Gestational Diabetes Mellitus (GDM) is one of the most prevalent conditions associated with pregnancy, and if untreated it can have a major negative impact on both the mother’s and the child’s health. It affects 3-8% of pregnancies and is defined by glucose intolerance identified during pregnancy due to obesity risk. The etiology of GDM remains poorly understood. The most widely accepted explanation states that human placental lactogen, prolactin, glucocorticoids, and progesterone all of which are released by the placenta during pregnancy cause GDM by lowering insulin sensitivity and boosting anti-insulin hormones. Adipocytes produce adipocytokines likes leptin that contribute to energy balance, metabolism of glucose and insulin. According to certain research, leptin may also play a major role in controlling the body’s overall glucose homeostasis. Leptin may therefore play a significant role in the onset and prognosis of GDM. There is a favorable relationship between plasma leptin concentrations and both direct and indirect markers of obesity. Leptin levels rise in expectant mothers who have altered maternal fat reserves and glucose metabolism. The concentration of leptin in mothers rises two to three times higher than in non-pregnant women, peaking at 28 weeks of gestation.

This study assessed the serum leptin concentrations for development of gestational diabetes mellitus. It is a case-control study, included 120 participants (60: Gestational Diabetes Mellitus Cases and 60: Healthy Controls). Authors assed BMI, FBS, HbA1c, Lipid Profile and serum leptin. Results: The serum leptin concentrations were significantly elevated in patients with gestational diabetes mellitus when compared to controls (P=0.001). There was a significant positive correlation between the serum leptin and BMI, FBS, HbA1c, Total Cholesterol and LDL (P=0.001).
The current study illustrated how maternal circulating leptin changes during gestational diabetes mellitus. Several studies have reported varying patterns of leptin variation with increasing gestational age in a typical pregnancy. The results of this investigation support the hypothesis that GDM and the mother’s circulating leptin profile are related. An adaptive reaction to insulin resistance and the inflammatory response linked to GDM could account for the variation in circulating leptin concentration observed in early gestation between women with and without GDM. By directly regulating the insulin receptor or indirectly through central neuronal pathways, leptin may enhance insulin sensitivity and it can also directly promote the absorption of glucose and the synthesis of glycogen in skeletal muscle.

It was also believed that the upregulation of the leptin gene and protein production constituted a sort of defense mechanism against the imbalance of proinflammatory cytokines that occurs in many abnormal pregnancies, including GDM.
Based on the present study findings, authors concluded that significant elevated levels of serum leptin might be served as a marker for detection of gestational diabetes mellitus.
Source: Thilak, Harika and Narayanswamy / Indian Journal of Obstetrics and Gynecology Research 2024;11(2):198–202