Longstanding systemic inequalities – fueling unequal access to critical resources such as healthcare, housing, education, and employment opportunities – are largely responsible for the significant race disparities in obesity and COVID-19. Because of this legacy, public health emergencies like the COVID-19 pandemic disproportionately impact communities of color, exacerbated by high rates of pre-existing

Patients with a metabolic syndrome (overweight, diabetes, hypertension, and dyslipidemia) have a particularly bad outcome if infected with SARS-CoV-2. Yu et al. (2020) suggest that insulin therapy itself may promote fatality in patients with COVID-19 and diabetes.

Adipose tissue is composed of a variety of cells distributed in different depots and playing various metabolic roles. In a recent issue of Nature, Sun et al. (2020) use snRNA-seq and functional studies to identify a population of adipocytes that can suppress the thermogenic activity of neighboring adipocytes by secretion of acetate.

Childhood obesity has been linked to early puberty in girls but the mechanism(s) by which overnutrition triggers pubertal onset remain unclear. In a recent issue of Cell Metabolism, Heras et al., 2020 implicate a non-canonical central ceramide to ovarian sympathetic innervation pathway as a novel mediator of obesity-induced pubertal acceleration in female rats.

Sustained proliferative potential of cancer cells creates heightened energetic and biosynthetic demands. The resulting overt dependence of cancer cells on unperturbed nutrient supply has prompted a widespread interest in amino acid restriction strategies as potential cancer therapeutics. However, owing to rapid signaling and metabolic reprogramming in cancer cells, the prospects for success of amino

Nonalcoholic fatty liver disease (NALFD) is now a leading cause of chronic liver disease worldwide, in part, as a consequence of rapidly rising levels of obesity and metabolic syndrome and is a major risk factor for cirrhosis, hepatocellular carcinoma, and liver-related mortality. From NAFLD stems a myriad of clinical challenges related to both diagnosis and management. A growing body of evidence suggests

Key pathological, including oncogenic, signaling pathways regulate the canonical functions of metabolic enzymes that serve the cellular metabolic needs. Importantly, these signaling pathways also confer a large number of metabolic enzymes to have noncanonical or nonmetabolic functions that are referred to as “moonlighting” functions. In this review, we highlight how aberrantly regulated metabolic enzymes

It is still unclear if the ability of key regulators of actin cytoskeletal remodeling to influence lipid metabolism contributes to kidney injury. In this issue of Cell Metabolism, Fu et al. (2020) show that junctional adhesion molecule-like (JAML) is a novel mediator of glomerular disease progression while suggesting a direct link between defects in cell adhesion and lipotoxicity.

Two recent studies published in Nature Immunology map out the link between dysregulated mitochondrial metabolism and terminal exhaustion of tumor-infiltrating T lymphocytes. Yu et al. (2020) and Vardhana et al. (2020) show that defective mitophagy or impaired oxidative phosphorylation triggers mitochondrial reactive oxygen species production, which in turn promotes a T cell exhaustion program, limiting

Metabolic reprogramming is a hallmark of T cell activation and function. As our understanding of T cell metabolism increases, so does our appreciation of its inherent complexity. The metabolic heterogeneity of T cells that reside in different locations, such as lymphoid and non-lymphoid tissues, presents a challenge to developing therapies that exploit metabolic vulnerabilities. The roots of metabolic

Acute or chronic cellular stress resulting from aberrant metabolic and biochemical processes may trigger a pervasive non-apoptotic form of cell death, generally known as ferroptosis. Ferroptosis is unique among the different cell death modalities, as it has been mostly linked to pathophysiological conditions and because several metabolic pathways, such as (seleno)thiol metabolism, fatty acid metabolism

Hepatic stellate cells (HSCs) are resident non-parenchymal liver pericytes whose plasticity enables them to regulate a remarkable range of physiologic and pathologic responses. To support their functions in health and disease, HSCs engage pathways regulating carbohydrate, mitochondrial, lipid, and retinoid homeostasis. In chronic liver injury, HSCs drive hepatic fibrosis and are implicated in inflammation

The consensus model of glucose-stimulated insulin secretion (GSIS) holds that ATP generation by oxidative phosphorylation directly regulates KATP channel activity and thus insulin granule release, a concept inconsistent with bioenergetic principles. Here, Lewandowski et al. (2020) and Abulizi et al. (2020) report that regulation of GSIS is much more complex as different sources of ATP generation are

Glia-neuron interactions underlie a number of homeostatic processes in the brain. In this issue of Cell Metabolism, Li et al. (2020) demonstrate that the regeneration of central nervous system axons is accelerated through modulation of neuronal GABA-B receptor activity by metabolic energy intermediaries released from glia.

The need for discovering new genes driving metabolic disease susceptibility is clear; even clearer is the need for their subsequent functional characterization. A new paper reports a role for miR-128-1 in metabolic control through a series of elegant mouse studies, and an intriguing hypothesis about its “thrifty” role in metabolism.

Nutrient acquisition and metabolism are integral components of cell growth, proliferation, and differentiation programs. In a recent study in Nature, Bian et al. (2020) revealed that cancer cells outcompete T cells for methionine uptake, resulting in diminished SAM production, attenuated H3K79 dimethylation, decreased STAT5 expression, and impaired T cell immunity to cancer.

Neurons within the arcuate nucleus control energy balance and represent the functional substrates through which FGF1 deploys its anti-diabetic action. Alonge et al. (2020) now report that the integrity of arcuate perineuronal nets, an extracellular matrix component that enmeshes GABAergic neurons, is reversibly altered in diabetic rats and a key component for FGF1-mediated diabetic remission. These

SARS-CoV-2 pneumonitis can quickly strike to incapacitate the lung, leading to severe disease and sometimes death. In this perspective, we suggest that vitamin D deficiency and the failure to activate the vitamin D receptor (VDR) can aggravate this respiratory syndrome by igniting a wounding response in stellate cells of the lung. The FDA-approved injectable vitamin D analog, paricalcitol, suppresses

Emerging research has identified metabolic pathways that are crucial for the proper regulation of immune cells and how, when deranged, they can cause immune dysfunction and disease progression. However, due to technical limitations such insights have relied heavily on bulk measurements in immune cells, often activated in vitro. But with the emergence of single-cell applications, researchers can now