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Extracellular-matrix remodelling contributes to tumour progression, results in intratumoural fibrosis and promotes metastatic behaviour. A new study by Papalazarou et al. now reveals that a pathway involved in ATP supply, the creatine phosphagen system, is a mechanosensitive target during pancreatic cancer invasion.
The ketogenic diet is a low-carbohydrate, high-fat diet that forces a metabolic switch towards fatty acid oxidation. Here, Goldberg et al. show that a ketogenic diet initially improves metabolic health and expands adipose tissue γδ T cells that are important for glycaemic control during obesity.
Extracellular-matrix remodelling promotes tumour progression and metastasis. Papalazarou et al. demonstrate that mechanosensing affects pancreatic cancer cell migration, metabolism and ultimately metastatic potential by targeting the creatine–phosphagen ATP-recycling system.
This study establishes reciprocal regulation between the two key nutrient sensors in cells, mTORC1 and AMPK, showing that mTORC1 directly inhibits AMPK by phosphorylation at S345 in the AMPK catalytic subunit α2.
Somatostatin is secreted by delta cells and inhibits insulin and glucagon secretion. Here Vergari et al. demonstrate a mechanism for somatostatin secretion that is dependent on decreased extracellular potassium and increased intracellular sodium levels, and is altered in islets from patients with diabetes.
Converting serine to pyruvate and ammonia, serine racemase is shown to support colon-cancer growth, thus highlighting a new strategy that cancer cells use to maintain cellular pyruvate levels and mitochondrial mass.