ADAPTATION TO HIGH-FAT DIETS - EFFECTS ON EATING BEHAVIOR AND PLASMA CHOLECYSTOKININ

Citation
Sj. French et al., ADAPTATION TO HIGH-FAT DIETS - EFFECTS ON EATING BEHAVIOR AND PLASMA CHOLECYSTOKININ, British Journal of Nutrition, 73(2), 1995, pp. 179-189
Citations number
17
Categorie Soggetti
Nutrition & Dietetics
ISSN journal
00071145
Volume
73
Issue
2
Year of publication
1995
Pages
179 - 189
Database
ISI
SICI code
0007-1145(1995)73:2<179:ATHD-E>2.0.ZU;2-G
Abstract
Twelve male subjects took part in a study to investigate the effects o f overfeeding a high-fat diet (19.17 MJ/d; 58% energy from fat) for 2 weeks on plasma cholecystokinin (CCK) levels, food intake, and subject ive feelings of hunger and fullness. Before and after the diet, subjec ts completed a 2-week weighed dietary inventory, formal measurements o f food intake from a pre-selected appetizing evening meal were carried out, and blood samples were taken after a standard breakfast for meas urement of CCK. Hunger and fullness were rated on visual analogue scal es before and after each of these meals and at evening meals during th e diet period. Following the high-fat diet there was a small non-signi ficant increase in food intake from the pre-selected meal (6919 (SE 61 5) kJ v. 6405 (SE 540) kJ; P = 0.1) and a significant increase in the average daily food consumption measured from the diaries (10.25 (SE 0. 49) MJ/d v. 9.59 (SE 0.62) MJ/d; P = 0.05). Corresponding trends of in creasing feelings of hunger and declining fullness also occurred over the study period. Plasma CCK responses to the standard breakfast were raised following the diet (1285 (SE 153) v. 897 (SE 78) pM min; 3 h in tegrated CCK production post v. pre diet; P < 0.01) with the major dif ferences observed at 90 and 120 min following the meal. These results suggest that the increase in food intake may be related to a down-regu lation in putative CCK receptors responsible for food intake. Elevated CCK levels might suggest a corresponding down-regulation in CCK recep tors responsible for feedback inhibition of CCK release.