Study of fasting plasma ghrelin hormone in obese non diabetic and obese type 2 diabetic patients

الملخص EN

Background: Ghrelin is a newly discovered circulating peptide hormone produced mainly by the stomach from gastric endocrine cells, hypothalamus, pituitary, placenta and gastroenteropancreatic tumors.

It has been identified as an endogenous ligand for the growth hormone secretagogue receptor.

Ghrelin has been shown to cause a positive energy balance by decreasing fat utilization through growth hormone independent mechanisms.

In addition, both intracerebroventricular and peripheral administration of ghrelin have been shown to elicit potent, long lasting stimulation of food intake via activation of neuropeptide Y neurons in the hypothalamic arcuate nucleus.

These findings raise the possibility that ghrelin play an important role in the regulation of metabolic balance. Objective: Is to study the possible role of ghrelin hormone in the pathogenesis of obesity in obese non-diabetic and obese type 2 diabetic patients. Study Design: 30 obese subjects classified as 15 obese type 2 diabetic, 15 obese non-diabetic subjects, and 15 healthy subjects age matched were chosen as control group.

All subjects were subjected to full history taking and through clinical examination including anthropometric measures, BMI, waist circumference and laboratory investigations including fasting plasma insulin, fasting plasma glucose, HbA1C and fasting plasma ghrelin. Results: Fasting plasma ghrelin level is significantly lower in obese subjects (31.7 ± 7.1 Pg / L) compared to control (42.3 ± 9.5 Pg / L) (P<0.05), and also significantly lower in type 2 obese diabetics (26.7 ± 7.1 Pg / L) compared to control (P<0.001).

Results showed significant negative correlation between ghrelin and fasting insulin, fasting blood glucose, body mass index, waist circumference in all studied groups. Conclusion: we concluded that fasting plasma ghrelin hormone seemed to be downregulated in human obesity and type 2 obese diabetics.

This downregulation may be a consequence of compensatory hyperinsulinaemia due to insulin resistance.