الفهرس 
Pre-diabetesOnly 14 pages are availabe for public view
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Abstract
Glucose homeostasis is a complicated process that involves insulin, glucagon, glucagon-like peptide-1(GLP-1), and glucose-dependant insulin-tropic poly-peptide (GIP). GLP-1 is a peptide secreted by L cells in the intestines with the ingestion of food (Egan et al., 2002).
GLP1 possesses several physiological properties that make it a subject of intensive investigation, the known physiological functions of it include;
- Increases insulin secretion from the pancreas in a glucose-dependant manner
- Decreases glucagon secretion from pancreas
- Increases beta cell mass and insulin gene expression
- Inhibits acid secretion and gastric emptying in the stomach
- Decreases food intake by increasing satiety (Meier et al., 2004).
People with pre-diabetes are 5-15 times more likely to develop type 2 diabetes than are people with normal glucose values (Santaguida et al., 2005), so interventions to prevent or delay progression of pre-diabetes to type 2 diabetes can be feasible and cost effective and many individuals could benefit from them particularly those who are overweight or obese (Kanaya and Narayan, 2003).
Since β-cell defects appear to drive the progression from pre-diabetes to diabetes, incretin-based therapies should in theory be effective for diabetes prevention. However, long term clinical trials are clearly needed to evaluate both the efficacy and safety of glucagon like peptide-1 agonists and dipeptidyle peptidase IV inhibitors for long-term use in diabetes prevention (Horton, 2008).
Obesity can no longer be regarded simply as a cosmetic problem affecting certain individuals but must be considered as an epidemic requiring effective measures for its prevention and management (Loscalzo et al., 2008).
A role for GLP-1 in the development of obesity was suggested partly because of the apparently physiological effects of the hormones on appetite and food intake and partly because of the reports that GLP-1 secretion may be reduced in obesity (Verdich et al., 2001).
The aim of the present study is to assess relation between obesity, pre-diabetes and GLP-1.
This study was conducted on 80 subjects who were divided into 4 groups:
Group 1: which included 20 control subjects had normal weight and normal blood glucose.
Group 2: included 20 obese subjects who had normal oral glucose tolerance test.
Group 3: included 20 obese subjects who had impaired fasting blood glucose.
Group 4: included 20 obese subjects who had impaired glucose tolerance.
All selected subjects were subjected to full medical history and full clinical examination and laboratory tests included fasting blood glucose, oral glucose tolerance test, fasting insulin and glucose-stimulated GLP-1.
In conclusion; the present study revealed that:
- Glucose- stimulated GLP-1 was significantly decreased in obese subjects than normal control and it was negatively correlated with BMI and waist circumference in all studied groups.
- Plasma glucose-stimulated GLP-1 was indirectly and significantly correlated with HOMA in all studied groups.
- No significant difference was found between glucose stimulated GLP-1 level in obese having normal glucose tolerance, obese having impaired fasting glucose and obese having impaired glucose tolerance.
- A significant positive correlation was noted between GLP-1 levels and increasing age only in control group.
- A statistically significant reduction of glucose-stimulated GLP-1 was found in hypertensive subjects in comparison to normotensive subjects in all studied groups.