Hormones, Obesity & Weight Loss
Specifically, the role of postprandial
releases of insulin and incretin hormones in meal-induced satiety effect
of obesity and weight reduction
Weight Loss Study Background
Previous studies have indicated that the secretion of the intestinal satiety
hormone glucagon-like peptide-1 (GLP-1) is attenuated in obese subjects.
Weight Loss Study Aim
To compare meal-induced response of GLP-1 and glucose-dependent insulinotropic
polypeptide (GIP) in obese and lean male subjects, to investigate the
effect of a major weight reduction in the obese subjects, and to look
for an association between these hormones and ad libitum food intake.
Weight Loss Study Method
Plasma concentrations of intestinal hormones and appetite sensations were
measured prior to, and every 30 min for 180 min after, ingestion of a
2.5 MJ solid test meal. Gastric emptying was estimated scintigraphically.
An ad libitum lunch was served 3 h after the test meal. Subjects included
19 non-diabetic obese and 12 lean
males. All obese subjects were re-examined after a mean stabilised weight
loss of 18.8 kg (95 percent CI 14.4-23.2).
Weight Loss Study Results
Total area under the GLP-1 response curve (AUCtotal, GLP-1) was lower
in obese before and after the weight loss compared to lean subjects, although
weight loss improved the response from 80 to 88 percent of that of the
lean subjects. The GIP response was similar in obese and lean subjects.
However, after the weight loss both AUCtotal, GIP and AUCincremental,
GIP were lowered. An inverse correlation was observed between AUCincremental,
GIP and energy intake at the subsequent ad libitum meal in all groups.
In lean subjects ad libitum energy intake was largely predicted by the
insulin response to the preceding meal.
Weight Loss Study Conclusion
Our study confirmed previous findings of a reduced postprandial GLP-1
response in severely obese subjects. Following weight reduction, GLP-1
response in the obese subjects apparently rose to a level between that
of obese and lean subjects. The data suggests that postprandial insulin
and GIP responses are key players in short-term appetite regulation.
Source: International Journal of Obesity
(2001)
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