Articles

Subcellular compartmentalization of the glycolytic enzyme PFKM regulates cell fate and metabolic switch during skeletal muscle differentiation.

Free fatty acids drive uncoupled respiration in white adipocytes, mediated in complex with ATP/ADP carriers, to modulate thermogenesis and cold tolerance in obese thermoneutral-adapted mice.

Cytosolic ScURA uncouples de novo pyrimidine synthesis from mitochondrial electron transport, and rescues pyrimidine production and cell proliferation under pharmacological or genetic mETC disruption.

The authors present a genetically encoded tool based on a bifunctional enzyme that can regenerate NAD⁺ while executing an engineered glycerol shunt. The tool successfully restored redox imbalance and modulated lipid metabolism in vitro and in a mouse hepatic steatosis model.

Boosting mitochondrial metabolism in neurons in central memory circuits by enhancing Ca²⁺ retention in the mitochondrial matrix is shown to improve long-term memory formation in flies and mice.

SLC6A6 localizes to the inner mitochondrial membrane and mediates mitochondrial taurine import, which sustains mitochondrial tRNA modifications and cell growth.

Hepatic glycogenolysis is essential for protein glycosylation and rhythmic secretion by the liver. Disruptions to hepatic glycogenolysis, caused by congenital diseases or physiological factors such as obesity, caloric restriction and changes to meal timing, alter hepatic protein secretion.

Mitochondrial superoxide production is shown to preserve nuclear envelope integrity by controlling lipid peroxidation, with impact on nuclear and organismal ageing in C. elegans.

Glucose deprivation triggers the secretion of the cytokine LIF, which promotes angiogenesis and immune suppression in lung cancer models.

Lamin A/C in the nuclear lamina is identified as a regulator of cysteine catabolic flux, necessary for cell fate decisions and function.

Analysing the causal links of gene expression and protein abundance on type 2 diabetes risk in blood and seven tissues related to the disease from individuals of four ancestries, the authors advance our understanding of the genetic architecture of type 2 diabetes

A pathogenic subset of NK cells is identified that promotes type 1 diabetes and is generated via T cell-derived IL-21.

Psychological stress-mediated dysregulation of catecholamine signalling rewires the hepatic kynurenine pathway, which in turn impairs liver CD8⁺ T cell function and promotes liver cancer progression.

Hexokinase detachment from the outer mitochondrial membrane is shown to support aerobic glycolysis in cancer cells. Differential localization of the HK1 isoform to the outer mitochondrial membrane, compared to the HK2 isoform, explains the conditional essentiality of HK2 in cancer cells cultured in physiologic media.

Prior hypoglycemia alters the paracrine interaction between islet α and δ cells, leading to impaired counter-regulatory glucagon secretion through somatostatin hypersecretion, increasing the risk of recurrent hypoglycemia.

Stable adipocytes resist lipolysis in healthy states but are highly susceptible to a catecholamine-independent, neurosystemic pathway-driven catabolic state.

Elevated adipocyte-derived AFABP in obesity disrupts iron homeostasis in intestinal stem cells (ISCs), which impairs PPARα signalling and blocks ISC differentiation after injury.

Multi-omics profiling of the mucosal mycobiome in individuals with Crohn’s disease identifies C. sphaerospermum as a protective fungal species that counteracts intestinal inflammation and reinforces the intestinal barrier.

Hepatocyte-specific GPR110 mediates metabolic dysfunction-associated steatohepatitis progression by regulating hepatic oestrogen sensitivity in a sex-specific manner, specifically in female mice.

The authors use Perturb-seq analysis in human pancreatic islet beta cells, as well as in vivo and in vitro analyses, to identify potential therapeutic targets for type 2 diabetes, including ZZEF1, which regulates insulin synthesis and cellular stress in islet β cells.