Background Many studies have been conducted on the genetic and epigenetic etiology of gestational diabetes mellitus (GDM) in the last two decades because of the disease’s increasing prevalence and role in global diabetes mellitus (DM) explosion. An update on the genetic and epigenetic etiology of GDM then becomes imperative to better understand and stem the rising incidence of the disease. This review, therefore, articulated GDM candidate genes and their pathophysiology for the awareness of stakeholders. Main body (genetic and epigenetic etiology, GDM) The search discovered 83 GDM candidate genes, of which TCF7L2, MTNR1B, CDKAL1, IRS1, and KCNQ1 are the most prevalent. Certain polymorphisms of these genes can modulate beta-cell dysfunction, adiposity, obesity, and insulin resistance through several mechanisms. Environmental triggers such as diets, pollutants, and microbes may also cause epigenetic changes in these genes, resulting in a loss of insulin-boosting and glucose metabolism functions. Early detection and adequate management may resolve the condition after delivery; otherwise, it will progress to maternal type 2 diabetes mellitus (T2DM) and fetal configuration to future obesity and DM. This shows that GDM is a strong risk factor for T2DM and, in rare cases, type 1 diabetes mellitus (T1DM) and maturity-onset diabetes of the young (MODY). This further shows that GDM significantly contributes to the rising incidence and burden of DM worldwide and its prevention may reverse the trend. Conclusion Mutations and epigenetic changes in certain genes are strong risk factors for GDM. For affected individuals with such etiologies, medical practitioners should formulate drugs and treatment procedures that target these genes and their pathophysiology.
The association between breastfeeding and type 1 diabetes mellitus (T1DM) is controversial. However, several recent studies have established a link between these two factors, necessitating a need to review this subject to raise public awareness. Current research indicates that breast milk contains a variety of bioactive substances including immunoglobulins, oligosaccharides, insulin, lactoferrin, lysozyme, cytokines, epidermal growth factors, leukocytes, nucleotides, beneficial bacteria and vitamins. Such substances strengthen the breastfeeding infant’s immune system, both directly, by increasing gut microbiota diversity and attacking harmful bacteria and proinflammatory molecules, and indirectly, by increasing thymus performance. Accordingly, a lack of or inadequate breastfeeding may predispose infants to several autoimmune disorders, including T1DM. Nursing mothers and caregivers are therefore advised to follow optimal breastfeeding practices prior to introducing complementary foods.Keywords: Breastfeeding; Type 1 Diabetes Mellitus; Autoimmune Diseases; Immunoglobulins; Oligosaccharides; Review Literature.
Introduction: Scientists are considering the possibility of treating diabetes mellitus (DM) using a personalized approach in which various forms of the diseases will be treated based on the causal gene and its pathogenesis. To this end, scientists have identified mutations in certain genes as probable causes of Type 2 diabetes mellitus (T2DM) with diverse mechanisms. Aim: This review was aimed at articulating already identified T2DM genes with their mechanisms of action and phenotypic presentations for the awareness of all stakeholders. Method: Method: The Google search engine was used to retrieve relevant information on the subject from reliable academic databases such as PubMed, Medline, and Google Scholar, among others. Results: At least seventy (70) genes are currently being suspected in the biogenesis of T2DM. However, mutations in, or variants of KCNJ11, PPARG, HNF1B and WFS1 genes, are the most suspected and reported in the pathogenesis of the disease. Mutations in these genes can cause disruption of insulin biosynthesis through the destruction of pancreatic beta cells, change of beta cell morphology, destruction of insulin receptors, among others. These cellular events may lead to insulin resistance and hyperglycemia and, along with environmental triggers such as obesity and overweight, culminate in T2DM. It was observed that each identified gene has its distinct mechanism by which it interacts with other genes and environmental factors to cause T2DM. Conclusion: Healthcare providers are advised to formulate T2DM drugs or treatment by targeting the causal genes along with their mechanisms.
Single gene mutations have been implicated in the pathogenesis of a form of diabetes mellitus (DM) known as the maturity-onset diabetes of the young (MODY). However, there are diverse opinions on the suspect genes and pathophysiology, necessitating the need to review and communicate the genes to raise public awareness. We used the Google search engine to retrieve relevant information from reputable sources such as PubMed and Google Scholar. We identified 14 classified MODY genes as well as three new and unclassified genes linked with MODY. These genes are fundamentally embedded in the beta cells, the most common of which are HNF1A, HNF4A, HNF1B, and GCK genes. Mutations in these genes cause β-cell dysfunction, resulting in decreased insulin production and hyperglycemia. MODY genes have distinct mechanisms of action and phenotypic presentations compared with type 1 and type 2 DM and other forms of DM. Healthcare professionals are therefore advised to formulate drugs and treatment based on the causal genes rather than the current generalized treatment for all types of DM. This will increase the effectiveness of diabetes drugs and treatment and reduce the burden of the disease.
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