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Adipose tissue varies depending on localization. Vijay et al. perform single-cell RNA sequencing in multiple adipose tissue depots from obese individuals and identify distinct subpopulations of endothelial cells, immune cells and pre-adipocytes.
Amyloid precursor protein contributes to the pathogenesis of Alzheimer’s disease. An et al. show that its increase in white adipose tissue under a high-fat diet promotes obesity and impairs mitochondrial function by blocking the protein import machinery.
Yu et al. report a bioluminescence- and paper-based assay for the rapid quantification of NAD+ levels in biological samples, such as blood and tissues.
Bevers and Litovchenko et al. sequence mitochondrial genomes from 169 different inbred Drosophila melanogaster strains to reveal mitochondrial population structure as well as links between mitochondrial haplotypes and metabolic variation in flies.
Persistent mitochondrial DNA stress is shown to upregulate nuclear DNA damage and repair responses via activation of the cGAS–STING pathway and a subset of interferon-stimulated genes.
The anti-diabetic drug metformin is shown to elevate plasma levels of the hormone GDF15. This increase in GDF15 is required for reductions in appetite and body mass, which are known to contribute to the beneficial metabolic effects of the drug.
Pulsatile GABA secretion from human beta cells via the volume regulatory anion channel (VRAC) and subsequent uptake by the GABA-permissive taurine transporter (TauT) is shown to regulate total insulin secretion and pulsatility.
Known as a regulator of lipolysis, ABHD5 is found to also act as a serine protease that cleaves HDAC4 in response to catecholaminergic stimulation, thus resulting in the formation of a polypeptide that protects against metabolic-stress-induced heart failure.
Liu et al. describe a molecular network wherein SIRT7 couples light-driven systemic body temperature cues to hepatic oscillators via HSP70 to ensure circadian phase coherence and glucose homeostasis in the liver.
Al Nabhani et al. show how excessive caloric intake during the postnatal period increases the risk of developing intestinal bowel disease during adulthood, owing to increased intestinal permeability, cytokines and hydrogen sulfide production by the microbiota.
Emerging findings identify important roles for brain lipoprotein receptors in the control of whole-body energy homoeostasis. Here Lee et al. reveal that IDOL-mediated regulation of VLDLR abundance in neurons, but not in peripheral metabolic tissues, regulates food intake and energy expenditure.
In addition to having direct anti-cancer effects, the cardiac glycoside ouabain is shown to kill a broad range of senescent cells, thus suggesting that cardiac glycosides represent a novel class of senolytics.
Dietary restriction (DR) late in life does not improve survival and has little benefit in metabolic health in mice. The absence of a DR gene-expression signature in fat tissue suggests that a ‘nutritional memory’ interferes with the benefits of DR.
Non-alcoholic steatohepatitis (NASH) is characterized by lipid accumulation within hepatocytes and fibrosis. Seitz et al. show that the GTPase protein Rab24 is increased in the livers of people who are obese or have NASH.
Here the authors provide a regulatory framework for the cardiac mitochondrial ATP synthase, which is shown to be dependent on cellular activity; levels of Ca2+, ADP and NADH; and the potential of the inner mitochondrial membrane.
Anoxia─lack of oxygen─commonly occurs during ischaemic heart disease. Using yeast, worms and mice, Hannich et al. show that anoxia-associated tissue injury and cell death are due to accumulation of a non-canonical sphingolipid, 1-deoxydihydroceramide, that damages the cytoskeleton.
Increased mitochondrial DNA (mtDNA) replication frequency is shown to lead to defects in maintenance of the nuclear genome due to reallocation of nucleotides to mitochondria, challenging the proposed direct role of mtDNA mutations as drivers of cellular and organismal ageing in mammalian progerias.
After development, adult skeletal muscle retains the capacity to regenerate by activating muscle stem cells. Here the authors demonstrate that the glycosylphosphatidylinositol-anchored membrane protein GAS1, which is induced in muscle stem cells with age, suppresses muscle regenerative capacity but can be inhibited by glial cell line-derived neurotrophic factor (GDNF).
The cellular effects of cold preservation in heart transplantation and how warm ischaemia leads to damage are unclear. Here the authors identify succinate accumulation as a major damaging metabolic change in warm ischaemia.