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Insulin Signaling Modulates Neuronal Metabolism
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Qian Huang, Jialin Fu, Kelly Anne Borges, Weikang Cai
Insulin, a pancreatic hormone, is essential for regulating glucose metabolism and energy homeostasis by acting on multiple classic insulin-sensitive peripheral tissues (1–6). While the brain is traditionally considered insulin-insensitive due to the lack of acute insulin-stimulated glucose uptake, evidence from the research over the last 40 years has demonstrated that insulin signaling plays a profound role in brain metabolism and higher-order neural functions. This chapter focuses on how insulin signaling regulates neuronal metabolism and discusses the impact of impaired neuronal insulin signaling on normal neural metabolism and functions.
Other Sleep Modulators
Published in Shojiro Inoué, Biology of Sleep Substances, 2020
Insulin is a 51-amino acid residue polypeptide originally known as a pancreatic hormone. Insulin is also regarded to be distributed in the brain, although its functional role in the brain is still an open question. Subsequent to the observation of Danguir and Nicolaidis,17 Sangiah et al.23 reported that an i.p. injection of a single nonconvulsive dose of insulin (1 unit/kg = 45.5 μg/kg = 7.6 nmol/kg) completely suppressed PS during the first 3-h postinjection period, returning to the normal level by the sixth hour without gross behavioral changes in rats. The administration of insulin concomitantly increased SWS over 5 h.
The physiology of glucose metabolism
Published in Janet Titchener, Diabetes Management, 2020
Amylin This is another pancreatic hormone. It is co-secreted with insulin from the pancreatic β-cells following the ingestion of food. Amylin suppresses postprandial glucagon secretion, thereby decreasing glucagon-stimulated hepatic glucose output (as described above). Amylin also slows the rate of gastric emptying. This reduces the rate at which glucose is delivered to the small intestine for absorption, thereby playing an important role in the control of postprandial blood sugars. By slowing gastric emptying, it is also possible that amylin reduces food intake and body weight – i.e. amylin has similar actions to the incretin hormones (see below).
Time of day difference in postprandial glucose and insulin responses: Systematic review and meta-analysis of acute postprandial studies
Published in Chronobiology International, 2020
Gloria K. W. Leung, Catherine E. Huggins, Robert S. Ware, Maxine P. Bonham
The actions of other glucoregulatory hormones such as glucagon and GLP-1 (Aronoff et al. 2004) should be examined, as some studies have shown that they also exhibit circadian rhythms. Glucagon, a pancreatic hormone, stimulates endogenous glucose production by the liver, thereby increasing blood glucose concentration. Results from a hypoglycemic clamp study showed that fasting and peak glucagon concentration is higher at night (2300h) compared to day (0900h) (Merl et al. 2004). GLP-1, an intestinal hormone, promotes glucose-dependent insulin secretion and suppresses glucagon secretion after food intake (Aronoff et al. 2004; Brubaker and Gil‐Lozano 2016). Gil-Lozano et al. (2016) showed that postprandial GLP-1 concentration was higher at night (2300h) compared to the day (1100h). In addition to the postprandial glucose elevation that occurs, this may also contribute to the increased postprandial insulin response observed at night.
Short-chain fatty acids and regulation of pancreatic endocrine secretion in mice
Published in Islets, 2019
Anne Ørgaard, Sara Lind Jepsen, Jens Juul Holst
SCFAs are produced from indigestible dietary fiber and malabsorbed carbohydrates by fermenting bacteria in the distal ileum and colon. SCFAs serve as fuel for enterocytes in the colon but may also influence host metabolism. We set out to explore the proposed impact of SCFAs on regulation of pancreatic endocrine secretions in mice using the in situ perfused mouse pancreas model. We believe this model has several advantages compared to islet- and cell-based models including e.g. preserved organ architecture with maintained microvasculature and islet organization, ensuring adequate respiration and metabolism for all cells and preserved paracrine relationships. Furthermore, this model offers the exclusive opportunity, compared to in vivo studies, to detect pancreatic hormone output before extraction occurs in the liver and before the secreted products are diluted into the systemic circulation or broken down by enzymatic mechanisms.
Psychopharmacological advances in eating disorders
Published in Expert Review of Clinical Pharmacology, 2018
Hubertus Himmerich, Janet Treasure
The hypothalamus plays a central role in the homeostatic system regulating of food intake and body weight. It integrates signals about the nutritional state and food supply from the periphery and modulates food intake and energy consumption [73,74]. An important orexigenic signal leading to hunger and food intake is ghrelin which is produced in the stomach [75]. Anorexigenic signals from the body periphery include glucose, the enterocyte hormone GLP-1 [76], the pancreatic hormone insulin, and the fatty tissue hormone leptin [74]. In the hypothalamus, the arcuate nucleus, the paraventricular nucleus, and the lateral hypothalamus are of particular relevance for weight regulation [74,77]. The arcuate nucleus integrates the incoming humoral signals of GLP-1, insulin, leptin, ghrelin, and other hormones and energy carriers such as glucose and converts them into neuronal signals. Orexigenic hypothalamic signaling molecules are NPY and AgRP which lead to an increase in appetite, while α-MSH as well as CART are anorexic signals which lead to a feeling of satiety [74]. α-MSH is produced by the so-called pro-opiomelanocortin (POMC) neurons [78]. In acute episodes of AN, for example, ghrelin has been found to be overexpressed, and leptin reduced as would be expected in starvation [94]. However, plasma levels of NPY (part of the orexigenic system) are anomalously low [94]. Abnormalities within the hormonal regulation of the homeostatic system have also been reported for BN [108] and BED [109].