Context Ketogenic diet has recently made a comeback as a part of lifestyle and dietary modifications in patients with polycystic ovary syndrome (PCOS). Despite studies suggesting its beneficial effects in reversing hormonal imbalance in women with PCOS, evidence has been patchy and derived from small populations under varying conditions. Objective To pool evidence from clinical trials to study the effects of ketogenic diet on reproductive hormones (LH/FSH ratio, free testosterone, serum progesterone) and observe evidence of weight change. Methods PubMed, ScienceDirect, Scopus, and Web of Science core collection were searched for clinical trials evaluating the effects of ketogenic diet in established PCOS women consistent with the Rotterdam classification. Single- or double-arm studies that included an outcome of interest were included. Two investigators worked independently to screen potential articles and a designated investigator extracted data on study characteristics and evaluated the outcomes. Data were pooled using a random-effects model. The quality of selected studies was assessed using the Cochrane Risk of Bias Tool. Results Following ≥45 days of intervention with ketogenic diet among women with PCOS, significant improvement was observed in reproductive hormone levels, with reduced LH/FSH ratio (d −0.851; 95% CI −1.015, −0.686; P < .001), reduced serum free testosterone (d −0.223; 95% CI −0.328, −0.119; P < .001), and an increased in serum sex hormone binding globulin (SHBG) (d 9.086; 95% CI 3.379, 14.792; P = .002). Significant weight loss was unanimously observed in all included studies (d −11.56; 95% CI −14.97, −8.15; P < .001). Conclusion Short-term ketogenic diet potentially improved hormonal imbalances commonly associated with PCOS.

Hypoglycemic disorders are rare in persons without diabetes, and clinical evaluation to identify its etiology can be challenging. We present a case of insulin autoimmune syndrome induced by carbimazole in a middle-aged Chinese man with underlying Graves’ disease, which was managed conservatively with a combination of dietary modification and alpha-glucosidase inhibitor.

Diabesotension refers to the pathophysiological association between diabetes mellitus, obesity, and hypertension. Despite their frequent coexistence, the underlying molecular mechanisms driving this triad remain poorly understood, and current therapeutic strategies typically address each condition in isolation rather than targeting their shared pathophysiological pathways. To identify potential hallmark genes underlying diabesotension, we mined gene associations with the triad from the NCBI database. Our analysis revealed that AKT1 and NF-κB1 are implicated in four major hallmarks of diabesotension, such as insulin resistance, inflammation, neurohormonal regulation, and oxidative stress. Collectively, these findings highlight the PI3K/Akt and NF-κB pathways as potential molecular drivers in the pathogenesis of diabesotension. This commentary will provide a comprehensive discussion of these findings within the broader context of current knowledge on the role of PI3K/Akt and NF-κB signaling in diabesotension.

Diabesotension, the coexistence of diabetes mellitus, obesity, and hypertension, represents an increasingly prevalent and clinically significant cardiometabolic syndrome. Epidemiological evidence highlights strong bidirectional relationships among these conditions, which together markedly elevate the risk of cardiovascular disease, stroke, nephropathy, and premature mortality. The pathophysiology of diabesotension is multifactorial, involving insulin resistance, chronic hyperglycemia, obesity-associated inflammation, endothelial dysfunction, sympathetic overactivity, and activation of the renin–angiotensin–aldosterone system (RAAS), culminating in adverse metabolic and hemodynamic interactions. Clinically, the synergistic presence of diabetes and hypertension accelerates both microvascular and macrovascular complications, leading to poorer outcomes than either condition alone. Recognizing diabesotension as a distinct clinical entity may facilitate more comprehensive care models and improved long-term outcomes, highlighting the need for continued research to refine risk stratification and optimize individualized treatment strategies. In this review, we focus on the genes implicated in key hallmarks of diabesotension, including insulin resistance, inflammation, RAAS activation, and oxidative stress, relevant clinical management strategies, and AI-based models for risk stratification of this triad of diseases.