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Journal articles on the topic 'Energy and glucose homeostasis'

Author: Grafiati

Published: 28 September 2024

Last updated: 31 July 2025

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1

Lam, Carol K. L., Madhu Chari, and Tony K. T. Lam. "CNS Regulation of Glucose Homeostasis." Physiology 24, no. 3 (2009): 159–70. http://dx.doi.org/10.1152/physiol.00003.2009.

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The past decade has hosted a remarkable surge in research dedicated to the central control of homeostatic mechanisms. Evidence indicates that the brain, in particular the hypothalamus, directly senses hormones and nutrients to initiate behavioral and metabolic responses to control energy and nutrient homeostasis. Diabetes is chiefly characterized by hyperglycemia due to impaired glucose homeostatic regulation, and a primary therapeutic goal is to lower plasma glucose levels. As such, in this review, we highlight the role of the hypothalamus in the regulation of glucose homeostasis in particula

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Assistant, Professor Farida Rozy. "Comparison of Insulin and Glucagon in the Regulation of Blood Glucose Levels." ISRG Journal of Arts Humanities & Social Sciences (ISRGJAHSS) III, no. III (2025): 147–52. https://doi.org/10.5281/zenodo.15454908.

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<em>Maintaining blood glucose levels is of vital importance, as glucose serves as the primary energy source for body cells. Therefore, to ensure adequate energy supply, body tissues and cells—particularly brain cells—rely on glucose as a principal energy substrate. The objectives of this study are to examine and compare the roles of insulin and glucagon in regulating blood glucose levels, explore their metabolic impacts, identify the mechanisms of action of these two hormones, and investigate how they interact to maintain glucose homeostasis. Furthermore, the study assesses complic

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Pattaranit, Ratchada, and Hugo Antonius van den Berg. "Mathematical models of energy homeostasis." Journal of The Royal Society Interface 5, no. 27 (2008): 1119–35. http://dx.doi.org/10.1098/rsif.2008.0216.

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Diabetes and obesity present a mounting global challenge. Clinicians are increasingly turning to mechanism-based mathematical models for a quantitative definition of physiological defects such as insulin resistance, glucose intolerance and elevated obesity set points, and for predictions of the likely outcomes of therapeutic interventions. However, a very large range of such models is available, making a judicious choice difficult. To better inform this choice, here we present the most important models published to date in a uniform format, discussing similarities and differences in terms of t

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4

Marty, Nell, Michel Dallaporta, and Bernard Thorens. "Brain Glucose Sensing, Counterregulation, and Energy Homeostasis." Physiology 22, no. 4 (2007): 241–51. http://dx.doi.org/10.1152/physiol.00010.2007.

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Neuronal circuits in the central nervous system play a critical role in orchestrating the control of glucose and energy homeostasis. Glucose, beside being a nutrient, is also a signal detected by several glucose-sensing units that are located at different anatomical sites and converge to the hypothalamus to cooperate with leptin and insulin in controlling the melanocortin pathway.

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López-Gambero, A. J., F. Martínez, K. Salazar, M. Cifuentes, and F. Nualart. "Brain Glucose-Sensing Mechanism and Energy Homeostasis." Molecular Neurobiology 56, no. 2 (2018): 769–96. http://dx.doi.org/10.1007/s12035-018-1099-4.

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Soty, Maud, Amandine Gautier-Stein, Fabienne Rajas, and Gilles Mithieux. "Gut-Brain Glucose Signaling in Energy Homeostasis." Cell Metabolism 25, no. 6 (2017): 1231–42. http://dx.doi.org/10.1016/j.cmet.2017.04.032.

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Wang, Yan, Markey C. McNutt, Serena Banfi, et al. "Hepatic ANGPTL3 regulates adipose tissue energy homeostasis." Proceedings of the National Academy of Sciences 112, no. 37 (2015): 11630–35. http://dx.doi.org/10.1073/pnas.1515374112.

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Angiopoietin-like protein 3 (ANGPTL3) is a circulating inhibitor of lipoprotein and endothelial lipase whose physiological function has remained obscure. Here we show that ANGPTL3 plays a major role in promoting uptake of circulating very low density lipoprotein-triglycerides (VLDL-TGs) into white adipose tissue (WAT) rather than oxidative tissues (skeletal muscle, heart brown adipose tissue) in the fed state. This conclusion emerged from studies of Angptl3−/− mice. Whereas feeding increased VLDL-TG uptake into WAT eightfold in wild-type mice, no increase occurred in fed Angptl3−/− animals. De

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Seo, J., E. S. Fortuno, J. M. Suh, et al. "Atf4 Regulates Obesity, Glucose Homeostasis, and Energy Expenditure." Diabetes 58, no. 11 (2009): 2565–73. http://dx.doi.org/10.2337/db09-0335.

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9

Giridharan, NV. "Glucose & energy homeostasis: Lessons from animal studies." Indian Journal of Medical Research 148, no. 5 (2018): 659. http://dx.doi.org/10.4103/ijmr.ijmr_1737_18.

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Pepino, Marta Y., and Christina Bourne. "Non-nutritive sweeteners, energy balance, and glucose homeostasis." Current Opinion in Clinical Nutrition and Metabolic Care 14, no. 4 (2011): 391–95. http://dx.doi.org/10.1097/mco.0b013e3283468e7e.

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11

van Praag, H., M. Fleshner, M. W. Schwartz, and M. P. Mattson. "Exercise, Energy Intake, Glucose Homeostasis, and the Brain." Journal of Neuroscience 34, no. 46 (2014): 15139–49. http://dx.doi.org/10.1523/jneurosci.2814-14.2014.

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12

Plum, L. "Central insulin action in energy and glucose homeostasis." Journal of Clinical Investigation 116, no. 7 (2006): 1761–66. http://dx.doi.org/10.1172/jci29063.

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13

Cheung, Grace W. C., Andrea Kokorovic, and Tony K. T. Lam. "Upper intestinal lipids regulate energy and glucose homeostasis." Cellular and Molecular Life Sciences 66, no. 18 (2009): 3023–27. http://dx.doi.org/10.1007/s00018-009-0062-y.

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14

Ali, Ifrah Ismail, Crystal D’Souza, Jaipaul Singh, and Ernest Adeghate. "Adropin’s Role in Energy Homeostasis and Metabolic Disorders." International Journal of Molecular Sciences 23, no. 15 (2022): 8318. http://dx.doi.org/10.3390/ijms23158318.

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Adropin is a novel 76-amino acid-peptide that is expressed in different tissues and cells including the liver, pancreas, heart and vascular tissues, kidney, milk, serum, plasma and many parts of the brain. Adropin, encoded by the Enho gene, plays a crucial role in energy homeostasis. The literature review indicates that adropin alleviates the degree of insulin resistance by reducing endogenous hepatic glucose production. Adropin improves glucose metabolism by enhancing glucose utilization in mice, including the sensitization of insulin signaling pathways such as Akt phosphorylation and the act

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Savino, Francesco, Stefania Alfonsina Liguori, Miriam Sorrenti, Maria Francesca Fissore, and Roberto Oggero. "Breast Milk Hormones and Regulation of Glucose Homeostasis." International Journal of Pediatrics 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/803985.

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Growing evidence suggests that a complex relationship exists between the central nervous system and peripheral organs involved in energy homeostasis. It consists in the balance between food intake and energy expenditure and includes the regulation of nutrient levels in storage organs, as well as in blood, in particular blood glucose. Therefore, food intake, energy expenditure, and glucose homeostasis are strictly connected to each other. Several hormones, such as leptin, adiponectin, resistin, and ghrelin, are involved in this complex regulation. These hormones play a role in the regulation of

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Shen, Minqian, and Haifei Shi. "Sex Hormones and Their Receptors Regulate Liver Energy Homeostasis." International Journal of Endocrinology 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/294278.

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The liver is one of the most essential organs involved in the regulation of energy homeostasis. Hepatic steatosis, a major manifestation of metabolic syndrome, is associated with imbalance between lipid formation and breakdown, glucose production and catabolism, and cholesterol synthesis and secretion. Epidemiological studies show sex difference in the prevalence in fatty liver disease and suggest that sex hormones may play vital roles in regulating hepatic steatosis. In this review, we summarize current literature and discuss the role of estrogens and androgens and the mechanisms through whic

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Aloqaily, Bahaa, Hyokjoon Kwon, Sarmed Al-Samerria, Ariel L. Negron, Fredric Edward Wondisford, and Sally Radovick. "Liver-Specific Kisspeptin Deletion Impairs Energy Metabolism in Mice." Journal of the Endocrine Society 5, Supplement_1 (2021): A440—A441. http://dx.doi.org/10.1210/jendso/bvab048.900.

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Abstract Kisspeptin, a neuroendocrine protein critical for the control of pubertal development and fertility has been shown to be modulated by nutritional signals. While the secretion of kisspeptin from specific hypothalamic nuclei is well-known to regulate GnRH-mediated pubertal maturation and reproduction, it remains unclear what role peripheral kisspeptin, specifically of hepatic origin, plays in regulating metabolism and glucose homeostasis. To define the role of kisspeptin in the liver, we developed a novel Kiss1f/f mouse line and targeted liver-specific Kiss1 ablation by injecting a AAV8

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Rourke, Jillian L., Shanmugam Muruganandan, Helen J. Dranse, Nichole M. McMullen, and Christopher J. Sinal. "Gpr1 is an active chemerin receptor influencing glucose homeostasis in obese mice." Journal of Endocrinology 222, no. 2 (2014): 201–15. http://dx.doi.org/10.1530/joe-14-0069.

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Chemerin is an adipose-derived signaling protein (adipokine) that regulates adipocyte differentiation and function, immune function, metabolism, and glucose homeostasis through activation of chemokine-like receptor 1 (CMKLR1). A second chemerin receptor, G protein-coupled receptor 1 (GPR1) in mammals, binds chemerin with an affinity similar to CMKLR1; however, the function of GPR1 in mammals is essentially unknown. Herein, we report that expression of murineGpr1mRNA is high in brown adipose tissue and white adipose tissue (WAT) and skeletal muscle. In contrast to chemerin (Rarres2) andCmklr1,G

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Sahu, Maitrayee, Prashanth Anamthathmakula, and Abhiram Sahu. "Hypothalamic PDE3B deficiency alters body weight and glucose homeostasis in mouse." Journal of Endocrinology 239, no. 1 (2018): 93–105. http://dx.doi.org/10.1530/joe-18-0304.

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Pharmacological studies have suggested hypothalamic phosphodiesterase-3B to mediate leptin and insulin action in regulation of energy homeostasis. Whereas Pde3b-null mice show altered energy homeostasis, it is unknown whether this is due to ablation of Pde3b in the hypothalamus. Thus, to address the functional significance of hypothalamic phosphodiesterase-3B, we used Pde3b flox/flox and Nkx2.1-Cre mice to generate Pde3b Nkx2.1KD mice that showed 50% reduction of phosphodiesterase-3B in the hypothalamus. To determine the effect of partial ablation of phosphodiesterase-3B in the hypothalamus on

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20

Levin, Barry E., Ambrose A. Dunn-Meynell, and Vanessa H. Routh. "Brain glucose sensing and body energy homeostasis: role in obesity and diabetes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 5 (1999): R1223—R1231. http://dx.doi.org/10.1152/ajpregu.1999.276.5.r1223.

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The brain has evolved mechanisms for sensing and regulating glucose metabolism. It receives neural inputs from glucosensors in the periphery but also contains neurons that directly sense changes in glucose levels by using glucose as a signal to alter their firing rate. Glucose-responsive (GR) neurons increase and glucose-sensitive (GS) decrease their firing rate when brain glucose levels rise. GR neurons use an ATP-sensitive K+ channel to regulate their firing. The mechanism regulating GS firing is less certain. Both GR and GS neurons respond to, and participate in, the changes in food intake,

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21

Perez, Katia M., Kathleen L. Curley, James C. Slaughter, and Ashley H. Shoemaker. "Glucose Homeostasis and Energy Balance in Children With Pseudohypoparathyroidism." Journal of Clinical Endocrinology & Metabolism 103, no. 11 (2018): 4265–74. http://dx.doi.org/10.1210/jc.2018-01067.

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22

Morton, Gregory J. "Hypothalamic leptin regulation of energy homeostasis and glucose metabolism." Journal of Physiology 583, no. 2 (2007): 437–43. http://dx.doi.org/10.1113/jphysiol.2007.135590.

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23

Rosen, Evan D., and Bruce M. Spiegelman. "Adipocytes as regulators of energy balance and glucose homeostasis." Nature 444, no. 7121 (2006): 847–53. http://dx.doi.org/10.1038/nature05483.

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24

Sridhar, Gumpeny R., and Gumpeny Lakshmi. "Bone-derived secretory proteins and glucose and energy homeostasis." Adipobiology 2 (December 31, 2010): 67. http://dx.doi.org/10.14748/adipo.v2.262.

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25

Katagiri, Hideki. "Neuronal information highways for maintaining glucose and energy homeostasis." Neuroscience Research 71 (September 2011): e26-e27. http://dx.doi.org/10.1016/j.neures.2011.07.113.

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26

Massart, Julie, and Juleen R. Zierath. "Role of Diacylglycerol Kinases in Glucose and Energy Homeostasis." Trends in Endocrinology & Metabolism 30, no. 9 (2019): 603–17. http://dx.doi.org/10.1016/j.tem.2019.06.003.

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27

Kleinridders, André, A. Christine Könner, and Jens C. Brüning. "CNS-targets in control of energy and glucose homeostasis." Current Opinion in Pharmacology 9, no. 6 (2009): 794–804. http://dx.doi.org/10.1016/j.coph.2009.10.006.

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28

Coué, Marine, and Cedric Moro. "Natriuretic peptide control of energy balance and glucose homeostasis." Biochimie 124 (May 2016): 84–91. http://dx.doi.org/10.1016/j.biochi.2015.05.017.

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29

Amoasii, Leonela, Efrain Sanchez-Ortiz, Teppei Fujikawa, Joel K. Elmquist, Rhonda Bassel-Duby, and Eric N. Olson. "NURR1 activation in skeletal muscle controls systemic energy homeostasis." Proceedings of the National Academy of Sciences 116, no. 23 (2019): 11299–308. http://dx.doi.org/10.1073/pnas.1902490116.

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Skeletal muscle plays a central role in the control of metabolism and exercise tolerance. Analysis of muscle enhancers activated after exercise in mice revealed the orphan nuclear receptor NURR1/NR4A2 as a prominent component of exercise-responsive enhancers. We show that exercise enhances the expression of NURR1, and transgenic overexpression of NURR1 in skeletal muscle enhances physical performance in mice. NURR1 expression in skeletal muscle is also sufficient to prevent hyperglycemia and hepatic steatosis, by enhancing muscle glucose uptake and storage as glycogen. Furthermore, treatment o

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McGrath, Thomas, Kevin G. Murphy, and Nick S. Jones. "Quantitative approaches to energy and glucose homeostasis: machine learning and modelling for precision understanding and prediction." Journal of The Royal Society Interface 15, no. 138 (2018): 20170736. http://dx.doi.org/10.1098/rsif.2017.0736.

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Obesity is a major global public health problem. Understanding how energy homeostasis is regulated, and can become dysregulated, is crucial for developing new treatments for obesity. Detailed recording of individual behaviour and new imaging modalities offer the prospect of medically relevant models of energy homeostasis that are both understandable and individually predictive. The profusion of data from these sources has led to an interest in applying machine learning techniques to gain insight from these large, relatively unstructured datasets. We review both physiological models and machine

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Shi, Haifei, April D. Strader, Stephen C. Woods, and Randy J. Seeley. "The effect of fat removal on glucose tolerance is depot specific in male and female mice." American Journal of Physiology-Endocrinology and Metabolism 293, no. 4 (2007): E1012—E1020. http://dx.doi.org/10.1152/ajpendo.00649.2006.

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Energy is stored predominately as lipid in white adipose tissue (WAT) in distinct anatomical locations, with each site exerting different effects on key biological processes, including glucose homeostasis. To determine the relative contributions of subcutaneous and visceral WAT on glucose homeostasis, comparable amounts of adipose tissue from abdominal subcutaneous inguinal WAT (IWAT), intra-abdominal retroperitoneal WAT (RWAT), male gonadal epididymal WAT (EWAT), or female gonadal parametrial WAT (PWAT) were removed. Gonadal fat removal in both male and female chow-fed lean mice resulted in l

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Liu, Zhuo, Yang Zhou, Xuecheng Qu, et al. "A Self-Powered Optogenetic System for Implantable Blood Glucose Control." Research 2022 (June 17, 2022): 1–13. http://dx.doi.org/10.34133/2022/9864734.

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Diabetes treatment and rehabilitation are usually a lifetime process. Optogenetic engineered designer cell-therapy holds great promise in regulating blood glucose homeostasis. However, portable, sustainable, and long-term energy supplementation has previously presented a challenge for the use of optogenetic stimulation in vivo. Herein, we purpose a self-powered optogenetic system (SOS) for implantable blood glucose control. The SOS consists of a biocompatible far-red light (FRL) source, FRL-triggered transgene-expressing cells, a power management unit, and a flexible implantable piezoelectric

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Jones, B. J., T. Tan, and S. R. Bloom. "Minireview: Glucagon in Stress and Energy Homeostasis." Endocrinology 153, no. 3 (2012): 1049–54. http://dx.doi.org/10.1210/en.2011-1979.

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Glucagon is traditionally thought of as an antihypoglycemic hormone, for example in response to starvation. However, it actually increases energy expenditure and has other actions not in line with protection from hypoglycemia. Furthermore, it is often found to be elevated when glucose is also raised, for example in circumstances of psychological and metabolic stress. These findings seem more in keeping with glucagon having some role as a hormone enhancing the response to stress.

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Hargett, Stefan R., Natalie N. Walker, and Susanna R. Keller. "Rab GAPs AS160 and Tbc1d1 play nonredundant roles in the regulation of glucose and energy homeostasis in mice." American Journal of Physiology-Endocrinology and Metabolism 310, no. 4 (2016): E276—E288. http://dx.doi.org/10.1152/ajpendo.00342.2015.

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The related Rab GTPase-activating proteins (Rab GAPs) AS160 and Tbc1d1 regulate the trafficking of the glucose transporter GLUT4 that controls glucose uptake in muscle and fat cells and glucose homeostasis. AS160- and Tbc1d1-deficient mice exhibit different adipocyte- and skeletal muscle-specific defects in glucose uptake, GLUT4 expression and trafficking, and glucose homeostasis. A recent study analyzed male mice with simultaneous deletion of AS160 and Tbc1d1 (AS160−/−/Tbc1d1−/− mice). Herein, we describe abnormalities in male and female AS160−/−/Tbc1d1−/− mice on another strain background. W

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Shi, Haifei, April D. Strader, Joyce E. Sorrell, James B. Chambers, Stephen C. Woods, and Randy J. Seeley. "Sexually different actions of leptin in proopiomelanocortin neurons to regulate glucose homeostasis." American Journal of Physiology-Endocrinology and Metabolism 294, no. 3 (2008): E630—E639. http://dx.doi.org/10.1152/ajpendo.00704.2007.

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Leptin regulates energy balance and glucose homeostasis, at least in part, via activation of receptors in the arcuate nucleus of the hypothalamus located in proopiomelanocortin (POMC) neurons. Females have greater sensitivity to central leptin than males, suggested by a greater anorectic effect of central leptin administration in females. We hypothesized that the regulation of energy balance and peripheral glucose homeostasis of female rodents would be affected to a greater extent than in males if the action of leptin in POMC neurons were disturbed. Male and female mice lacking leptin receptor

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Song, Seon, and Eun Hwang. "A Rise in ATP, ROS, and Mitochondrial Content upon Glucose Withdrawal Correlates with a Dysregulated Mitochondria Turnover Mediated by the Activation of the Protein Deacetylase SIRT1." Cells 8, no. 1 (2018): 11. http://dx.doi.org/10.3390/cells8010011.

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Glucose withdrawal has been used as a model for the study of homeostatic defense mechanisms, especially for how cells cope with a shortage of nutrient supply by enhancing catabolism. However, detailed cellular responses to glucose withdrawal have been poorly studied, and are controversial. In this study, we determined how glucose withdrawal affects mitochondrial activity, and the quantity and the role of SIRT1 in these changes. The results of our study indicate a substantial increase in ATP production from mitochondria, through an elevation of mitochondrial biogenesis, mediated by SIRT1 activa

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Guan, Xinfu. "The CNS glucagon-like peptide-2 receptor in the control of energy balance and glucose homeostasis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 6 (2014): R585—R596. http://dx.doi.org/10.1152/ajpregu.00096.2014.

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The gut-brain axis plays a key role in the control of energy balance and glucose homeostasis. In response to luminal stimulation of macronutrients and microbiota-derived metabolites (secondary bile acids and short chain fatty acids), glucagon-like peptides (GLP-1 and -2) are cosecreted from endocrine L cells in the gut and coreleased from preproglucagonergic neurons in the brain stem. Glucagon-like peptides are proposed as key mediators for bariatric surgery-improved glycemic control and energy balance. Little is known about the GLP-2 receptor (Glp2r)-mediated physiological roles in the contro

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Pydi, Sai P., Luiz F. Barella, Lu Zhu, Jaroslawna Meister, Mario Rossi та Jürgen Wess. "β-Arrestins as Important Regulators of Glucose and Energy Homeostasis". Annual Review of Physiology 84, № 1 (2022): 17–40. http://dx.doi.org/10.1146/annurev-physiol-060721-092948.

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β-Arrestin-1 and -2 (also known as arrestin-2 and -3, respectively) are ubiquitously expressed cytoplasmic proteins that dampen signaling through G protein–coupled receptors. However, β-arrestins can also act as signaling molecules in their own right. To investigate the potential metabolic roles of the two β-arrestins in modulating glucose and energy homeostasis, recent studies analyzed mutant mice that lacked or overexpressed β-arrestin-1 and/or -2 in distinct, metabolically important cell types. Metabolic analysis of these mutant mice clearly demonstrated that both β-arrestins play key roles

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Myers, Martin G., Alison H. Affinati, Nicole Richardson, and Michael W. Schwartz. "Central nervous system regulation of organismal energy and glucose homeostasis." Nature Metabolism 3, no. 6 (2021): 737–50. http://dx.doi.org/10.1038/s42255-021-00408-5.

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Ren, Decheng, Yingjiang Zhou, David Morris, Minghua Li, Zhiqin Li, and Liangyou Rui. "Neuronal SH2B1 is essential for controlling energy and glucose homeostasis." Journal of Clinical Investigation 117, no. 2 (2007): 397–406. http://dx.doi.org/10.1172/jci29417.

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Li, C., P. Chen, J. Vaughan, K. F. Lee, and W. Vale. "Urocortin 3 regulates glucose-stimulated insulin secretion and energy homeostasis." Proceedings of the National Academy of Sciences 104, no. 10 (2007): 4206–11. http://dx.doi.org/10.1073/pnas.0611641104.

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Kocalis, Heidi E., Scott L. Hagan, Leena George, et al. "Rictor/mTORC2 facilitates central regulation of energy and glucose homeostasis." Molecular Metabolism 3, no. 4 (2014): 394–407. http://dx.doi.org/10.1016/j.molmet.2014.01.014.

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WANG, CHUNMEI, YANLIN HE, PINGWEN XU, YONGJIE YANG, and YONG XU. "TAp63 in Mature POMC Neurons Regulates Glucose and Energy Homeostasis." Diabetes 67, Supplement 1 (2018): 1796—P. http://dx.doi.org/10.2337/db18-1796-p.

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Kaneko, Kentaro, Pingwen Xu, Elizabeth L. Cordonier, et al. "Neuronal Rap1 Regulates Energy Balance, Glucose Homeostasis, and Leptin Actions." Cell Reports 16, no. 11 (2016): 3003–15. http://dx.doi.org/10.1016/j.celrep.2016.08.039.

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El-Mehdi, Mouna, Saloua Takhlidjt, Fayrouz Khiar, et al. "Glucose homeostasis is impaired in mice deficient in the neuropeptide 26RFa (QRFP)." BMJ Open Diabetes Research & Care 8, no. 1 (2020): e000942. http://dx.doi.org/10.1136/bmjdrc-2019-000942.

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Introduction26RFa (pyroglutamyl RFamide peptide (QRFP)) is a biologically active peptide that has been found to control feeding behavior by stimulating food intake, and to regulate glucose homeostasis by acting as an incretin. The aim of the present study was thus to investigate the impact of 26RFa gene knockout on the regulation of energy and glucose metabolism.Research design and methods26RFa mutant mice were generated by homologous recombination, in which the entire coding region of prepro26RFa was replaced by the iCre sequence. Energy and glucose metabolism was evaluated through measuremen

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Hill, Jennifer W., Yong Xu, Frederic Preitner, et al. "Phosphatidyl Inositol 3-Kinase Signaling in Hypothalamic Proopiomelanocortin Neurons Contributes to the Regulation of Glucose Homeostasis." Endocrinology 150, no. 11 (2009): 4874–82. http://dx.doi.org/10.1210/en.2009-0454.

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Recent studies demonstrated a role for hypothalamic insulin and leptin action in the regulation of glucose homeostasis. This regulation involves proopiomelanocortin (POMC) neurons because suppression of phosphatidyl inositol 3-kinase (PI3K) signaling in these neurons blunts the acute effects of insulin and leptin on POMC neuronal activity. In the current study, we investigated whether disruption of PI3K signaling in POMC neurons alters normal glucose homeostasis using mouse models designed to both increase and decrease PI3K-mediated signaling in these neurons. We found that deleting p85α alone

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Beckoff, Katherine, Caroline G. MacIntosh, Ian M. Chapman, et al. "Effects of glucose supplementation on gastric emptying, blood glucose homeostasis, and appetite in the elderly." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 2 (2001): R570—R576. http://dx.doi.org/10.1152/ajpregu.2001.280.2.r570.

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The aims of this study were to evaluate the effects of dietary glucose supplementation on gastric emptying (GE) of both glucose and fat, postprandial blood glucose homeostasis, and appetite in eight older subjects (4 males, 4 females, aged 65–84 yr). GE of a drink (15 ml olive oil and 33 g glucose dissolved in 185 ml water), blood glucose, insulin, gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), and appetite (diet diaries, visual analog scales, and food intake at a buffet meal consumed after the GE study) were evaluated twice, after 10 days on a standard or a glucose-

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Escolero, Vanessa, Laica Tolentino, Abdul Bari Muhammad, Abdul Hamid, and Kabirullah Lutfy. "The Involvement of Endogenous Enkephalins in Glucose Homeostasis." Biomedicines 11, no. 3 (2023): 671. http://dx.doi.org/10.3390/biomedicines11030671.

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Obesity has nearly tripled since 1975 and is predicted to continue to escalate. The surge in obesity is expected to increase the risk of diabetes type 2, hypertension, coronary artery disease, and stroke. Therefore, it is essential to better understand the mechanisms that regulate energy and glucose homeostasis. The opioid system is implicated in regulating both aspects (hedonic and homeostatic) of food intake. Specifically, in the present study, we investigated the role of endogenous enkephalins in changes in food intake and glucose homeostasis. We used preproenkephalin (ppENK) knockout mice

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Olson, Ann Louise, and Kenneth Humphries. "Recent advances in understanding glucose transport and glucose disposal." F1000Research 9 (June 24, 2020): 639. http://dx.doi.org/10.12688/f1000research.22237.1.

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Deficient glucose transport and glucose disposal are key pathologies leading to impaired glucose tolerance and risk of type 2 diabetes. The cloning and identification of the family of facilitative glucose transporters have helped to identify that underlying mechanisms behind impaired glucose disposal, particularly in muscle and adipose tissue. There is much more than just transporter protein concentration that is needed to regulate whole body glucose uptake and disposal. The purpose of this review is to discuss recent findings in whole body glucose disposal. We hypothesize that impaired glucos

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Eržen, Stjepan, Gašper Tonin, Dubravka Jurišić Eržen, and Jasna Klen. "Amylin, Another Important Neuroendocrine Hormone for the Treatment of Diabesity." International Journal of Molecular Sciences 25, no. 3 (2024): 1517. http://dx.doi.org/10.3390/ijms25031517.

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Diabetes mellitus is a devastating chronic metabolic disease. Since the majority of type 2 diabetes mellitus patients are overweight or obese, a novel term—diabesity—has emerged. The gut–brain axis plays a critical function in maintaining glucose and energy homeostasis and involves a variety of peptides. Amylin is a neuroendocrine anorexigenic polypeptide hormone, which is co-secreted with insulin from β-cells of the pancreas in response to food consumption. Aside from its effect on glucose homeostasis, amylin inhibits homeostatic and hedonic feeding, induces satiety, and decreases body weight

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