The Central Nervous System, Pancreatic Hormones, Feeding, and Obesity

Woods, Stephen C.; Porte, Daniel

doi:10.1016/b978-0-12-027309-6.50020-3

Cited by 69 publications

(24 citation statements)

References 178 publications

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“…4) Finally, it is possible that insulin, as a body weight regulator (Woods and Porte Jr. 1978), may have as yet, an unknown role in the hypothalamus, and that inhibits the cephalic phase of insulin secretion in the obese.…”

Section: Discussionmentioning

confidence: 99%

Cephalic Phase of Insulin Secretion in Obese Women

Ji¹,

Pages²,

Ma³

et al. 1986

Horm Metab Res

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The cephalic phase of reflex insulin secretion was studied in normoglycemic and normoinsulinemic female patients, obese (more than 30% over IBW) and normal subjects. After an overnight fasting, at the sight of breakfast food, the obese group did not present a cephalic response. Their glycemia and insulinemia levels remained at base levels. One minute after visual and olfactory stimulation, a statistically significant rise in immunoreactive insulin levels which was maintained throughout the test, was observed in the control group.

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Section: Discussionmentioning

confidence: 99%

Cephalic Phase of Insulin Secretion in Obese Women

Ji¹,

Pages²,

Ma³

et al. 1986

Horm Metab Res

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“…Obese humans have higher insulin levels and it was proposed that CSF insulin serves as an adiposity-signal (Woods and Porte, 1978). Insulin is also claimed to play the role of a satiety hormone (Anika et al, 1980).…”

Section: Endogenous Anorectic Substances In Comparison To Satietinmentioning

confidence: 99%

Satietin; a 50,000 dalton glycoprotein in human serum with potent, long-lasting and selective anorectic activity

Knoll

1984

J. Neural Transmission

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Satietin, a 50,000 dalton anorectic glycoprotein was isolated from human serum. Its isoelectric point is 7.0. It contains 14-15% amino acids and 70-75% carbohydrates. Its biological activity survives digestion with proteases and boiling. Satietin is a highly potent anorectic substance. The intracerebroventricular administration of 10-20 micrograms satietin suppresses food intake in rats during the first day of feeding after deprivation of food for 96 hours to half of the amount eaten by untreated controls (ID50). The onset of the effect can be detected within 30 minutes, the peak effect is reached within an hour. The effect lasts 24-30 hours. Satietin acts both at intravenous and subcutaneous administration (ID50 = 0.5-0.75 mg/kg) in rats deprived of food for 96 hours. The peak effect is reached within an hour and lasts over 24 hours. In contrast to the anorectic drugs in clinical use and to the endogenous anorectic substances (like cholecystokinin and calcitonin) satietin proved to be highly selective in suppressing food intake. Considering that satietin is widely distributed in the world of vertebrates, its concentration in the blood is amazingly high, its site of effect is in the central nervous system and it induces satiety without having any other detectable central or peripheral effect, the hypothesis was forwarded that satietin may play the role of a rate limiting blood-borne satiety signal in the negative feedback of food intake, i.e. serving as the essential chemical link connecting the gastrointestinal tract and the brain in the regulation of feeding.

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“…Insulin was the first peripheral hormone to be identified as important in energy homoeostasis [3], however, evidence for another hormone came from a series of classic parabioses studies carried out in mice by Coleman in the early 1970s [4]. A putative factor was discovered 2 decades later by Zhang et al [5], who first identified leptin through positional cloning of the obese (ob) gene in mice.…”

Section: Leptinmentioning

confidence: 99%