Nutrition and weight gain during pregnancy can influence the life-course health of offspring. Clinical practice guidelines play an important role in ensuring appropriate nutrition and weight gain among pregnant women. This study aims to identify clinical practice guidelines on gestational weight gain and/or maternal nutrition across the Asia-Pacific region and to determine the quality of the guidelines and variability in the recommendations. Through a systematic search of grey literature from 38 Asia-Pacific countries, 23 published guidelines were obtained. Of these, 10 eligible clinical practice guidelines reporting nutrition- or/and weight-related recommendations for pregnant women were selected and reviewed. Guideline quality was determined using the Assessment of Guidelines for Research Evaluation II (AGREE II) instrument. Of the 10 guidelines, 90% were classified as low-quality in the AGREE II appraisal. Several variations were found with respect to recommendations on gestational weight gain, including those specific to Asian populations. The recommendations on dietary advice, additional energy intake, and nutritional supplementation during pregnancy were varied. Clinical practice guidelines on weight gain and nutrition in pregnancy across the Asia-Pacific region are generally of poor quality, reflecting significant variation, and need to be improved to ensure pregnant women receive appropriate advice. (PROSPERO registration no. CRD42021291395).

Background: Recent findings have highlighted that abnormal energy metabolism is a key feature of autosomal-dominant polycystic kidney disease (ADPKD). Emerging evidence suggests that nutritional ketosis could offer therapeutic benefits, including potentially slowing or even reversing disease progression. This systematic review aims to synthesise the literature on ketogenic interventions to evaluate the impact in ADPKD. Methods: A systematic search was conducted in Medline, Embase, and Scopus using relevant Medical Subject Headings (MeSH) and keywords. Studies assessing ketogenic interventions in the management of ADPKD in both human and animal models were selected for data extraction and analysis. Results: Three animal reports and six human studies were identified. Ketogenic diets (KD) significantly slowed polycystic kidney disease (PKD) progression in rats with improved renal function and reduced cystic areas. There was reduced renal fibrosis and cell proliferation. The supplementation of beta-hydroxybutyrate (BHB) in rats also reduced PKD progression in a dose-dependent manner. Human studies (n = 129) on KD in ADPKD reported consistent body mass index (BMI) reduction across trials, with an average weight loss of ∼4 kg. Improvements in blood pressure were also noted. Ketosis was achieved in varying degrees. Effects on kidney function (eGFR) were beneficial. Results for kidney volume were mixed but most studies were underpowered for this outcome. Lipid profiles showed increases in total cholesterol (∼1 mmol/L) and LDL cholesterol (∼0.4 mmol/L) in most studies. Safety concerns such as “keto flu” symptoms, elevated uric acid levels, and occasional kidney stones were noted. Overall feasibility and adherence to the KD were rated positively by most participants. Conclusions: Human studies are promising; however, they have been limited by small sample sizes and short durations. Larger, long-term trials are needed to assess the efficacy, adherence, and safety of ketogenic diets in people with ADPKD.

Type 2 diabetes (T2D) is a pressing global health challenge, primarily driven by modern dietary and lifestyle patterns. Central to T2D progression is the dysfunction of insulin-secreting pancreatic β-cells, which critically disrupts glucose homeostasis. The progression to T2D relies on the β-cells’ inability to compensate for increasing insulin resistance. Initially, β-cells enhance the insulin output, but chronic nutrient overload, ER stress and inflammation ultimately compromise their function and survival. This review examines the molecular and cellular drivers of β-cell failure, focusing on endoplasmic reticulum stress, mitochondrial dysfunction and inflammatory pathways amid chronic metabolic stress. We also explore the loss of β-cell identity and altered interactions within the islet microenvironment. Understanding these mechanisms is essential for developing strategies to prevent β-cell dysfunction and slow T2D progression, ultimately supporting better metabolic health outcomes.

A ketogenic diet (KD) is a low-carbohydrate, high-fat dietary approach. Beyond treating neurologic disorders, KDs have attracted significant media attention for their potential to improve obesity and diabetes. The diet induces a metabolic shift from glucose toward fatty acid oxidation and ketone body production. This shift leads to ketosis, which may reduce hunger, partly through the anorexigenic effects of ketone bodies, thereby contributing to weight loss and improved metabolic parameters, including glycaemic control and insulin sensitivity. In particular, the positive effects of KDs lower insulin demand and may thereby improve β-cell function. However, the long-term efficacy, safety, and sustainability of KDs, especially for diabetes, remain debated. This review offers current insights into the effects of ketogenesis and ketosis, as well as the potential mechanisms underlying them. We explore the metabolic effects of KDs in obesity and diabetes, drawing on preclinical and clinical studies, and suggest that combining KDs with antidiabetic agents may provide synergistic benefits. However, combining KDs with these pharmacotherapies, particularly SGLT-2 inhibitors, requires careful clinical supervision because of potential risks, including euglycaemic diabetic ketoacidosis. We explore how a KD alters the composition of the gut microbiota, thereby affecting host health. We conclude by highlighting challenges and future directions for optimising KD-based therapies and by outlining the limitations of the current review.

Background: Vitamin D signalling, primarily through the vitamin D receptor (VDR), regulates cellular survival and programmed cell death. This systematic review aims to synthesise current evidence on the role of vitamin D in pancreatic β-cell apoptosis. Methods: Medline, Embase, and Scopus were searched for original studies investigating vitamin D, vitamin D analogues, or VDR-related interventions in experimental models of β-cell apoptosis or programmed cell death. Results: 26 studies were included. Across in vitro, ex vivo, and in vivo models, vitamin D signalling protected β-cells against apoptosis induced by cytokine-mediated inflammation, oxidative stress, glucotoxicity, lipotoxicity, streptozotocin exposure, and diabetic stress. These effects were associated with reduced NF-κB signalling, nitric oxide and reactive oxygen species production, improved mitochondrial stability, modulation of Bcl-2 family proteins, inhibition of endoplasmic reticulum stress, and regulation of pyroptosis, ferroptosis, and autophagy-related survival mechanisms. VDR activation also supported β-cell identity, insulin secretion, and β-cell mass preservation. In contrast, calcitriol-associated growth inhibition and increased apoptosis were reported in βTC insulinoma models. Conclusion: Vitamin D signalling generally appears cytoprotective in β-cells exposed to inflammatory, oxidative, and metabolic stress. However, its effects on β-cell survival are model- and context-dependent, reflecting differences in cellular background, experimental stressors, and methods used to assess cell death.

A ketogenic diet (KD) is a low-carbohydrate, high-fat dietary approach. Beyond treating neurologic disorders, KD has attracted significant media attention for its potential to improve obesity and diabetes. The diet induces a metabolic shift from glucose toward fatty acid oxidation and ketone body production. This shift leads to ketosis, which may reduce hunger, cause weight loss, and improve glycaemic control and insulin sensitivity. In particular, the positive effects of KD lower insulin demand and may thereby improve β-cell function. However, the long-term efficacy, safety, and sustainability of KD, especially for diabetes, remain debated. This review offers current insights into the effects of ketogenesis and ketosis and the potential mechanisms underlying them. We examine the metabolic effects of KD in obesity and diabetes, drawing on preclinical and clinical studies, and suggest that combining KD with antidiabetic agents may provide synergistic benefits. We explore how KD alters the composition of the gut microbiota, thereby impacting host metabolism and systemic inflammation. We conclude by highlighting challenges and future directions for optimizing KD-based therapies through personalized nutrition and pharmacological combination treatments.