Basic nutritional investigationPassiflora edulis peel intake improves insulin sensitivity, increasing incretins and hypothalamic satietogenic neuropeptide in rats on a high-fat diet

- Passiflora edulis peel intake improves insulin sensitivity in high-fat-fed rats.
- P. edulis peel intake increases satietogenic neuropeptide, incretins, glucose-dependent insulinotropic polypeptide, and glucagon-like peptide-1 in high-fat-fed rats.
- P. edulis peel intake modulates adiponectin and leptin in high-fat-fed rats.

ObjectiveThis study aimed to investigate the effect of Passiflora edulis peel flour (PEPF) intake on hypothalamic neuropeptides messenger RNA expression, insulin sensitivity, and other metabolic parameters in Sprague-Dawley rats fed a high-fat (HF) diet.MethodsSprague-Dawley rats were divided in 3 groups: a control group, fed on a normal fat diet; a HF group, fed on a high-fat diet (35% fat [w/w]); and a high-fat Passiflora flour (HFPF) group, fed on a HF diet containing PEPF. The rats from the HFPF group as well as the HF group were kept on an HF diet for the first 4 wk to induce metabolic conditions related to obesity. Then the HFPF group was switched to a HF diet containing PEPF for additional 6 wk. Other groups were kept on normal-fat and HF diet without addition of PEPF during the whole period of experiment. The glucose tolerance and insulin sensitivity were evaluated through the glucose tolerance test (GTT) and the insulin tolerance test (ITT). Gut hormones and adipokines were measured through an immunoassay. The hypothalamic neuropeptides expression was assessed by real-time polymerase chain reaction.ResultsThe PEPF intake increased the hypothalamic cocaine- and amphetamine-regulated transcript expression (CART) (P < 0.05), counteracted cumulative body weight gain (P < 0.001), decreased adiposity (P < 0.05) and leptin level (P < 0.01), whereas increased adiponectin (P < 0.01), glucose-dependent insulinotropic polypeptide (P < 0.01), and glucagon-like peptide-1 (GLP-1) (P < 0.001) improved the insulin sensitivity in diet-induced obesity rats by increasing the kITT (glucose disappearance rate) (P < 0.01), which was calculated during the ITT. Other gut hormones (peptide tyrosine tyrosine, pancreatic polypeptide, and amylin) and interleukins (IL) (IL-6, tumor necrosis factor-α, IL-1β, and monocyte chemoattractant protein-1) were not changed by the PEPF intake.ConclusionOur findings provide a further understanding of how the PEPF works as a dietary component to improve glucose homeostasis and demonstrate a molecular mechanism that may increase satiety by PEPF in diet-induced obesity.