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Hypothalamus insulin

Somatostatin, a 14-amino-acid peptide (Figure 37-2), is found in the hypothalamus, other parts of the central nervous system, the pancreas, and other sites in the gastrointestinal tract. It inhibits the release of GH, glucagon, insulin, and gastrin. [Pg.832]

Peptide Hormones Peptide hormones may have from 3 to 200 or more amino acid residues. They include the pancreatic hormones insulin, glucagon, and somatostatin, the parathyroid hormone, calcitonin, and all the hormones of the hypothalamus and pituitary (described below). These hormones are synthesized on ribosomes in the form of longer precursor proteins (prohormones),... [Pg.886]

The effects of treatment with selegiline, an MAO-B inhibitor, on plasma levels of insulin-like growth factor I (IGF-I) (as indicator of GH secretion), levels of monoamines and their metabolites, and the activity and content of tyrosine hydroxylase — the rate-limiting enzyme in the biosynthesis of catecholamines — in the hypothalamus and hypophysis of old animals have been studied. It is believed that the antiaging effects of selegiline are due to restoration of hypothalamic hormones. [Pg.182]

Fig. 21.2 Major effects of AMPK activation on numerous tissues. AMPK plays a key role in regulating whole body energy storage and expenditure. In hypothalamus, AMPK is involved in regulation of satiety and food intake. Activation of AMPK in the hypothalamus increases food intake, whereas inhibition decreases intake. In peripheral tissues such as skeletal muscle and liver, activation of AMPK increases energy expenditure by stimulating mitochondrial genesis and energy substrate utilization. AMPK also regulates lipolysis in adipose tissue and insulin secretion in pancreas. Fig. 21.2 Major effects of AMPK activation on numerous tissues. AMPK plays a key role in regulating whole body energy storage and expenditure. In hypothalamus, AMPK is involved in regulation of satiety and food intake. Activation of AMPK in the hypothalamus increases food intake, whereas inhibition decreases intake. In peripheral tissues such as skeletal muscle and liver, activation of AMPK increases energy expenditure by stimulating mitochondrial genesis and energy substrate utilization. AMPK also regulates lipolysis in adipose tissue and insulin secretion in pancreas.
Glucose sensitive neurons are present in the hypothalamus. They depend on glucokinase and act in many ways similar to beta cells [51]. They influence both insulin secretion and glucose uptake, and there appear to be neural connections between all glucose sensing cells [15]. The output may be part of the hepato-portal system, but also conditioned reflexes may participate in the neural stimulation of insulin release and glucose uptake [52]. In this sense the CNS also participates in predictive control. [Pg.160]

Serotonin. Serotonin central receptors appear to play a major role in glucose homeostasis. Experiments in obese mice have demonstrated that small doses of a classical serotonin agonist, metachlorophenylpiperazine (mCPP), markedly lower plasma insulin levels and increase insulin sensitivity, without affecting food intake, body weight or fat mass. The downstream target of the involved serotonin receptor appears to be melanocortin-4 receptors, in the arcuate nucleus of the hypothalamus. [Pg.59]


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Hypothalamus

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