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Ghrelin and glucagon-like peptide-1 according to body adiposity and glucose homeostasis. | LitMetric

Ghrelin and glucagon-like peptide-1 according to body adiposity and glucose homeostasis.

Arch Endocrinol Metab

Unidade de Obesidade, Centro de Pesquisas Clínicas Multiusuário (CePeM), Hospital Universitário Pedro Ernesto (HUPE), Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brasil.

Published: May 2023

Objective: We investigated the biological behavior of ghrelin and glucagon-like peptide-1 (GLP-1) after a standard liquid meal according to body adiposity and glucose homeostasis.

Subjects And Methods: This cross-sectional study included 41 individuals (92.7% women; aged 38.3 ± 7.8 years; BMI 32.2 ± 5.5 kg/m) allocated into three groups according to body adiposity and glucose homeostasis, as follows: normoglycemic eutrophic controls (CON, = 11), normoglycemic with obesity (NOB, n = 15), and dysglycemic with obesity (DOB, = 15). They were tested at fasting and 30 and 60 min after the ingestion of a standard liquid meal in which we measured active ghrelin, active GLP-1, insulin, and plasma glucose levels.

Results: As expected, DOB exhibited the worst metabolic status (glucose, insulin, HOMA-IR, HbA1c) and an inflammatory status (TNF-α) at fasting, besides a more significant increase in glucose than postprandial NOB ( ≤ 0.05). At fasting, no differences between groups were detected in lipid profile, ghrelin, and GLP-1 ( ≥ 0.06). After the standard meal, all groups exhibited a reduction in ghrelin levels between fasting 60 min ( ≤ 0.02). Additionally, we noticed that GLP-1 and insulin increased equally in all groups after the standard meal (fasting 30 and 60 min). Although glucose levels increased in all groups after meal intake, these changes were significantly more significant in DOB CON and NOB at 30 and 60 min post-meal ( ≤ 0.05).

Conclusion: Time course of ghrelin and GLP-1 levels during the postprandial period was not influenced by body adiposity or glucose homeostasis. Similar behaviors occurred in controls and patients with obesity, independently of glucose homeostasis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10665067PMC
http://dx.doi.org/10.20945/2359-3997000000611DOI Listing

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