Influence of food deprivation on intestinal cholecystokinin and somatostatin

Kanayama, Shuji; Liddle, Rodger A.

doi:10.1016/0016-5085(91)90263-k

Cited by 37 publications

(19 citation statements)

References 22 publications

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“…Lipid-stimulated plasma cholecystokinin was reduced after the 4-d dietary restriction. These changes were consistent with a study in rats in which a 3-d food deprivation led to a rapid decrease in plasma cholecystokinin associated with reduced duodenal concentrations of cholecystokinin messenger RNA (33) as well as a study in lean humans which reported that overfeeding for a period of 2 wk increased plasma-cholecystokinin responses to a mixed meal (34). In analogy to the interpretation by the authors (34), a reduction in cholecystokinin concentrations may be indicative of a corresponding upregulation in and enhanced sensitivity of cholecystokinin receptors that are responsible for the feedback inhibition of cholecystokinin release.…”

Section: Discussionsupporting

confidence: 78%

Effects of acute and longer-term dietary restriction on upper gut motility, hormone, appetite, and energy-intake responses to duodenal lipid in lean and obese men

Seimon¹,

Taylor²,

Little³

et al. 2014

The American Journal of Clinical Nutrition

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Background: A 4-d 70% energy restriction enhances gastrointestinal sensitivity to nutrients associated with enhanced energy-intake suppression by lipid. To our knowledge, it is unknown whether these changes occur with 30% energy restriction and are sustained in the longer term. Objectives: We hypothesized that 1) a 4-d 30% energy restriction would enhance effects of intraduodenal lipid on gastrointestinal motility, gut hormones, appetite, and energy intake in lean and obese men and 2) a 12-wk energy restriction associated with weight loss would diminish effects of acute energy restriction on responses to lipid in in obese men. Design: Twelve obese males were studied before (day 0) and after 4 d (day 5), 4 wk (week 4), and 12 wk (week 12), and 12 lean males were studied before and after 4 d of consumption of a 30% energyrestricted diet. On each study day, antropyloroduodenal pressures, gut hormones, and appetite during a 120-min (2.86-kcal/min) intraduodenal lipid infusion and energy intake at a buffet lunch were measured. Results: On day 5, fasting cholecystokinin was less, and ghrelin was higher, in lean (P , 0.05) but not obese men, and lipid-stimulated cholecystokinin and peptide YY and the desire to eat were greater in both groups (P , 0.05), with no differences in energy intakes compared with on day 0. In obese men, a 12-wk energy restriction led to weight loss (9.7 6 0.7 kg). Lipid-induced basal pyloric pressures (BPPs), peptide YY, and the desire to eat were greater (P , 0.05), whereas the amount eaten was less (P , 0.05), at weeks 4 and 12 compared with day 0. Conclusions: A 4-d 30% energy restriction modestly affects responses to intraduodenal lipid in health and obesity but not energy intake, whereas a 12-wk energy restriction, associated with weightloss, enhances lipid-induced BPP and peptide YY and reduces food intake, suggesting that energy restriction increases gastrointestinal sensitivity to lipid. This trial was registered at the Australian New Zealand Clinical Trials Registry (www.anzctr.org.au) as 12609000943246. Am J Clin Nutr 2014;99:24-34.

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Section: Discussionsupporting

confidence: 78%

Effects of acute and longer-term dietary restriction on upper gut motility, hormone, appetite, and energy-intake responses to duodenal lipid in lean and obese men

Seimon¹,

Taylor²,

Little³

et al. 2014

The American Journal of Clinical Nutrition

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“…Rats were not food deprived and food intake was investigated in the active dark phase, since it was shown that fasting leads to changes in the central and peripheral CCK system (see Baile et al 1986 for review; Kanayama and Liddle 1991). In a preliminary experiment we determined 10 and 40 Bg/kg CCK-8S as clearcut satiating doses.…”

Section: Discussionmentioning

confidence: 99%

Obesity induced by unspecific early postnatal overfeeding in male and female rats: hypophagic effect of CCK-8S

Voits

Forster

Rödel

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

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The response to cholecystokinin (CCK) as a satiety peptide in obesity or anorexia has been tested mainly in extreme models of food intake control. In the present study, the effect of CCK-8S on food intake was investigated in a nongenetic and less-stressful model of obesity due to unspecific early postnatal overfeeding in male and female rats. Reducing the normal litter size of ten to three newborn rats on day 3 of life led to an enhanced food intake resulting in an increased body weight until adulthood. Freely fed male and female, normal and obese rats were given 10 micrograms/kg CCK-8S i.p. on day 41 and 40 micrograms/kg CCK-8S on day 91 of life and food intake was measured for 24 h. Compared with treatment with saline (i.p.) 1 day before the test, the lower dose of 10 micrograms/kg CCK-8S reduced food intake for 2 h in normal, but not in obese rats. Conversely, the higher dose of 40 micrograms/kg CCK-8S reduced food intake in both normal and obese rats for 2 h, but this effect was more evident in the obese rats. Moreover, the satiating effect of CCK-8S was more pronounced and longer lasting in male than in female rats. In summary, the data suggest that the response to CCK-8S differs in normal and obese rats and depends on sex.

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“…Feldman et al (1976) listed four ways in which the absence of nutrients from the lumen of the small intestine causes mucosal hypoplasia, and it is likely that some, if not all, of these mechanisms were implicated in the results observed in this experiment: (1) the absence of food may have changed the balance or numbers of bacterial flora in the gut, leading to secondary changes in the small intestine mucosa; (2) ingested food may have been used directly by the intestinal mucosa during transport, either as an energy source or as substrates for cell synthesis; (3) the absence of luminal contents could have led to smaller than normal release of gastrointestinal polypeptide hormones which, themselves, may be trophic to the intestine (e.g. enteroglucagon) (Williamson, 1978); and (4) the absence of food in the gut may have failed to trigger cholecystokinin (Kanayama and Liddle, 1991) and secretin release from the intestinal mucosa and, in turn, the resultant exocrine pancreatic hyposecretion may have led to hypoplasia (Altmann and Leblond, 1970;Altmann, 1971;Tivey and Shulman, 1991).…”

Section: Villous Height and Crypt Depth After Weaningmentioning

confidence: 99%

Villous height and crypt depth in piglets in response to increases in the intake of cows' milk after weaning

1996

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Influence of food deprivation on intestinal cholecystokinin and somatostatin

Cited by 37 publications

References 22 publications

Effects of acute and longer-term dietary restriction on upper gut motility, hormone, appetite, and energy-intake responses to duodenal lipid in lean and obese men

Effects of acute and longer-term dietary restriction on upper gut motility, hormone, appetite, and energy-intake responses to duodenal lipid in lean and obese men

Obesity induced by unspecific early postnatal overfeeding in male and female rats: hypophagic effect of CCK-8S

Villous height and crypt depth in piglets in response to increases in the intake of cows' milk after weaning

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