Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Evers et al. explore the interconnection between cellular mechanics and metabolism, emerging paradigms and the role of this interaction in cancer, cardiovascular disease and fibrosis.
Irx3 and Irx5 are effectors of the FTO locus, which is associated with obesity. Son et al. show regulation of hypothalamic neurogenesis by Irx3 and Irx5, uncovering a role for these genes in leptin response and energy homeostasis.
Teijeiro et al. find that IL-17A pathogenically reprograms adipocytes and that pharmacological targeting of IL-17A production with digoxin protects mice from diet-induced obesity.
Colchicine is an anti-inflammatory agent that suppresses myeloid cell activation and is commonly used to treat gout. In this issue of Nature Metabolism, Weng et al. demonstrate that colchicine exerts its anti-inflammatory effects in mice via the induction of the hormone GDF-15 in the liver.
Brown adipose tissue acquires increased thermogenic capacity with prolonged cold exposure through de novo recruitment of brown adipocytes. Studies by Shamsi et al. and Angueira et al. identify novel cellular origins of cold-induced brown adipocytes and further elucidate the molecular mechanism regulating the expansion of brown adipose tissue.
Weng et al. demonstrate that colchicine’s well-known anti-inflammatory effects are not due its direct action on immune cells but are indirect effects, mediated by hepatokines such as GDF15, which are released as a result of colchicine action in the liver.
Shamsi et al. identify vascular smooth muscle cells marked by expression of Trpv1 as a part of the cellular lineage of brown and beige fat. Cold stimulates the expansion and differentiation of Trpv1-expressing progenitors to highly thermogenic adipocytes.
Wyatt et al. explore glycaemic responses after a standardized meal and find that postprandial glycaemic dip is a predictor of hunger and subsequent energy intake.
Redox cofactors are essential for the metabolic reactions that support cell proliferation. NADPH is important both to combat oxidative stress and to facilitate reductive reactions in biosynthesis. In this issue, Tran et al. find that the enzyme that produces mitochondrial NADPH is critical in enabling proline synthesis to support cell proliferation when environmental proline is limited.
NADPH exists in separate cellular pools within the cytosol and mitochondria. Tran et al. find that mitochondrial NADPH is essential to enable proline biosynthesis during cell growth.
Using whole-exome sequencing data, Gorelick et al. identify lineage-specific somatic mutations in mitochondrial DNA that affect cancer progression and patient prognosis.
Learning to balance work, family, optimism and setbacks is a process for all early-career investigators. Stephanie Correa and Leng Han share their stories in this instalment of Career pathways.
The Drosophila white mutant has been used extensively for genetics studies. Sasaki et al. show a metabolic role of white, which is found to regulate intestinal stem cell proliferation during ageing through folate metabolism.
Some ‘species differences’ between mice and humans can be diminished simply by housing mice at warmer temperatures. Failure to strategically turn up the thermostat may undermine the translation of findings in mice to insights into human metabolic diseases.
Ludwig et al. map transcription and chromatin accessibility in single cells across the brainstem dorsal vagal complex, thereby identifying neuronal populations, including some that control feeding.
Obesity is associated with mitochondrial dysfunction and chronic metabolic derailment. Cho et al. report that elevated adipose expression of the Hippo kinases STK3 and STK4 (STK3/4) in obesity and type 2 diabetes decreases the mass and oxidative capacity of adipocyte mitochondria. Genetic or pharmacological inhibition of STK3/4 restores mitochondrial mass and function in adipocytes and improves glucose homeostasis in mice with diet-induced obesity. These findings support STK3/4 as new targets for obesity-related diseases.
Cho et al. show regulation of mitophagy, and thereby energy expenditure, in adipocytes by the Hippo pathway kinases STK3 and STK4, independently of classical Hippo signalling. Genetic inactivation of Stk3 and Stk4 is shown to protect mice from the adverse metabolic effects of diet-induced obesity.
Glycogen accumulation is a hallmark of clear cell renal cell carcinoma. Xie et al. uncover that under metabolic stress or hypoxia, these glycogen deposits are dispensable for tumour cell proliferation and survival, both in vivo and in vitro.
It is self-evident that consuming alcohol affects brain function and behaviour. What is not clear, however, is how alcohol does so. A new study shows that impairments in balance and motor coordination evoked by low-dose alcohol are mediated not by ethanol itself but by one of its metabolites, which is produced locally by astrocytes in the brain rather than in the liver.
