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Under a high-fat diet, the amyloid precursor protein, which is involved in the development of Alzheimer’s disease, accumulates at the protein-entry gate of mitochondria in white adipose tissue, thus leading to mitochondrial dysfunction, adipocyte hypertrophy and obesity.
GDF15 is an anorectic hormone that relays systemic stress to the brain. In the current issue of Nature Metabolism, Day et al. elegantly demonstrate that the frontline anti-diabetes drug, metformin, lowers body weight by increasing circulating levels of GDF15.
Di Gioia and colleagues report on how the oxidized phospholipid oxPAPC alters metabolism in macrophages via glutamine and oxaloacetate, thus boosting production of the cytokine IL-1β and promoting atherosclerosis.
A study in Nature Metabolism reveals a hitherto-unknown enzymatic and physiological role of ABHD5, which acts as a protease that couples extracellular cues to the epigenome of cardiomyocytes by cleaving histone deacetylase 4 (HDAC4).
A new study by Menegaz et al. in this issue of Nature Metabolism addresses fundamental questions on the acute regulation and role of GABA secretion in pancreatic islets.
The mechanism of alcohol-induced changes in the brain is multi-faceted. Acetate, the product of hepatic alcohol metabolism, might contribute to addictive behaviour by regulating gene expression.
Lifespan is increased and ageing is delayed by lifelong dietary restriction. A study in Nature Metabolism shows that these benefits are reduced when dietary restriction is started in old age, owing to the development of an inflexible nutritional memory within white adipose tissue.
Nuclear DNA damage has detrimental effects on cellular homoeostasis and accelerates the ageing process. A new study causally links error-prone mitochondrial replication to increased nuclear DNA damage, thus suggesting that the hallmarks of ageing are associated with nuclear genome instability, a potential unifying denominator in the ageing process.
GDF15 is an anorectic hormone that signals organismal stress to the brain. New data suggest that GDF15 enhances tolerance to acute inflammation by modulating liver lipid metabolism and triglyceride availability in mice.
Findeisen et al. have engineered IC7Fc, a cytokine for the treatment of type 2 diabetes, that selectively activates beneficial metabolic pathways systemically and in metabolic tissues without promoting an inflammatory response.
In this issue, Diehl et al. report that exogenous serine is essential for the cellular redox state and cancer nucleotide production, despite the ability of cancer cells to synthesize serine de novo in vitro.
Obesity is the result of an imbalance between caloric intake from the diet and energy expenditure. A new study provides evidence that alterations in calcium transport efficiency in muscle lead to an increased metabolic rate and protect mice against diet-induced obesity.
Systemic accumulation of branched-chain amino acids (BCAAs) is a major metabolic hallmark and contributor to insulin resistance associated with obesity. A recent report identifies SLC25A44 as the BCAA transporter in mitochondrial membranes and shows that BCAA catabolism in brown adipose tissue significantly affects thermogenic activity, systemic BCAA clearance, energy expenditure and overall metabolic health.
Dopamine is an important neurotransmitter with essential roles in movement control and salience, and implications in addiction as well as weight loss, decreased food intake and a reduced motivational drive to eat. Folgueira et al. now demonstrate that dopamine causes weight loss and increases brown adipose tissue temperature via activation of the dopamine receptor D2R in hypothalamic GABA-expressing neurons in mice, and treatment with the dopamine agonist cabergoline causes weight loss in humans.
Cells contributing to atherosclerotic disease are highly plastic and can shift their phenotype in a changing microenvironment. A study in Nature Metabolism now reveals that transforming growth factor-β (TGF-β) can transform endothelial cells into pro-inflammatory cells and that inhibition of TGF-β-receptor signalling in the endothelium can reverse atherosclerosis in mice.
The gene encoding the RagC GTPase (RRAGC), an activator of a nutrient-sensing pathway that drives cellular anabolism, is mutated in 15% of follicular lymphoma cases. A new study provides evidence that RRAGC mutations promote lymphomagenesis by distorting the nutrient-dependent control of paracrine signals from the microenvironment, thus enhancing B-cell activation.
A recent study by Esteghamat et al., published in Nature Genetics, has reported that CELA2A, encoding a pancreatic enzyme, is a novel genetic cause of metabolic syndrome and atherosclerosis.
Diabetes mellitus invariably involves impaired regulation of insulin secretion from pancreatic β cells, as a result of unfavourable environmental influences in combination with aberrant expression of risk genes at either the transcriptional or the translational level. A recent report in Nature Metabolism explores a novel role of mRNA methylation in β-cell function and suggests that its downregulation causes type 2 diabetes.
Mitochondrial H+ leak, which is responsible for basal respiration, appears to be a transport process mediated by the ADP/ATP carrier and regulated by fatty acids and adenine nucleotides.
Lymphedema, a condition of fluid retention and tissue swelling, is currently incurable and is treated primarily with physical therapy. Studies in mice reveal that intake of a ketogenic diet or exogenous ketone bodies may alleviate lymphedema by increasing the formation of lymphatic vessels, which can drain excess lymph fluid.
