Intestinal fatty acid sensor (FFAR4) and transporter (CD36) expression are significantly correlated with body mass index, and are not altered by acute fat exposure in lean, overweight or obese humans — ASN Events
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  3. Intestinal fatty acid sensor (FFAR4) and transporter (CD36) expression are significantly correlated with body mass index, and are not altered by acute fat exposure in lean, overweight or obese humans

Intestinal fatty acid sensor (FFAR4) and transporter (CD36) expression are significantly correlated with body mass index, and are not altered by acute fat exposure in lean, overweight or obese humans (#6)

Nada Cvijanovic 1 2 , Nicole J Isaacs 1 2 , Christopher K Rayner 1 3 4 , Christine Feinle-Bisset 1 3 , Richard L Young 1 2 3 4 , Tanya J Little 1 3
  1. Discipline of Medicine, University of Adelaide, Adelaide, SA, Australia
  2. South Australian Health and Medical Research Institute, Adelaide, SA, Australia
  3. Centre of Research Excellence in Translating Nutritional Science to Good Health, University of Adelaide, Adelaide, SA, Australia
  4. Department of Gastroenterology and Hepatology, Royal Adelaide Hospital, Adelaide, SA, Australia

Dietary free-fatty acids (FAs) are detected by FFAR4 on enteroendocrine cells within the proximal small intestine, while the FA transporter CD36 on enterocytes is responsible for their absorption. There is limited knowledge in humans regarding the effects of acute fat exposure on expression of FFAR4 and CD36, and their subsequent roles in mediating fat-induced satiety hormone release and suppression of energy intake. Fifty fasted, lean (n=19; BMI: 22 ± 1 kg/m2), overweight (n=14; BMI: 27 ± 1 kg/m2) and obese (n=17; BMI: 36 ± 1 kg/m2) subjects were studied on 2 occasions. The effects of intraduodenal (ID) lipid infusion (10% Intralipid®; 2kcal/min for 120 min) on energy and fat intake at a subsequent ad libitum buffet-meal were assessed on Day 1, while relative expression of FFAR4 and CD36 in duodenal biopsies was assessed prior to, and after, a 30 min ID lipid infusion on Day 2. Baseline FFAR4 expression was lower in obese compared to lean (P<0.05), and negatively correlated with BMI (r= -0.32, P<0.05). Baseline CD36 expression was higher in the obese (P<0.05) and positively correlated with BMI (r=0.33, P<0.05). No target was significantly altered by 30 min ID fat compared to baseline. Following ID fat, FFAR4 was comparable between groups, and CD36 remained higher in obese individuals compared to lean (P<0.05), and was positively correlated with BMI (r=0.4, P<0.05). Buffet energy intake (kJ) was comparable between groups, although obese subjects consumed a higher % of fat compared to overweight subjects (34.8 ± 1.6% vs 29.4 ± 1.7%, P < 0.05). We conclude that duodenal sensing of medium-long chain fatty acids (FFAR4) may be impaired in obesity, while capacity for FA absorption is higher (CD36). These changes may alter the release of gut satiety hormones, and potentially, diminish satiety feedback and subsequent regulation of fat intake in obese individuals.