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Journal articles on the topic 'Energy and glucose homeostasis'

Author: Grafiati

Published: 28 September 2024

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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 (June 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 particular and discuss the cellular and molecular mechanisms by which this neural pathway is orchestrated.

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2

Pattaranit, Ratchada, and Hugo Antonius van den Berg. "Mathematical models of energy homeostasis." Journal of The Royal Society Interface 5, no. 27 (July 8, 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 the decisions faced by modellers. We review models for glucostasis, based on the glucose–insulin feedback control loop, and consider extensions to long-term energy balance, dislipidaemia and obesity.

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3

Marty, Nell, Michel Dallaporta, and Bernard Thorens. "Brain Glucose Sensing, Counterregulation, and Energy Homeostasis." Physiology 22, no. 4 (August 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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4

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 (May 24, 2018): 769–96. http://dx.doi.org/10.1007/s12035-018-1099-4.

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5

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

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6

Wang, Yan, Markey C. McNutt, Serena Banfi, Michael G. Levin, William L. Holland, Viktoria Gusarova, Jesper Gromada, Jonathan C. Cohen, and Helen H. Hobbs. "Hepatic ANGPTL3 regulates adipose tissue energy homeostasis." Proceedings of the National Academy of Sciences 112, no. 37 (August 24, 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. Despite the reduction in delivery to and retention of TG in WAT, fat mass was largely preserved by a compensatory increase in de novo lipogenesis in Angptl3−/− mice. Glucose uptake into WAT was increased 10-fold in KO mice, and tracer studies revealed increased conversion of glucose to fatty acids in WAT but not liver. It is likely that the increased uptake of glucose into WAT explains the increased insulin sensitivity associated with inactivation of ANGPTL3. The beneficial effects of ANGPTL3 deficiency on both glucose and lipoprotein metabolism make it an attractive therapeutic target.

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7

Seo, J., E. S. Fortuno, J. M. Suh, D. Stenesen, W. Tang, E. J. Parks, C. M. Adams, T. Townes, and J. M. Graff. "Atf4 Regulates Obesity, Glucose Homeostasis, and Energy Expenditure." Diabetes 58, no. 11 (August 18, 2009): 2565–73. http://dx.doi.org/10.2337/db09-0335.

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8

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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9

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 (July 2011): 391–95. http://dx.doi.org/10.1097/mco.0b013e3283468e7e.

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10

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 (November 12, 2014): 15139–49. http://dx.doi.org/10.1523/jneurosci.2814-14.2014.

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11

Plum, L. "Central insulin action in energy and glucose homeostasis." Journal of Clinical Investigation 116, no. 7 (July 3, 2006): 1761–66. http://dx.doi.org/10.1172/jci29063.

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12

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 (June 10, 2009): 3023–27. http://dx.doi.org/10.1007/s00018-009-0062-y.

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13

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 (July 28, 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 activation of the glucose transporter 4 receptor. Several studies have also demonstrated that adropin improves cardiac function, cardiac efficiency and coronary blood flow in mice. Adropin can also reduce the levels of serum triglycerides, total cholesterol and low-density lipoprotein cholesterol. In contrast, it increases the level of high-density lipoprotein cholesterol, often referred to as the beneficial cholesterol. Adropin inhibits inflammation by reducing the tissue level of pro-inflammatory cytokines such as tumor necrosis factor alpha and interleukin-6. The protective effect of adropin on the vascular endothelium is through an increase in the expression of endothelial nitric oxide synthase. This article provides an overview of the existing literature about the role of adropin in different pathological conditions.

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14

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 which estrogen receptors and androgen receptors regulate lipid and glucose metabolism in the liver. In females, estradiol regulates liver metabolism via estrogen receptors by decreasing lipogenesis, gluconeogenesis, and fatty acid uptake, while enhancing lipolysis, cholesterol secretion, and glucose catabolism. In males, testosterone works via androgen receptors to increase insulin receptor expression and glycogen synthesis, decrease glucose uptake and lipogenesis, and promote cholesterol storage in the liver. These recent integrated concepts suggest that sex hormone receptors could be potential promising targets for the prevention of hepatic steatosis.

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15

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 glucose metabolism and are involved in the development of obesity, diabetes, and metabolic syndrome. Recently, their presence in breast milk has been detected, suggesting that they may be involved in the regulation of growth in early infancy and could influence the programming of energy balance later in life. This paper focuses on hormones present in breast milk and their role in glucose homeostasis.

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16

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 (May 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-TBG-iCre virus via the tail vein (LKiss1KO). Control mice included Kiss1f/f male and female mice injected with AAV-GFP (LKiss1WT). We previously showed that deletion of hepatic kisspeptin did not affect body weight, but resulted in decreased insulin secretion and glucose intolerance in both sexes. To clarify the effects of liver-specific Kiss1 knockout on insulin action and glucose homeostasis in vivo, we conducted hyperinsulinemic-euglycemic clamp studies three weeks after tail injections. We noted a sexual dimorphism in the glucose infusion rate (GIR), female mice have a higher GIR to maintain euglycemia associated with an elevated glucose consumption rate, suggesting that female mice are more insulin sensitive than male mice. However, the deletion of liver kisspeptin had no effect on the glucose production rate in either sex. Indirect calorimetry assessment was conducted 4 weeks post-injection. Both male and female LKiss1KO mice showed significantly higher oxygen consumption, carbon dioxide production, and increased energy expenditure as compared to the LKiss1WT groups. However, there were no differences in either the respiratory exchange ratio or total ambulatory activity among treatments. These findings clearly define a pivotal role for hepatic Kiss1 in the modulation of insulin secretion to maintain glucose homeostasis without modulating glucose production as well as in maintaining energy homeostasis in both male or female mice.

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17

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 (August 3, 2018): 4265–74. http://dx.doi.org/10.1210/jc.2018-01067.

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18

Morton, Gregory J. "Hypothalamic leptin regulation of energy homeostasis and glucose metabolism." Journal of Physiology 583, no. 2 (August 30, 2007): 437–43. http://dx.doi.org/10.1113/jphysiol.2007.135590.

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19

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

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20

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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21

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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22

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

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23

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 (December 2009): 794–804. http://dx.doi.org/10.1016/j.coph.2009.10.006.

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24

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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25

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 (June 3, 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,Gpr1expression predominates in the non-adipocyte stromal vascular fraction of WAT. Heterozygous and homozygousGpr1-knockout mice fed on a high-fat diet developed more severe glucose intolerance than WT mice despite having no difference in body weight, adiposity, or energy expenditure. Moreover, mice lackingGpr1exhibited reduced glucose-stimulated insulin levels and elevated glucose levels in a pyruvate tolerance test. This study is the first, to our knowledge, to report the effects ofGpr1deficiency on adiposity, energy balance, and glucose homeostasisin vivo. Moreover, these novel results demonstrate that GPR1 is an active chemerin receptor that contributes to the regulation of glucose homeostasis during obesity.

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26

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 (May 1, 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, sympathoadrenal activity, and energy expenditure produced by extremes of hyper- and hypoglycemia. It is less certain that they respond to the small swings in plasma glucose required for the more physiological regulation of energy homeostasis. Both obesity and diabetes are associated with several alterations in brain glucose sensing. In rats with diet-induced obesity and hyperinsulinemia, GR neurons are hyporesponsive to glucose. Insulin-dependent diabetic rats also have abnormalities of GR neurons and neurotransmitter systems potentially involved in glucose sensing. Thus the challenge for the future is to define the role of brain glucose sensing in the physiological regulation of energy balance and in the pathophysiology of obesity and diabetes.

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27

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 (May 20, 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 of obese mice with putative NURR1 agonists increases energy expenditure, improves glucose tolerance, and confers a lean phenotype, mimicking the effects of exercise. These findings identify a key role for NURR1 in governance of skeletal muscle glucose metabolism, and reveal a transcriptional link between exercise and metabolism. Our findings also identify NURR1 agonists as possible exercise mimetics with the potential to ameliorate obesity and other metabolic abnormalities.

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28

Sahu, Maitrayee, Prashanth Anamthathmakula, and Abhiram Sahu. "Hypothalamic PDE3B deficiency alters body weight and glucose homeostasis in mouse." Journal of Endocrinology 239, no. 1 (October 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 energy and glucose homeostasis, males and females were subjected to either a low- or high-fat diet for 19–21 weeks. Only female but not male Pde3b Nkx2.1KD mice on the low-fat diet showed increased body weight from 13 weeks onward with increased food intake, decreased fat pad weights and hypoleptinemia. Glucose tolerance was improved in high-fat diet-fed male Pde3b Nkx2.1KD mice in association with decreased phosphoenolpyruvate carboxykinase-1 and glucose-6-phosphatase mRNA levels in the liver. Also, insulin sensitivity was increased in male Pde3b Nkx2.1KD mice on the low-fat diet. Changes in body weight or in glucose homeostasis were not associated with any alteration in hypothalamic proopiomelanocortin, neuropepide Y and agouti-related peptide mRNA levels. These results suggest that partial loss of phosphodiesterase-3B in the hypothalamus produces a sex-specific response in body weight and glucose homeostasis, and support a role, at least in part, for hypothalamic phosphodiesterase-3B in regulation of energy and glucose homeostasis in mice.

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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 (January 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 learning results across a diverse range of applications in energy homeostasis, and highlight how modelling and machine learning can work together to improve predictive ability. We collect quantitative details in a comprehensive mathematical supplement. We also discuss the prospects of forecasting homeostatic behaviour and stress the importance of characterizing stochasticity within and between individuals in order to provide practical, tailored forecasts and guidance to combat the spread of obesity.

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30

Jones, B. J., T. Tan, and S. R. Bloom. "Minireview: Glucagon in Stress and Energy Homeostasis." Endocrinology 153, no. 3 (March 1, 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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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 (October 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 lowered glucose levels across glucose tolerance tests. Female lean C57BL/6J mice as well as male and female lean FVBN mice significantly improved glucose tolerance, indicated by decreased areas under glucose clearance curves. For the C57BL/6J mice maintained on a high-fat butter-based diet, glucose homeostasis was improved only in female mice with PWAT removal. Removal of IWAT or RWAT did not affect glucose tolerance in either dietary condition. We conclude that WAT contribution to glucose homeostasis is depot specific, with male gonadal EWAT contributing to glucose homeostasis in the lean state, whereas female gonadal PWAT contributes to glucose homeostasis in both lean and obese mice. These data illustrate both critical differences among various WAT depots and how they influence glucose homeostasis and highlight important differences between males and females in glucose regulation.

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Liu, Zhuo, Yang Zhou, Xuecheng Qu, Lingling Xu, Yang Zou, Yizhu Shan, Jiawei Shao, 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 nanogenerator (i-PENG) to supply long-term energy by converting biomechanical energy into electricity. Our results show that this system can harvest energy from body movement and power the FRL source, which then significantly enhanced production of a short variant of human glucagon-like peptide 1 (shGLP-1) in vitro and in vivo. Indeed, diabetic mice equipped with the SOS showed rapid restoration of blood glucose homeostasis, improved glucose, and insulin tolerance. Our results suggest that the SOS is sufficiently effective in self-powering the modulation of therapeutic outputs to control glucose homeostasis and, furthermore, present a new strategy for providing energy in optogenetic-based cell therapy.

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33

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 (February 15, 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. We confirm the earlier observation that GLUT4 expression and glucose uptake defects of single-knockout mice join in AS160−/−/Tbc1d1−/− mice to affect all skeletal muscle and adipose tissues. In large mixed fiber-type skeletal muscles, changes in relative basal GLUT4 plasma membrane association in AS160−/− and Tbc1d1−/− mice also combine in AS160−/−/Tbc1d1−/− mice. However, we found different glucose uptake abnormalities in isolated skeletal muscles and adipocytes than reported previously, resulting in different interpretations of how AS160 and Tbc1d1 regulate GLUT4 translocation to the cell surface. In support of a larger role for AS160 in glucose homeostasis, in contrast with the previous study, we find similarly impaired glucose and insulin tolerance in AS160−/−/Tbc1d1−/− and AS160−/− mice. However, in vivo glucose uptake abnormalities in AS160−/−/Tbc1d1−/− skeletal muscles differ from those observed previously in AS160−/− mice, indicating additional defects due to Tbc1d1 deletion. Similar to AS160- and Tbc1d1-deficient mice, AS160−/−/Tbc1d1−/− mice show sex-specific abnormalities in glucose and energy homeostasis. In conclusion, our study supports nonredundant functions for AS160 and Tbc1d1.

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Pydi, Sai P., Luiz F. Barella, Lu Zhu, Jaroslawna Meister, Mario Rossi, and Jürgen Wess. "β-Arrestins as Important Regulators of Glucose and Energy Homeostasis." Annual Review of Physiology 84, no. 1 (February 10, 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 in regulating the function of most of these cell types, resulting in striking changes in whole-body glucose and/or energy homeostasis. These studies also revealed that β-arrestin-1 and -2, though structurally closely related, clearly differ in their metabolic roles under physiological and pathophysiological conditions. These new findings should guide the development of novel drugs for the treatment of various metabolic disorders, including type 2 diabetes and obesity.

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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 (June 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 (February 1, 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 (February 27, 2007): 4206–11. http://dx.doi.org/10.1073/pnas.0611641104.

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Kocalis, Heidi E., Scott L. Hagan, Leena George, Maxine K. Turney, Michael A. Siuta, Gloria N. Laryea, Lindsey C. Morris, et al. "Rictor/mTORC2 facilitates central regulation of energy and glucose homeostasis." Molecular Metabolism 3, no. 4 (July 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 (May 2018): 1796—P. http://dx.doi.org/10.2337/db18-1796-p.

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Kaneko, Kentaro, Pingwen Xu, Elizabeth L. Cordonier, Siyu S. Chen, Amy Ng, Yong Xu, Alexei Morozov, and Makoto Fukuda. "Neuronal Rap1 Regulates Energy Balance, Glucose Homeostasis, and Leptin Actions." Cell Reports 16, no. 11 (September 2016): 3003–15. http://dx.doi.org/10.1016/j.celrep.2016.08.039.

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41

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 (March 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 receptors only in POMC neurons gained significantly more body weight and accumulated more body fat. However, female mice gained disproportionately more visceral adiposity than males, and this appeared to be largely the result of differences in energy expenditure. When maintained on a high-fat diet (HFD), both male and female mutants had higher levels of insulin following exogenous glucose challenges. Chow- and HFD-fed males but not females had abnormal glucose disappearance curves following insulin administrations. Collectively, these data indicate that the action of leptin in POMC neurons is sexually different to influence the regulation of energy balance, fat distribution, and glucose homeostasis.

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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 (December 27, 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 activation that is driven by increased NAD+/NADH ratio. Moreover, mitochondria persisted in the cells as elongated forms, and apparently evaded mitophagic removal. This led to a steady increase in mitochondria content and the reactive oxygen species (ROS) generated from them, indicating failure in ATP and ROS homeostasis, due to a misbalance in SIRT1-mediated mitochondria turnover in conditions of glucose withdrawal. Our results suggest that SIRT1 activation alone cannot properly manage energy homeostasis under certain metabolic crisis conditions.

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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 (September 15, 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 control of food intake and glucose homeostasis, yet Glp1r has been studied extensively. This review will highlight the physiological relevance of the central nervous system (CNS) Glp2r in the control of energy balance and glucose homeostasis and focuses on cellular mechanisms underlying the CNS Glp2r-mediated neural circuitry and intracellular PI3K signaling pathway. New evidence (obtained from Glp2r tissue-specific KO mice) indicates that the Glp2r in POMC neurons is essential for suppressing feeding behavior, gastrointestinal motility, and hepatic glucose production. Mice with Glp2r deletion selectively in POMC neurons exhibit hyperphagic behavior, accelerated gastric emptying, glucose intolerance, and hepatic insulin resistance. GLP-2 differentially modulates postsynaptic membrane excitability of hypothalamic POMC neurons in Glp2r- and PI3K-dependent manners. GLP-2 activates the PI3K-Akt-FoxO1 signaling pathway in POMC neurons by Glp2r-p85α interaction. Intracerebroventricular GLP-2 augments glucose tolerance, suppresses glucose production, and enhances insulin sensitivity, which require PI3K (p110α) activation in POMC neurons. Thus, the CNS Glp2r plays a physiological role in the control of food intake and glucose homeostasis. This review will also discuss key questions for future studies.

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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 (February 22, 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 and their wildtype littermates/controls to assess changes in body weight, food intake, and plasma glucose levels when mice were fed a high-fat diet for 16 weeks. Body weight and food intake were measured every week (n = 21–23 mice per genotype), and at the end of the 16-week exposure period, mice were tested using the oral glucose tolerance test (OGTT, n = 9 mice per genotype) and insulin tolerance test (n = 5 mice per genotype). Our results revealed no difference in body weight or food intake between mice of the two genotypes. However, HFD-exposed enkephalin-deficient mice demonstrated impaired OGTT associated with reduced insulin sensitivity compared to their wildtype controls. The impaired insulin sensitivity is possibly due to the development of peripheral insulin resistance. Our results reveal a potential role of enkephalins in the regulation of glucose homeostasis and in the pathophysiology of diabetes type 2.

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El-Mehdi, Mouna, Saloua Takhlidjt, Fayrouz Khiar, Gaëtan Prévost, Jean-Luc do Rego, Jean-Claude do Rego, Alexandre Benani, et al. "Glucose homeostasis is impaired in mice deficient in the neuropeptide 26RFa (QRFP)." BMJ Open Diabetes Research & Care 8, no. 1 (February 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 measurement of complementary parameters. Morphological and physiological alterations of the pancreatic islets were also investigated.ResultsOur data do not reveal significant alteration of energy metabolism in the 26RFa-deficient mice except the occurrence of an increased basal metabolic rate. By contrast, 26RFa mutant mice exhibited an altered glycemic phenotype with an increased hyperglycemia after a glucose challenge associated with an impaired insulin production, and an elevated hepatic glucose production. Two-dimensional and three-dimensional immunohistochemical experiments indicate that the insulin content of pancreatic β cells is much lower in the 26RFa−/− mice as compared with the wild-type littermates.ConclusionDisruption of the 26RFa gene induces substantial alteration in the regulation of glucose homeostasis, with in particular a deficit in insulin production by the pancreatic islets. These findings further support the notion that 26RFa is an important regulator of glucose homeostasis.

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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 glucose uptake and disposal is a consequence of mismatched energy input and energy output. Decreasing the former while increasing the latter is key to normalizing glucose homeostasis.

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Peier, Andrea M., Kunal Desai, James Hubert, Xiaobing Du, Liming Yang, Ying Qian, Jennifer R. Kosinski, et al. "Effects of Peripherally Administered Neuromedin U on Energy and Glucose Homeostasis." Endocrinology 152, no. 7 (May 17, 2011): 2644–54. http://dx.doi.org/10.1210/en.2010-1463.

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Neuromedin U (NMU) is a highly conserved peptide reported to modulate energy homeostasis. Pharmacological studies have shown that centrally administered NMU inhibits food intake, reduces body weight, and increases energy expenditure. NMU-deficient mice develop obesity, whereas transgenic mice overexpressing NMU become lean and hypophagic. Two high-affinity NMU receptors, NMUR1 and NMUR2, have been identified. NMUR1 is found primarily in the periphery and NMUR2 primarily in the brain, where it mediates the anorectic effects of centrally administered NMU. Given the broad expression pattern of NMU, we evaluated whether peripheral administration of NMU has effects on energy homeostasis. We observed that acute and chronic peripheral administration of NMU in rodents dose-dependently reduced food intake and body weight and that these effects required NMUR1. The anorectic effects of NMU appeared to be partly mediated by vagal afferents. NMU treatment also increased core body temperature and metabolic rate in mice, suggesting that peripheral NMU modulates energy expenditure. Additionally, peripheral administration of NMU significantly improved glucose excursion. Collectively, these data suggest that NMU functions as a peripheral regulator of energy and glucose homeostasis and the development of NMUR1 agonists may be an effective treatment for diabetes and obesity.

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Hill, Jennifer W., Yong Xu, Frederic Preitner, Makota Fukuda, You-Ree Cho, Ji Luo, Nina Balthasar, et al. "Phosphatidyl Inositol 3-Kinase Signaling in Hypothalamic Proopiomelanocortin Neurons Contributes to the Regulation of Glucose Homeostasis." Endocrinology 150, no. 11 (October 9, 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 induced resistance to diet-induced obesity. In contrast, deletion of the p110α catalytic subunit of PI3K led to increased weight gain and adipose tissue along with reduced energy expenditure. Independent of these effects, increased PI3K activity in POMC neurons improved insulin sensitivity, whereas decreased PI3K signaling resulted in impaired glucose regulation. These studies show that activity of the PI3K pathway in POMC neurons is involved in not only normal energy regulation but also glucose homeostasis.

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Rodriguez, Susana, Xia Lei, Pia S. Petersen, Stefanie Y. Tan, Hannah C. Little, and G. William Wong. "Loss of CTRP1 disrupts glucose and lipid homeostasis." American Journal of Physiology-Endocrinology and Metabolism 311, no. 4 (October 1, 2016): E678—E697. http://dx.doi.org/10.1152/ajpendo.00087.2016.

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C1q/TNF-related protein 1 (CTRP1) is a conserved plasma protein of the C1q family with notable metabolic and cardiovascular functions. We have previously shown that CTRP1 infusion lowers blood glucose and that transgenic mice with elevated circulating CTRP1 are protected from diet-induced obesity and insulin resistance. Here, we used a genetic loss-of-function mouse model to address the requirement of CTRP1 for metabolic homeostasis. Despite similar body weight, food intake, and energy expenditure, Ctrp1 knockout (KO) mice fed a low-fat diet developed insulin resistance and hepatic steatosis. Impaired glucose metabolism in Ctrp1 KO mice was associated with increased hepatic gluconeogenic gene expression and decreased skeletal muscle glucose transporter glucose transporter 4 levels and AMP-activated protein kinase activation. Loss of CTRP1 enhanced the clearance of orally administered lipids but did not affect intestinal lipid absorption, hepatic VLDL-triglyceride export, or lipoprotein lipase activity. In contrast to triglycerides, hepatic cholesterol levels were reduced in Ctrp1 KO mice, paralleling the reduced expression of cholesterol synthesis genes. Contrary to expectations, when challenged with a high-fat diet to induce obesity, Ctrp1 KO mice had increased physical activity and reduced body weight, adiposity, and expression of lipid synthesis and fibrotic genes in adipose tissue; these phenotypes were linked to elevated FGF-21 levels. Due in part to increased hepatic AMP-activated protein kinase activation and reduced expression of lipid synthesis genes, Ctrp1 KO mice fed a high-fat diet also had reduced liver and serum triglyceride and cholesterol levels. Taken together, these results provide genetic evidence to establish the significance of CTRP1 to systemic energy metabolism in different metabolic and dietary contexts.

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Beckoff, Katherine, Caroline G. MacIntosh, Ian M. Chapman, Judith M. Wishart, Howard A. Morris, Michael Horowitz, and Karen L. Jones. "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 (February 1, 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-supplemented diet (70 g glucose 3 times a day). Glucose supplementation accelerated GE of glucose ( P < 0.05), but not oil; there was a trend for an increase in GIP (at 15 min, P = 0.06), no change in GLP-1, an earlier insulin peak ( P < 0.01), and a subsequent reduction in blood glucose (at 75 min, P < 0.01). Glucose supplementation had no effect on food intake during each diet so that energy intake was greater ( P < 0.001) during the glucose-supplemented diet. Appetite ratings and energy intake at the buffet meal were not different. We conclude that, in older subjects, glucose supplementation 1) accelerates GE of glucose, but not fat; 2) modifies postprandial blood glucose homeostasis; and 3) increases energy intake.

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