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. 2006 Summer;3(2):54-60.
doi: 10.1900/RDS.2006.3.54. Epub 2006 Aug 10.

Central control of glucose homeostasis

Antonella Puglianiello  1 , Stefano Cianfarani
Affiliations

Central control of glucose homeostasis

Antonella Puglianiello et al. Rev Diabet Stud. 2006 Summer.
No abstract available

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Figures

Figure 1
Figure 1
The activation of insulin signaling in hypothalamic arcuate nucleus (ARC) is sufficient to decrease blood glucose levels via the inhibition of hepatic glucose production (GP). This effect is mediated by the activation of efferent vagal fibers which innervate the liver. The effects of central leptin on glucose homeostasis involve both melanocortin-dependent and melanocortin-independent pathways. Acute activation of hypothalamic melanocortin receptors, results in an increased rate of hepatic gluconeogenesis. The effect of central leptin on the suppression of glucose production and glycogenolysis is mediated by the stimulation of melanocortin-independent pathways involving insulin-like pathways such as the PI3K signaling cascade. Glucagon-like peptide-1 (GLP-1) is produced in a discrete set of hindbrain neurons that project to a specific population of GLP-1 receptor-containing cells in the hypothalamus. During hyperglycemia following a meal, GLP-1 inhibits muscle glucose utilization and increases insulin secretion to favor hepatic glycogen storage. The intracellular pool of long-chain fatty acids (LCFA-CoAs) is under the control of several biochemical events including a free fatty acids (FFA) flux. Accumulation of LCFA-CoAs reduces hepatic glucose production.
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