METHODS: Using a randomized, crossover and double-blinded design, 15 men and 15 women with metabolic syndrome consumed high-fat meals enriched with SFA, MUFA or n-6 PUFA, or a low-fat/high-sucrose (SUCR) meal. C-peptide, insulin, glucose, gastrointestinal peptides and satiety were measured up to 6 h.
RESULTS: As expected, SUCR meal induced higher C-peptide (45 %), insulin (45 %) and glucose (49 %) responses compared with high-fat meals regardless of types of fatty acids (P < 0.001). Interestingly, incremental area under the curve (AUC0-120min) for glucagon-like peptide-1 was higher after SUCR meal compared with MUFA (27 %) and n-6 PUFA meals (23 %) (P = 0.01). AUC0-120min for glucose-dependent insulinotropic polypeptide was higher after SFA meal compared with MUFA (23 %) and n-6 PUFA meals (20 %) (P = 0.004). Significant meal x time interaction (P = 0.007) was observed for ghrelin, but not cholecystokinin and satiety.
CONCLUSIONS: The amount of fat regardless of the types of fatty acids affects insulin and glycemic responses. Both the amount and types of fatty acids acutely affect the gastrointestinal peptide release in metabolic syndrome subjects, but not satiety.
Methods: 53 women with GDM (30 managed with diet only (GDM-diet) and 23 treated with insulin (GDM-insulin)) and 43 pregnant women with normal glucose tolerance (NGDM) were studied, with GIP and GLP-1 levels measured at 24-28 weeks (E1), prior (E2) and after (E3) delivery, and postpuerperium (E4).
Results: Basal GIP was shown to be low in GDM groups compared to NGDM in E1, and in E4 for GDM-diet. GLP-1 was low in GDM groups during pregnancy and afterwards. At E1, serum GIP and GLP-1 were inversely associated with GDM and participants with lower levels of GIP (<0.23 ng/mL) and GLP-1 (<0.38 ng/mL) had a 6 (95% CI 2.5-14.5)- and 7.6 (95% CI 3.0-19.1)-fold higher risk of developing GDM compared with the higher level, respectively. In the postpuerperium, when there is a drop in β-cell function, participants with previous GDM (pGDM) presented lower GLP-1 (in both GDM subgroups) and lower GIP in GDM-diet subgroup compared to controls.
Conclusion: There is an independent, inverse association between fasting incretins and higher risk of GDM. Furthermore, lowered levels of these peptides may play an important role in the abnormality of glucose regulation following pregnancy.