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Maternal circadian rhythms influence the health of infants. Cui, Xu and colleagues find that disruption of maternal rhythms impairs neonatal immune cell function and aggravates neonatal inflammatory disorders, which can be rescued by the administration of docosahexaenoic acid (a metabolite found in breast milk).
In mice, disruption of circadian rhythms during pregnancy aggravates neonatal inflammation via metabolic reprograming of myeloid cells in the offspring.
A new sensor that detects optoacoustic signals generated by mid-infrared light enables measurement of glucose concentration from intracutaneous tissue rich in blood. This technology does not rely on glucose measurements in interstitial fluid or blood sampling and might yield the next generation of non-invasive glucose-sensing devices for improved diabetes management.
A new methodology uses intravital time-gated mid-infrared optoacoustic signals for accurate non-invasive measurements of glucose concentrations in blood-rich volumes of the skin.
AMPK directly phosphorylates the mitochondrial protein SYNJ2BP to facilitate its interaction with the RNA-binding protein SYNJ2a, which transports Pink1 mRNA into neurites. AMPK inhibition downstream of insulin signalling untethers Pink1 mRNA from neuronal mitochondria and favours PINK1-dependent mitophagy in neurons. ApoE4-induced insulin receptor internalization reverses the process by stabilizing Pink1 mRNA binding to neuronal mitochondria.
When preparing your manuscript, clear presentation of the data and concise writing are key. In this Editorial, we offer tips on how to better communicate your results.
Hees et al. identify a mechanism that integrates insulin signalling with distal mitochondrial quality control in neurons via AMPK/PINK1, with implications for mitochondrial dysfunction in the context of insulin resistance in neurons.
The mechanisms that drive cancer cachexia are unclear. Adipocyte activation of GPR81 by high levels of lactate is now shown to drive adipose tissue browning, thermogenesis and a loss of body weight in mouse models of cancer.
The mechanism by which metformin affects food intake remains controversial. Now, two studies link metformin treatment with the induction of the appetite-suppressing metabolite N-lactoyl-phenylalanine, which is produced by the intestine.
Metformin treatment was found to be associated with acute increases in the appetite-suppressing metabolite Lac-Phe in several human observational and interventional studies.
Tumour-derived lactate activates adipose GPR81, which in turn leads to cachexia. Targeting GPR81 and its downstream signalling pathway holds therapeutic potential for treating cancer cachexia.
Metformin is shown to trigger production and release of Lac-Phe from gut epithelial cells, which is required for its effects on food intake and loss of body weight.
Eating requires the sensing in the stomach of not only nutrients, but also volume. A study in Nature Metabolism shows that stretch activation of PIEZO1 on X/A-like cells of the stomach reduces ghrelin production and secretion, which consequently reduces food intake.
Sharma et al. review the regulation and biological functions of apparently ‘futile’ dynamic lipid cycle in regulating whole-body metabolic homeostasis.
Zhang, Fang, et al. develop a method to perform an in-depth lysine succinylation analysis in the mouse liver. This approach allows them to identify a previously unappreciated mechanism of regulation of the urea cycle and ammonia detoxification.
A recent study in Nature Metabolism uncovers a mechanism for pain sensitization that involves a regulatory protein of glycogen metabolism in spinal astrocytes. Targeting this protein, or the lactate fluxes linked to glycogen breakdown, may provide novel opportunities for pain management.