What gestational diabetes mellitus is?
Gestational diabetes mellitus (GDM) is a common occurrence in pregnant women. It typically regresses after delivery. Is the problem, however, truly solved? Or is this, in fact, just the tip of the iceberg? GDM has been linked to type 2 diabetes (T2DM) and cardiovascular disease (CVD) later in life, according to research. Furthermore, GDM might result in short-term complications in the offspring, such as birth damage and premature birth. Concerning long-term implications on offspring’s body composition, measurement, and metabolic functions were seen, in keeping with Freikel’s hypothesis. N. Freikel had postulated the critical role of the uterine environment in shaping development over 20 years ago and speculated that in-utero over-nutrition was important in the long run. In the context of diabetes in pregnancy, he introduced the concept of fuel-mediated teratogenesis, or changes in cell differentiation, and fetal organogenesis, which is caused by excessive exposure to nutrients of the fetal-placental unit and has immediate, but mostly long-term effects on metabolic and physiologic functions. The most apparent thought on the prevalence of gestational diabetes mellitus in women could be ascribed to risk factors, such as obesity and being overweight. We might believe so, but many women with GDM are neither obese nor overweight, which is unexpected. This could indicate the presence of other risk factors for GDM. According to recent molecular technology studies, Zhang et al, a systematic review, there are seven genes that are strongly associated with GDM risk, which is also directly related to T2DM and CVD. Six of these (TCF7L2, GCK, KCNJ11, CDKAL1, IGF2BP2, MTNR1B) were linked to insulin secretion, while one (IRS1) was linked to insulin resistance, suggesting that inherited anomalies of pancreatic islet b-cell function and/or b-cell mass may play a role in GDM aetiology. All these genes have previously been linked to the risk of T2DM.
Nutrigenetics is the study of the impact of genetic variation on food response, as well as the consequences of these interactions on health and nutrition-related disorders. Dietary variables, according to new findings, can cause epigenetic changes, which can influence genome stability and the production of proteins involved in metabolism. A study on the relationship between several clinical parameters and nine single nucleotide polymorphisms (SNPs) involved in nutrition and metabolism revealed that gene variants (mutations) in women with and without GDM are highly correlated with the likelihood of acquiring GDM. Lipid parameters and polymorphisms in five genes were shown to have a positive correlation. In women with GDM, the variation, which was located near one of the five genes, was linked to pre-pregnancy BMI. The considerable links between GDM women’s nutritional characteristics and specific gene variations involved in nutrition and metabolism may be crucial in the development of efficient GDM prevention measures. In another study, scientists evaluated 9 SNPs from 9 genes associated with nutrition and metabolism in 29 women with a history of GDM to assess the role of novel nutrigenetic indicators, in addition to traditional parameters, in predicting early, subclinical atherosclerosis. All of the women received an oral glucose tolerance test (OGTT), their carotid artery intima-media thickness (cIMT) was assessed, and their metabolic parameters were examined during a 3-year postpartum follow-up. The APOA5-CC genotype (The apolipoprotein A5 gene (APOA5) is a key regulator of lipid levels) and cIMT were found to have significant relationships. This preliminary research reveals that a lipid profile during pregnancy, as well as other genetic variations, may play a role in predicting cIMT, a cardiovascular disease early marker. Human health and fertility are heavily influenced by eating choices. Appropriate nutrition for a developing fetus provides correct hypothalamic programming, including balanced production of anorexigenic (appetite suppressant) and orexigenic (appetite stimulant) peptides, which leads to normal feeding patterns in adulthood. If a pregnant woman is malnourished, her offspring acquire an altered hypothalamic function, leading to a worsening of the orexigenic state, which leads to excessive eating, decreased satiety, and metabolic syndrome later in life. To conclude, avoiding the harmful effects of genetic and epigenetic alterations requires a healthy lifestyle and nutrition. The transcription factor Hhnf4a, which is linked to the development of type 2 diabetes, is epigenetically regulated by a pregnant woman’s diet, according to a study on rat pancreatic islets, showing a relationship between maternal nutrition and offspring long-term health. Finally, a protective effect for bioactive food substances has recently been proposed in terms of lowering epigenetic alterations. The integration of genetic reports with high-specific omics technologies will allow researchers to get new insights into nutrient-gene interactions based on genotype and build tailored nutrition plans for optimal health and disease prevention.