Effect of low fat diet on lipid absorption and fatty-acid transport following bowel resection

Abstract

Low-fat diets (LFD) are used extensively in many different clinical conditions. However, the effect of this diet on lipid absorption and cellular long-chain fatty-acid (LCFA) transport is unknown. Fatty-acid translocase (FAT), the rat homologue of human CD36, is one of several LCFA plasma-membrane transport proteins that may play an important role in intestinal lipid uptake. The purpose of this study was to investigate the effects of a LFD on intestinal expression of FAT/CD36, enterocyte fatty-acid transport, and in-vivo lipid absorption in rats following bowel resection. Adult male Sprague-Dawley rats were divided into five experimental groups: normal rats fed normal chow(NR-NC) (10 kcal% fat), normal rats fed a LFD (NR-LFD) (3 kcal% fat), sham rats fed normal chow (Sham-NC), short-bowel syndrome rats fed normal chow (SBS-NC), and SBS rats fed a LFD (SBS-LFD). SBS rats underwent 75% small-bowel resection, while sham animals underwent bowel transection and reanastomosis. Food intake, fecal mass, and fecal fat were measured over the last 3 days before death on day 14. Final body weight, plasma lipids and protein, and tissue total lipids in liver, adipose tissue, and intestine were determined at death. Total RNA from the mucosa of the duodenum, jejunum, and ileum was extracted for Northern blot analysis to determine fatty-acid translocase (FAT)/CD36 mRNA levels. An established cellular LCFA transport assay was used to determine isolated enterocyte [3H]-oleate uptake. Students t-test was used to determine statistical significance (P < 0.05). NR-LFD rats demonstrated a small increase in overall food absorption and no change in fat absorption compared to NR-NC animals. A significant decrease in FAT/CD36 mRNA levels was seen in the duodenum and jejunum in NF-LFD rats (vs NR-NC) and was accompanied by reduced LCFA transport by isolated enterocytes from the jejunum and ileum. SBS-LFD rats demonstrated decreased FAT/CD36 mRNA levels in all three segments and a concomitant decrease in LCFA uptake enterocytes compared to the SBS-NC group. In addition, SBS-LFD rats showed significantly lower final body weight and plasma lipids compared to SBS-NC animals.

The role of enteral fat as a modulator of body composition after small bowel resection

“…A previous study has found that rats given a low fat diet with 3% kcal/fat after SBR were found to have decreased body weight, mucosal weight, and attenuated villus height/proliferation/apoptosis in the ileum when compared to normal chow. 5, 6 However, our results reveal that at least 10% kcal fat as in LFD is adequate to demonstrate adaptive changes.…”

“…4 However, the mechanism for high fat induced intestinal adaptation remains unknown. While it has been suggested that a low fat diet is detrimental to adaptation 5, 6 , it is unknown how much fat is needed to generate an augmented adaptation response. Additionally, it is unknown what kind of fat produces the optimal response after resection.…”

Advances in short bowel syndrome: an updated review

“…A lowfat diet affected adaptive responses by an inhibition of enterocyte proliferation and did so independent of enterocyte apoptosis [18]. In another investigation [19], we reported that depletion of dietary fat inhibited cellular and molecular mechanisms of LCFA absorption by isolated enterocytes in the same model. This was associated with a decrease in LCFA plasma-membrane transport protein fatty-acid translocase (FAT) (the rat homologue of human CD36) and with a decrease in isolated enterocyte [3H]-oleate uptake as measured by an established cellular LCFA transport assay [19].…”

Mécanisme d’absorption intestinale des acides gras à longue chaîne : rôle émergent du CD36

“…L'expression intestinale du CD36 est etroitement corr el ee avec la teneur en lipides du r egime. Alors qu'un r egime pauvre en lipides diminue son expression (Sukhotnik et al, 2001), un r egime hyperlipidique chronique l'induit fortement (Poirier et al, 1996). Cependant, a la diff erence de l'adipocyte et du myocyte, la contribution significative de CD36 dans le captage ent erocytaire des AGLC est mise en doute.…”