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By analysing microbial profiles in three adipose tissue depots and the liver and plasma of morbidly obese individuals, a new study uncovers a unique organ-specific microbial signature, or potential internal ‘tissue microbiota’, in obese people with diabetes.
By introducing a rationally designed metabolic pathway into the genome of Escherichia coli, Kim et al. have re-engineered central carbon metabolism to utilize the one-carbon intermediates formate and methanol for the first time, thus generating a biological platform for sustainable fuel and chemical production.
A recent study by Yuan et al., published in Nature Genetics, demonstrates multidimensional molecular alterations in mitochondrial DNA in human cancers and provides an online catalogue of mitochondrial genomes in many cancer types.
Current pharmacological options for diabetes treatment help patients control blood glucose levels but do not reverse the decline in insulin-secreting β-cells. A new study now shows that a pharmacological combination of insulin and a GLP-1–oestrogen conjugate not only decreases daily insulin requirements but also improves β-cell function.
Inherited deficiencies in oxidative phosphorylation cause severe mitochondrial disease. A recent study in Nature Biotechnology demonstrates that an engineered bifunctional enzyme can rescue the biochemical consequences of mitochondrial dysfunction.
Xu and colleagues provide a comprehensive overview of cholesterol metabolism in cancer cells and its effects on immune cells of the tumour microenvironment, highlighting its effects on cancer growth as well as opportunities for therapeutic intervention.
New research in this issue of Nature Metabolism shows how a high-protein diet increases amino acids in blood and atherosclerotic plaques, and in plaque macrophages activates mTOR signalling, suppresses mitophagy and increases apoptosis, thereby exacerbating atherosclerotic-plaque build-up in genetically modified mouse models.
A new study in mice reveals time-dependent effects of a ketogenic diet on resident immune cells in visceral adipose tissue, which have consequences for whole-body metabolic homeostasis.
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.
