx.doi.org/10.1152/ajpendo.00175.2004.

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To investigate early secretory defects in prediabetes, we evaluated β-Cell function and insulin sensitivity (M value, by euglycemic clamp) in 26 normotolerant first-degree relatives of type 2 diabetic patients (FDR) and 17 age- and weight-matched control subjects. β-Cell function was assessed by modeling analysis of glucose and C-peptide concentrations measured during 24 h of standardized living conditions. Fasting and total insulin secretion (ISR) were increased in FDR, as was ISR at a reference 5 mM glucose level (ISR5, 107 ± 6 vs. 87 ± 6 pmol· min−1·m−2, P < 0.05). ISR5 was inversely rel

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32

Eva, SN, GM Mollah, DK Sunyal, and R. Zinnat. "Type 2 diabetes mellitus is associated with lower serum adiponectin level in Bangladeshi population." Mediscope 2, no. 2 (2015): 16–21. http://dx.doi.org/10.3329/mediscope.v2i2.25405.

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The aim of the observational case control study was to find out the association of type 2 diabetes mellitus (T2DM) with serum adiponectin level in Bangladeshi population. This was conducted in the Biomedical Research Group, Research Division, Bangladesh Institute of Research and Rehabilitation in Diabetes, Endocrine and Metabolic Disorders (BIRDEM), Dhaka, Bangladesh. Sixty six T2DM subjects and seventy four healthy control subjects were included. Diabetes was diagnosed and classified as per World Health Organization criteria. Serum adiponectin was measured by Enzyme Linked Immunosorbent Assay

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33

Chamberlain, L. H., M. E. Graham, S. Kane, et al. "The synaptic vesicle protein, cysteine-string protein, is associated with the plasma membrane in 3T3-L1 adipocytes and interacts with syntaxin 4." Journal of Cell Science 114, no. 2 (2001): 445–55. http://dx.doi.org/10.1242/jcs.114.2.445.

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Adipocytes and muscle cells play a major role in blood glucose homeostasis. This is dependent upon the expression of Glut4, an insulin-responsive facilitative glucose transporter. Glut4 is localised to specialised intracellular vesicles that fuse with the plasma membrane in response to insulin stimulation. The insulin-induced translocation of Glut4 to the cell surface is essential for the maintenance of optimal blood glucose levels, and defects in this system are associated with insulin resistance and type II diabetes. Therefore, a major focus of recent research has been to identify and charac

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34

Leahy, Jack L., and Mark S. Fineman. "Impaired phasic insulin and amylin secretion in diabetic rats." American Journal of Physiology-Endocrinology and Metabolism 275, no. 3 (1998): E457—E462. http://dx.doi.org/10.1152/ajpendo.1998.275.3.e457.

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We have proposed that a hyperstimulated insulin secretion causing β-cell degranulation is the basis for the impaired glucose-potentiated insulin secretion in type 2 diabetes (“overworked β-cell”). To confirm this idea, we previously investigated tolbutamide-infused euglycemic rats. Two novel kinds of β-cell dysfunction were observed: altered phasic glucose-potentiated insulin secretion with preferential sparing of the first phase and a raised secreted ratio of amylin to insulin. The current study tested these parameters in 90% (intact β-cell insulin stores) and 95% (markedly lowered insulin st

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35

Morin, L., M. H. Giroix, M. N. Gangnerau, D. Bailbe, and B. Portha. "Impaired phosphoinositide metabolism in glucose-incompetent islets of neonatally streptozotocin-diabetic rats." American Journal of Physiology-Endocrinology and Metabolism 272, no. 5 (1997): E737—E745. http://dx.doi.org/10.1152/ajpendo.1997.272.5.e737.

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The effects of nutrient and neurotransmitter stimuli on insulin release, loss of phosphoinositides (PI), and production of inositol phosphates (InsP) were investigated in islets from neonatally streptozotocin-injected (nSTZ) rats. In islets from nSTZ rats, insulin secretory responses to 16.7 mM D-glucose and 10.0 mM D-glyceraldehyde were reduced compared with controls. Contents in phosphatidylinositol 4-monophosphate [PtdIns(4)P] and phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2], but not in phosphatidylinositol, were diminished. Glucose effects on breakdown of PtdIns(4)P and PtdIns(4,5

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36

Kalwat, Michael A., In Hyun Hwang, Jocelyn Macho та ін. "Chromomycin A2 potently inhibits glucose-stimulated insulin secretion from pancreatic β cells". Journal of General Physiology 150, № 12 (2018): 1747–57. http://dx.doi.org/10.1085/jgp.201812177.

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Modulators of insulin secretion could be used to treat diabetes and as tools to investigate β cell regulatory pathways in order to increase our understanding of pancreatic islet function. Toward this goal, we previously used an insulin-linked luciferase that is cosecreted with insulin in MIN6 β cells to perform a high-throughput screen of natural products for chronic effects on glucose-stimulated insulin secretion. In this study, using multiple phenotypic analyses, we found that one of the top natural product hits, chromomycin A2 (CMA2), potently inhibited insulin secretion by at least three p

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Jia, Dong Mei, Akinari Tabaru, Hayato Nakamura, Ken-Ichiro Fukumitsu, Toshiharu Akiyama, and Makoto Otsuki. "Troglitazone prevents and reverses dyslipidemia, insulin secretory defects, and histologic abnormalities in a rat model of naturally occurring obese diabetes." Metabolism 49, no. 9 (2000): 1167–75. http://dx.doi.org/10.1053/meta.2000.8599.

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38

Misler, Stanley. "Unifying concepts in stimulus-secretion coupling in endocrine cells and some implications for therapeutics." Advances in Physiology Education 33, no. 3 (2009): 175–86. http://dx.doi.org/10.1152/advan.90213.2008.

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Stimulus-secretion coupling (SSC) in endocrine cells remains underappreciated as a subject for the study/teaching of general physiology. In the present article, we review key new electrophysiological, electrochemical, and fluorescence optical techniques for the study of exocytosis in single cells that have made this a fertile area for recent research. Based on findings using these techniques, we developed a model of SSC for adrenal chromaffin cells that blends features of Ca2+ entry-dependent SSC (characteristic of neurons) with G protein receptor-coupled, Ca2+ release-dependent, and second me

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Curtis, S. B., та A. M. J. Buchan. "Proinsulin mRNA and peptide are present in β-cells of diabetic BB rats". Canadian Journal of Physiology and Pharmacology 73, № 1 (1995): 92–97. http://dx.doi.org/10.1139/y95-013.

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Previous studies have demonstrated that islets isolated from newly diabetic BB rat pancreata retain the ability to release insulin in culture, although in vivo the insulin response to stimulation is absent. The purpose of this study was to determine whether the β-cells in these newly diabetic animals were releasing stored insulin or whether they were still capable of insulin biosynthesis, since secretory defects may reflect abnormalities in insulin synthetic capacity. Insulin gene transcription was examined using in situ hybridization to detect preproinsulin mRNA (ppImRNA) at the level of the

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Zhang, Peichuan, Barbara McGrath, Sheng'ai Li та ін. "The PERK Eukaryotic Initiation Factor 2α Kinase Is Required for the Development of the Skeletal System, Postnatal Growth, and the Function and Viability of the Pancreas". Molecular and Cellular Biology 22, № 11 (2002): 3864–74. http://dx.doi.org/10.1128/mcb.22.11.3864-3874.2002.

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ABSTRACT Phosphorylation of eukaryotic initiation factor 2α (eIF-2α) is typically associated with stress responses and causes a reduction in protein synthesis. However, we found high phosphorylated eIF-2α (eIF-2α[P]) levels in nonstressed pancreata of mice. Administration of glucose stimulated a rapid dephosphorylation of eIF-2α. Among the four eIF-2α kinases present in mammals, PERK is most highly expressed in the pancreas, suggesting that it may be responsible for the high eIF-2α[P] levels found therein. We describe a Perk knockout mutation in mice. Pancreata of Perk−/− mice are morphologica

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Delghingaro-Augusto, Viviane, Simon Décary, Marie-Line Peyot та ін. "Voluntary running exercise prevents β-cell failure in susceptible islets of the Zucker diabetic fatty rat". American Journal of Physiology-Endocrinology and Metabolism 302, № 2 (2012): E254—E264. http://dx.doi.org/10.1152/ajpendo.00360.2011.

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Physical activity improves glycemic control in type 2 diabetes (T2D), but its contribution to preserving β-cell function is uncertain. We evaluated the role of physical activity on β-cell secretory function and glycerolipid/fatty acid (GL/FA) cycling in male Zucker diabetic fatty (ZDF) rats. Six-week-old ZDF rats engaged in voluntary running for 6 wk (ZDF-A). Inactive Zucker lean and ZDF (ZDF-I) rats served as controls. ZDF-I rats displayed progressive hyperglycemia with β-cell failure evidenced by falling insulinemia and reduced insulin secretion to oral glucose. Isolated ZDF-I rat islets sho

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Wilson, M. R., and S. J. Hughes. "The effect of maternal protein deficiency during pregnancy and lactation on glucose tolerance and pancreatic islet function in adult rat offspring." Journal of Endocrinology 154, no. 1 (1997): 177–85. http://dx.doi.org/10.1677/joe.0.1540177.

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Abstract To test the hypothesis that poor foetal–neonatal nutrition predisposes adult animals to impaired glucose tolerance or diabetes, pregnant and lactating rats were fed a low (5%) protein diet and glucose tolerance and pancreatic islet function then assessed in the adult offspring. To expose any underlying defects the offspring were allowed access to a sucrose supplement (35%) or fed a high fat diet. Offspring born to low protein-fed females had significantly lower body weights than controls. In islets from previously malnourished rats, insulin release in batch incubations or perifusion w

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Parton, Laura E., Patrick J. McMillen, Yingnian Shen, et al. "Limited role for SREBP-1c in defective glucose-induced insulin secretion from Zucker diabetic fatty rat islets: a functional and gene profiling analysis." American Journal of Physiology-Endocrinology and Metabolism 291, no. 5 (2006): E982—E994. http://dx.doi.org/10.1152/ajpendo.00067.2006.

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Accumulation of intracellular lipid may contribute to defective insulin secretion in type 2 diabetes. Although Zucker diabetic fatty (ZDF; fa/fa) rat islets are fat-laden and overexpress the lipogenic master gene, sterol regulatory element binding protein 1c (SREBP-1c), the contribution of SREBP-1c to the secretory defects observed in this model remains unclear. Here we compare the gene expression profile of lean control ( fa/+) and ZDF rat islets in the absence or presence of dominant-negative SREBP-1c (SREBP-1c DN). ZDF islets displayed elevated basal insulin secretion at 3 mmol/l glucose bu

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Jia, Dongmei, Masashi Taguchi, and Makoto Otsuki. "Synthetic protease inhibitor camostat prevents and reverses dyslipidemia, insulin secretory defects, and histological abnormalities of the pancreas in genetically obese and diabetic rats." Metabolism 54, no. 5 (2005): 619–27. http://dx.doi.org/10.1016/j.metabol.2004.12.005.

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Vauhkonen, Ilkka, Leo Niskanen, Mikael Knip, et al. "Subtle hyperproinsulinaemia characterises the defective insulin secretory capacity in offspring of glutamic acid decarboxylase antibody-positive patients with latent autoimmune diabetes mellitus in adults." European Journal of Endocrinology 153, no. 2 (2005): 265–73. http://dx.doi.org/10.1530/eje.1.01972.

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Objective: We set out to assess whether hyperproinsulinaemia is an early finding in latent autoimmune diabetes in adults (LADA). Research design and methods: We measured plasma proinsulin and C-peptide responses during a 2-h oral glucose tolerance test (OGTT) and in the hyperglycaemic clamp in 21 normoglycaemic offspring of LADA patients testing positive for glutamic acid decarboxylase antibodies (GADA) or islet cell antibodies (ICA), and in 17 healthy control subjects without a family history of diabetes. Results: The study groups had comparable areas under the curves of blood glucose, plasma

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Chen, Jianguo, Per Bendix Jeppesen, Iver Nordentoft та Kjeld Hermansen. "Stevioside improves pancreatic β-cell function during glucotoxicity via regulation of acetyl-CoA carboxylase". American Journal of Physiology-Endocrinology and Metabolism 292, № 6 (2007): E1906—E1916. http://dx.doi.org/10.1152/ajpendo.00356.2006.

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Chronic hyperglycemia is detrimental to pancreatic β-cells, causing impaired insulin secretion and β-cell turnover. The characteristic secretory defects are increased basal insulin secretion (BIS) and a selective loss of glucose-stimulated insulin secretion (GSIS). Several recent studies support the view that the acetyl-CoA carboxylase (ACC) plays a pivotal role for GSIS. We have shown that stevioside (SVS) enhances insulin secretion and ACC gene expression. Whether glucotoxicity influences ACC and whether this action can be counteracted by SVS are not known. To investigate this, we exposed is

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Tang, Kechun, Teresa Pasqua, Angshuman Biswas, et al. "Muscle injury, impaired muscle function and insulin resistance in Chromogranin A-knockout mice." Journal of Endocrinology 232, no. 2 (2017): 137–53. http://dx.doi.org/10.1530/joe-16-0370.

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Chromogranin A (CgA) is widely expressed in endocrine and neuroendocrine tissues as well as in the central nervous system. We observed CgA expression (mRNA and protein) in the gastrocnemius (GAS) muscle and found that performance of CgA-deficient Chga-KO mice in treadmill exercise was impaired. Supplementation with CgA in Chga-KO mice restored exercise ability suggesting a novel role for endogenous CgA in skeletal muscle function. Chga-KO mice display (i) lack of exercise-induced stimulation of pAKT, pTBC1D1 and phospho-p38 kinase signaling, (ii) loss of GAS muscle mass, (iii) extensive format

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Chen, Pei-Chun, Erik M. Olson, Qing Zhou, et al. "Carbamazepine as a Novel Small Molecule Corrector of Trafficking-impaired ATP-sensitive Potassium Channels Identified in Congenital Hyperinsulinism." Journal of Biological Chemistry 288, no. 29 (2013): 20942–54. http://dx.doi.org/10.1074/jbc.m113.470948.

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ATP-sensitive potassium (KATP) channels consisting of sulfonylurea receptor 1 (SUR1) and the potassium channel Kir6.2 play a key role in insulin secretion by coupling metabolic signals to β-cell membrane potential. Mutations in SUR1 and Kir6.2 that impair channel trafficking to the cell surface lead to loss of channel function and congenital hyperinsulinism. We report that carbamazepine, an anticonvulsant, corrects the trafficking defects of mutant KATP channels previously identified in congenital hyperinsulinism. Strikingly, of the 19 SUR1 mutations examined, only those located in the first t

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Roma, L. P., S. M. Pascal, J. Duprez, and J. C. Jonas. "Mitochondrial oxidative stress contributes differently to rat pancreatic islet cell apoptosis and insulin secretory defects after prolonged culture in a low non-stimulating glucose concentration." Diabetologia 55, no. 8 (2012): 2226–37. http://dx.doi.org/10.1007/s00125-012-2581-6.

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Dalan, Rinkoo, Stefan R. Bornstein, Ali El-Armouche, et al. "The ACE-2 in COVID-19: Foe or Friend?" Hormone and Metabolic Research 52, no. 05 (2020): 257–63. http://dx.doi.org/10.1055/a-1155-0501.

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AbstractCOVID-19 is a rapidly spreading outbreak globally. Emerging evidence demonstrates that older individuals and people with underlying metabolic conditions of diabetes mellitus, hypertension, and hyperlipidemia are at higher risk of morbidity and mortality. The SARS-CoV-2 infects humans through the angiotensin converting enzyme (ACE-2) receptor. The ACE-2 receptor is a part of the dual system renin-angiotensin-system (RAS) consisting of ACE-Ang-II-AT1R axis and ACE-2-Ang-(1–7)-Mas axis. In metabolic disorders and with increased age, it is known that there is an upregulation of ACE-Ang-II-

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