Unravelling the Crosstalk between Estrogen deficiency and Gut-biota Dysbiosis in the development of Diabetes Mellitus

• Published in: Current diabetes reviews
• Main Authors: Chaudhary, Rishabh, Bansal, Seema, Goel, Akriti, Gupta, Sumeet, Malik, Deepti, Bansal, Nitin
• Format: Journal Article
• Language: English
• Published: United Arab Emirates 01.01.2024
• Subjects: Gut-biota dysbiosis; Diabetes Mellitus; Menopause; Estrogen
• ISSN: 1875-6417
• DOI: 10.2174/0115733998275953231129094057

Estrogens are classically considered essential hormonal signals, but they exert profound effects in a number of physiological and pathological states, including glucose homeostasis and insulin resistance. Estrogen deficiency after menopause in most women leads to increased androgenicity and changes in body composition, and it is recommended to manipulate the β-cell function of the pancreas, insulin-induced glucose transport, and hepatic glucose output, hence, the increasing incidence of type 2 diabetes mellitus. Recently, studies have reported that gut biota alteration due to estrogen deficiency contributes to altered energy metabolism and, hence, accentuates the pathology of diabetes mellitus. Emerging research suggests estrogen deficiency via genetic disposition or failure of ovaries to function in old age modulates the insulin resistance and glucose secretion workload on pancreatic beta cells by decreasing the levels of good bacteria such as Akkermansia muciniphila, Bifidobacterium spp., Lactobacillus spp., Faecalibacterium prausnitzii, Roseburia spp., and Prevotella spp., and increasing the levels of bad bacteria's such as Bacteroides spp., Clostridium difficile, Escherichia coli, and Enterococcus spp. Alteration in these bacteria's concentrations in the gut further leads to the development of impaired glucose uptake by the muscles, increased gluconeogenesis in the liver, and increased lipolysis and inflammation in the adipose tissues. Thus, the present review paper aims to clarify the intricate interactions between estrogen deficiency, gut microbiota regulation, and the development of diabetes mellitus.