CNS nutrient sensing and afferent endocrine signalling are established as parallel systems communicating metabolic status and energy availability in vertebrates. The only afferent endocrine signal known to require modification with a fatty acid side chain is the orexigenic hormone ghrelin. We find that the ghrelin O-acyl transferase (GOAT) which is essential for ghrelin acylation, is regulated by nutrient availability, depends on specific dietary lipids as acylation substrates and modulates body fat mass in mice.Two discoveries have softened the traditional differentiation between the classic model of nutrient sensing 1 and the concept of endocrine signals controlling energy status 2 and drawn attention to the regulation of energy homeostasis by circulating long chain fatty acids (LCFAs). Hotamisligil and colleagues recently reported that one specific adipocyte derived long chain fatty acid (C16:1n7), the lipokine palmitoleate, functions as a hormone regulating systemic insulin sensitivity 3. A recent study followed with the discovery that a gastrointestinal lipid metabolite, N-acylphosphatidylethanolamine (NAPE), can function as an endocrine signal which targets hypothalamic energy balance centers to control food intake, particularly when the acyl NAPE species is C16:0 4. Ten years after the discovery of the only orexigenic gut hormone ghrelin 5,6, this unique medium-chain fatty acid (MCFA)-peptide chimera is now revealing itself as yet another nutrient-hormone hybrid with the specific role of linking macronutrient composition with CNS energy balance regulation. It is further intriguing that the only peptide hormone known to require a fatty acid modification 5 is also the only known afferent endocrine factor which depends on intra-neuronal fatty acid metabolism 7. Unique characteristics of the predominantly stomach derived ghrelin include Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use

Bariatric surgeries, such as gastric bypass, result in dramatic and sustained weight loss that is usually attributed to a combination of gastric volume restriction and intestinal malabsorption. However, studies parceling out the contribution of enhanced intestinal stimulation in the absence of these two mechanisms have received little attention. Previous studies have demonstrated that patients who received intestinal bypass or Roux-en-Y surgery have increased release of gastrointestinal hormones. One possible mechanism for this increase is the rapid transit of nutrients into the intestine after eating. To determine whether there is increased secretion of anorectic peptides produced in the distal small intestine when this portion of the gut is given greater exposure to nutrients, we preformed ileal transpositions (IT) in rats. In this procedure, an isolated segment of ileum is transposed to the jejunum, resulting in an intestinal tract of normal length but an alteration in the normal distribution of endocrine cells along the gut. Rats with IT lost more weight (P < 0.05) and consumed less food (P < 0.05) than control rats with intestinal transections and reanastomosis without transposition. Weight loss in the IT rats was not due to malabsorption of nutrients. However, transposition of distal gut to a proximal location caused increased synthesis and release of the anorectic ileal hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY; P < 0.01). The association of weight loss with increased release of GLP-1 and PYY suggests that procedures that promote gastrointestinal endocrine function can reduce energy intake. These findings support the importance of evaluating the contribution of gastrointestinal hormones to the weight loss seen with bariatric surgery.

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Dietary DHA intake and associated elevations in erythrocyte DHA composition are associated with alterations in functional activity in cortical attention networks during sustained attention in healthy boys. This trial was registered at clinicaltrials.gov as NCT00662142.

Background & Aims-Studies are aimed to determine the role of CD36 in intestinal lipid absorption.