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Adipose tissue is a major source of energy for the human body. It is also a source of major adipocytokines adiponectin and leptin. Insulin resistance is a condition in which insulin action is impaired in adipose tissue and is more strongly linked to intra-abdominal fat than to fat in other depots. The expression of adiponectin decreases with increase in the adiposity. Adiponectin mediates insulin-sensitizing effect through binding to its receptors AdipoR1 and AdipoR2, leading to activation of adenosine monophosphate dependent kinase (AMPK), PPAR-α, and presumably other yet-unknown signalling pathways. Weight loss significantly elevates plasma adiponectin levels. Reduction of adiponectin has been associated with insulin resistance, dyslipidemia, and atherosclerosis in humans. The other major adipokine is leptin. Leptin levels increase in obesity and subcutaneous fat has been a major determinant of circulating leptin levels. The leptin signal is transmitted by the Janus kinase, signal transducer and activator of transcription ((JAK-STAT) pathway. The net action of leptin is to inhibit appetite, stimulate thermogenesis, enhance fatty acid oxidation, decrease glucose, and reduce body weight and fat., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Gestational Diabetes Mellitus (GDM) exposes women to a higher risk for development of type 2 diabetes mellitus in later years of life. Newborns of mothers with GDM are at increased risk for acute perinatal complications including hypoglycaemia, jaundice and being large for gestational age. One of the mechanisms underlying glucose metabolism in pregnancy are a group of substances, which includes leptin and adiponectin, produced mainly in the adipose tissue; in this paper we analyze the role of these mediators in women with GDM. This case control study was performed in 90 females (30 GDM patients and 60 control subjects without GDM) referred to a tertiary care hospital. Blood samples were analyzed for fasting blood glucose, leptin and adiponectin. Leptin and Adiponectin were analyzed using ELISA technique. In our study, the levels of fasting blood glucose were statistically significantly higher (p=0.000) in gestational diabetes patients as compared to controls. There was statistically significant positive correlation between blood glucose and leptin (p = 0.000, r = 0.585). There was statistically significant negative correlation between blood glucose and adiponectin(p = 0.000, r = -0.661). An amplification of the low-grade inflammation already existing in normal pregnancy may lead to increase in leptin and decrease in adiponectin. These factors may play a role in development of gestational diabetes mellitus. Further studies are required for establishing them as a marker for gestational diabetes mellitus. [ABSTRACT FROM AUTHOR]