The response of functionally related gut hormones, ghrelin and GLP-1 to overfeeding

Introduction: Ghrelin and glucagon-like peptide-1 (GLP-1) are peripherally secreted hormones from the gut. GLP-1 is secreted from the distal gastrointestinal tract in response to a meal and is involved in the insulin response and energy homeostasis. Ghrelin is secreted mainly from the fundus of the...

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Bibliographic Details
Main Author: Wadden, Danny
Format: Thesis
Language:English
Published: Memorial University of Newfoundland 2014
Subjects:
Eia
Online Access:https://research.library.mun.ca/6374/
https://research.library.mun.ca/6374/1/DannyW-thesisPDF.pdf
https://research.library.mun.ca/6374/3/DannyW-thesisPDF.pdf
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Summary:Introduction: Ghrelin and glucagon-like peptide-1 (GLP-1) are peripherally secreted hormones from the gut. GLP-1 is secreted from the distal gastrointestinal tract in response to a meal and is involved in the insulin response and energy homeostasis. Ghrelin is secreted mainly from the fundus of the stomach and has been shown to increase appetite. Although both hormones have been linked to the development of obesity and diabetes, data is lacking as to how GLP-1 and ghrelin respond to a positive energy challenge (PEC) and whether the response differs according to obesity status. Thus the present study was designed to investigate the response of these functionallyrelated gut hormones to a period of energy surplus (overfeeding). Methods: A total range of 68-72 young men (68 in the ghrelin study, 72 for GLP-1) were overfed 70% more calories than baseline requirements for 7 days. Fasting blood samples, anthropometric measures and body composition utilizing dual-energy X-ray absorptiometry (DXA) were taken pre- and post- overfeeding. Biochemical markers measured included glucose, insulin, cholesterol, HDL-C, LDL-C, and triglycerols. Serum total GLP-1 and acylated ghrelin were measured using enzyme-linked immunosorbent assays (ELISA) and enzyme immune assays (EIA), respectively. Results: As expected, serum GLP-1 increased in response to the energy surplus, however unexpectingly, circulating acylated ghrelin also increased. The increase in both GLP-1 and ghrelin were independent of adiposity status. At baseline, there was no difference in fasting GLP-1 and ghrelin between the normal weight, overweight, and obese groups. In the overweight/obese cohort, baseline GLP-1 concentration was negatively associated with HDL-cholesterol and positively associated with triacylglycerols and markers of insulin resistance. Also in the overweight/obese subjects, a negative relationship was present between baseline GLP-1 concentration and change in percent gynoid fat. Baseline acylated ghrelin was inversely correlated with weight and BMI in the normal weight group and inversely correlated with BMI in the overweight group. Additionally, baseline acylated ghrelin was negatively associated with change in weight and BMI in the overweight group and positively associated with the same variables in the obese group. Percentage change in GLP-1 was positively associated with percentage change in triacylglycerols in both the normal weight and overweight/obese groups. Percent change in GLP-1 was negatively correlated with percent change in gynoid fat in the normal weight group and positively correlated with percent change in cholesterol in the overweight/obese group. Conclusion: Serum GLP-1 and ghrelin increased in response to a 7-day overfeeding period in young Newfoundland men, regardless of obesity status. Our results suggest a protective role for GLP-1, increasing to counteract the energy surplus. We also suggest that the increase in ghrelin is attempting to offset the rise in insulin resistance.