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Glucose-6-Phosphatase (G6Pase), a key enzyme in gluconeogenesis and glycogenolysis in the mammalian liver and kidney, converts glucose-6-phosphate to glucose for maintaining systemic blood glucose homeostasis during nutrient deprivation. However, its function has remained elusive in insects, which have no need for G6Pase in sugar homeostasis since they convert glucose-6-phosphate to trehalose, their main circulating sugar, via trehalose phosphate synthase (TPS1). In this study we identify an unexpected and essential requirement for G6Pase in male fertility, specifically to produce motile sperm.

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Background: With the global increase in metabolic disorders, identifying effective dietary strategies is crucial for enhancing health outcomes. While various health advantages of alkaline reduced water (ARW) have been documented, its specific impacts on glucose and lipid metabolism in both healthy and diabetic conditions are still not well understood.

Methods: This study investigates how ARW affects carbohydrate and lipid metabolism in male Wistar rats, which were induced to develop glucose metabolism disorders through subcutaneous injections of nicotinamide and streptozotocin (STZ).

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Aims/hypothesis: Immunotherapeutics targeting T cells are crucial for inhibiting autoimmune disease progression proximal to disease onset in type 1 diabetes. There is an outstanding need to augment the durability and effectiveness of T cell targeting therapies by directly restraining proinflammatory T cell subsets, while simultaneously augmenting regulatory T cell (Treg) activity. Here, we present a novel strategy for preventing diabetes incidence in the NOD mouse model using a blocking monoclonal antibody targeting the type 1 diabetes risk-associated T cell co-stimulatory receptor, CD226.

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This study investigates the impact of β-fructofuranosidase (Bmsuc1) on the development of the silk gland in silkworms (Bombyx mori). Previous research shows that Bmsuc1 is highly expressed in the silk glands and may be involved in silk gland development and protein synthesis. However, the precise mechanism by which Bmsuc1 regulates silk gland development remains unclear.

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G6PC3 deficiency is a monogenic immunometabolic disorder that causes severe congenital neutropenia type 4. Patients display heterogeneous extra-hematological manifestations, contributing to delayed diagnosis. Here, we investigated the origin and functional consequence of the G6PC3 c.

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