Endocrine Abstracts

Ghrelin is known to play an important role in overweight formation and glucose metabolism regulation. The aim was to assess ghrelin basal secretion features in persons with metabolic syndrome (MS).

We examined 39 patients (age 35–55years) with MS (IDF criteria) and 28 healthy persons of comparable age. Ghrelin, insulin and C-peptide serum concentrations were measured by immunoenzyme method, lipid spectrum parameters - by spectrophotometry. For IR assessment we used HOMA-IR and Reciprocal of HOMA-IR indexes.

Basal insulinemia and C-peptide levels in S significantly exceeded the ones in healthy persons: 21.3±3.86 vs 9.96±1.18 mU/l and 2.86±0.56 vs 1.28±0.76 ng/ml. HOMA-IR in MS significantly exceeded the value of control group (5.03±1.03 vs 2.06±0.23). Reciprocal of HOMA-IR showed the opposite results. Ghrelin level was significantly lower in MS 61.06±11.9 vs 88.76±16.9 ng/ml in control group. Progressive decrease of ghrelin from 71.59±7.09 to 50.34±6.58 ng/ml was marked at BMI increase that is confirmed at correlation analysis: ghrelin levels negatively correlated with BMI (r=0.41; P<0.05), waist-to-hip ratio (r=0.37; P<0.05) and waist circumference (r=0.39; P<0.05). Ghrelin levels also showed negative correlation with systolic (r=0.40; P<0.01) and diastolic blood pressure (r=0.39; P<0.01).

We observed significant negative correlation of ghrelin and insulin (r=0.18), C-peptide (r=0.15), HOMA-IR (r=0.23) and positive with Reciprocal of HOMA-IR (r=0.22). We revealed significant negative correlation of ghrelin and atherogenecity index (r=0.32), while there was no significant connection with other parameters of lipid spectrum.

Conclusion: Progressive decrease of basal ghrelin levels with increase of BMI, waist-to-hip ratio and waist circumference was revealed that can testify to ghrelin influence on formation of visceral obesity. Obtained results are proved by negative correlation of ghrelin level with basal insulinemia, HOMA-IR and positive one with Reciprocal of HOMA-IR that confirms ghrelin role in formation of insulin resistance in MS and dictates essential necessity for further studies.