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Brain insulin release

Hepoxylins are metabolites of arachidonic acid which arise from 12-HPETE in tissues such as pancreatic islet cells (where they stimulate glucose-dependent insulin release) and brain (where they appear to have a neuromodulatory role). The structure of the hepoxylins was confirmed by synthesis which also has provided this scarce material for biological investigation. [Pg.337]

K+ channels K-atp Rat brain Diabetes, asthma, cardiac arrythmia, angina, cardiac and cerebral ischemia, thrombosis, hypertension, incontinence, pain, neurogenic inflammation, epilepsy, stroke, hair growth Control of insulin release, vasodilatation, protection against cell ischemia... [Pg.124]

Several hours after the intake of dietary carbohydrate, blood glucose levels fall slightly because of the ongoing oxidation of glucose by the brain and other tissues. Lowered blood glucose triggers secretion of glucagon and decreases insulin release (Fig. 23-27). [Pg.904]

B Located in heart, brain, kidney, and liver Vascular remodeling with -agonist Cardiac hypertrophy with aragonist Glucose metabolism and insulin sensitivity Brain dopamine release and addictive behavior... [Pg.233]

CCK is a peptide with 33 amino acids originally isolated from pork intestine. Its action on insulin secretion is very weak in humans. Several smaller molecular forms, however, have been isolated from gut mucosa and from brain. Both the C-terminal octapeptide (CCK8) and the tetrapeptide (CCK4) stimulate insulin release in vitro (Okabayashi et al., 1983 Herman-sen, 1984 Verspohl et al.. 1986b Zawalich et al., 1987). [Pg.98]

Phenoxy- benzamine (Dibenzyline) a1, a2 Irreversible alkylation of alpha receptor. Vasodilation (a1). Blocks sympathetic outflow from the brain and feedback inhibition of norepinephrine release at [Pg.22]

Answer C. Insulin increases glucose transport in only two tissues, adipose and muscle. The major site of glucose uptake is muscle, which decreases hyperglycemia. Glucose and ketone transport and metabolism are insulin independent in the brain (choice D). Insulin would slow gluconeogenesis (choice A) and fatty acid release from adipose (choice B). Insulin would inhibit glycogenolysis in the liver (choice E). [Pg.160]

Receptor-mediated endocytosis may be possible because receptors have a high affinity for BDNF (Deckner et al. 1993). A linear relation between intranasal administration of -labeled NGF and brain concentrations of the compound suggest that this transportation is not mediated by receptors and that this releasing method of agents to the brain via olfactory nerves may be effective for many therapies (Frey et al. 1995). BDNF and the insulin-type growth factor (IGF-1) are currently used in clinical studies (Appel 1997). [Pg.507]

Adipokinetic hormones control metabolism of insects during long-distance flight.359 363 In the migratory locust these hormones consist of a pair of related octapeptides and a decapeptide (Table 30-5). The hormones stimulate triacylglycerol lipase in the insects fat bodies, induce release of carbohydrates from body stores, and affect many other aspects of metabolism.363 Insects also have hormones of the insulin family, proteins consisting of disulfide-linked A and B chains as in insulin. The silkworm Bombyx mori has 38 genes for the insulinlike bombyxins, which are synthesized in the brain.364... [Pg.1760]


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Insulin release

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