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The author discusses how metabolic engagements and reconfiguration of immune and non-immune cells following virus recognition modulate the natural course of viral infections, and how such early metabolic alterations are likely to influence longer-term disease manifestations of infection.
Gut commensal bacteria and their metabolites can contribute to metabolic diseases. Qiao, Liu et al. reveal that expansion of Parabacteroides merdae attenuates experimental atherosclerosis.
Microglia require a large amount of energy to clear plaques in the brains of people with Alzheimer’s disease. Leng et al. found that increased activity of the glycolytic enzyme hexokinase 2 (HK2) blocks microglial phagocytosis in Alzheimer’s disease. Inhibition of HK2 results in increased microglial energy production by a compensatory lipid metabolism response, restores phagocytosis and improves cognitive function.
Hepatocellular carcinoma (HCC) is the 4th leading cause of cancer mortality. Modulation of tumour metabolism may represent a novel therapeutic strategy. Hexokinase 1, secreted into extracellular vesicles by activated hepatic stellate cells, is shown to be taken up by tumour cells, where it accelerates glycolysis and HCC growth.
SARS-CoV-2-induced anorexia triggers systemic metabolic alterations. In a study published in Nature, Karagiannis et al. show that the ketone body β-hydroxybutyrate (BHB) improves COVID-19 disease outcomes. Further, BHB metabolically and functionally reprograms CD4+ T cells, highlighting immunometabolic tuning of immunity in COVID-19.
Decreased insulin action and insulin receptor signalling contribute to the pathology of diabetes. Liu et al. uncover a role for the Ephrin type-B receptor 4 in insulin receptor degradation regulating liver and systemic insulin sensitivity.
This Review summarizes emerging concepts for diabetes therapy aimed at specifically altering β cell biology and function, such as β cell insulin signalling, proliferation, differentiation, apoptosis, as well as the selective killing of senescent β cells.
It has long been recognized that some phenotypic variation in mammals cannot be explained by known genetic or environmental variables. Here, the authors show that the absence of Nnat expression is associated with polyphenism in mice with the same genotype. Broadly consistent effects are also found in humans.
PRDM16 is a key mediator of thermogenic fat, counteracting adipose fibrosis and inflammation. Kajimura and co-authors demonstrate that a CUL2–APPBP2 ubiquitin E3 ligase complex destabilizes the PRDM16 protein, resulting in declined metabolic activity in an age-dependent manner.
Mass spectrometry imaging holds promise for mapping the intricate organization of metabolism in complex tissues. Wang et al. combine this exciting technique with metabolic tracing ex vivo to uncover metabolic specialization and adaptation in the mouse kidney.
New research shows that a drug conjugate that links the dual PPAR𝛼/𝛾 agonist tesaglitazar to a GLP-1 receptor agonist has superior effects on weight loss and glucose metabolism compared with monotherapy in mice. The conjugate has actions in the hypothalamus that may contribute to its benefits.
Adipose tissue plays a critical role in systemic metabolism. This work describes how perturbations in the adipocyte progenitor cell repertoire during the perinatal period exert long-lasting metabolic effects in adulthood.
Measurements of oxygen consumption rates have been central to the resurgent interest in studying cellular metabolism. To enhance the overall reproducibility and reliability of these measurements, Divakaruni and Jastroch provide a guide advising on the selection of experimental models and instrumentation as well as the analysis and interpretation of data.
The authors of this Perspective summarize the state of human islet research and compare available islet procurement methods, proposing strategies to increase collaboration and standardization to accelerate discoveries on diabetes.
Evanna Mills and Edward Chouchani share the experience of their successful mentor–mentee relationship and talk about the challenges of starting a new lab — both from a recent perspective and five years on.
New research reports that targeting the asialoglycoprotein receptor (ASGR1) in mice promotes cholesterol excretion through a mechanism involving stabilization of LXR without lipogenesis activation, strengthening the idea of therapeutically targeting ASGR1 to lower blood cholesterol and risk of atherosclerotic cardiovascular disease.
Longer duration of breastfeeding is shown to have long-lasting effects in rodents, which lead to an adult phenotype that is resistant to diet-induced obesity and has increased brown adipose tissue activity through a process dependent on hypothalamic FGF21 signalling.
Nampoothiri et al. discuss the most recent literature that places glial cells as key mediators of energy balance through integration of peripheral signals in discrete brain regions, highlighting the relevance of glia in the pathophysiology of metabolic diseases.
The hindbrain is mostly known to participate in eating behaviour by controlling short-term meal parameters and aversive responses to gut malaise. Cheng et al. review current evidence revealing non-aversive neuronal circuits in the hindbrain that are relevant for initiation and termination of homeostatic feeding, as well as for the long-term control of body weight.
Alcantara and Miranda-Tapia et al. discuss the central mechanisms that dictate eating behaviour, by dissecting the neural circuits involved in food procurement, food consumption, and meal termination.
