Regulation of redox homeostasis by ATF4-MTHFD2 axis during white adipose tissue browning.

Maintaining redox balance is crucial for mitochondrial homeostasis. During browning of white adipocytes, both the quality and quantity of mitochondria undergo dramatic changes. However, the mechanisms controlling the redox balance in the mitochondria during this process remain unclear.

Chrononutrition: Potential, Challenges, and Application in Managing Obesity.

The circadian clock orchestrates nearly every aspect of physiology, aligning metabolic processes with environmental cues, such as light and food intake. While the central pacemaker in the suprachiasmatic nucleus synchronizes peripheral clocks across key metabolic tissue, feeding behavior emerges as the dominant cue for peripheral clock alignment. This interaction reveals a crucial link between circadian biology and metabolism.

In vivo brown adipogenic reprogramming induced by a small molecule cocktail.

Research on the browning of adipocytes has been increasing in recent years owing to the prevalence of lifestyle diseases such as obesity and diabetes. Accumulation of brown fat enhances energy expenditure and could be a strategy to fight obesity. While approaches to induce browning in animals for therapeutic purposes have been tested, clinically applicable options are limited.

Cross-talks between Metabolic and Translational Controls during Beige Adipocyte Differentiation.

Whether and how regulatory events at the translation stage shape the cellular and metabolic features of thermogenic adipocytes is hardly understood. In this study, we report two hitherto unidentified cross-talk pathways between metabolic and translational regulation in beige adipocytes. By analysing temporal profiles of translation activity and protein level changes during precursor-to-beige differentiation, we found selective translational down-regulation of OXPHOS component-coding mRNAs.

H19X-encoded microRNAs induced by IL-4 in adipocyte precursors regulate proliferation to facilitate differentiation.

Adipose tissue, an organ critical for systemic energy homeostasis, is influenced by type 2 immunity in its development and function. The type 2 cytokine interleukin (IL)-4 induces the proliferation of bipotential adipocyte precursors (APs) in white fat tissue and primes these cells for differentiation into beige adipocytes, which are specialized for thermogenesis. However, the underlying mechanisms have not yet been comprehensively examined.

The Influence of Ambient Temperature on Adipose Tissue Homeostasis, Metabolic Diseases and Cancers.

Adipose tissue is a recognized energy storage organ during excessive energy intake and an endocrine and thermoregulator, which interacts with other tissues to regulate systemic metabolism. Adipose tissue dysfunction is observed in most obese mouse models and humans. However, most studies using mouse models were conducted at room temperature (RT), where mice were chronically exposed to mild cold.

Reduction in endoplasmic reticulum stress activates beige adipocytes differentiation and alleviates high fat diet-induced metabolic phenotypes.

Endoplasmic reticulum (ER) stress is closely associated with various metabolic diseases, such as obesity and diabetes. Development of beige/brite adipocytes increases thermogenesis and helps to reduce obesity. Although the relationship between ER stress and white adipocytes has been studied considerably, the possible role of ER stress and the unfolded protein response (UPR) induction in beige adipocytes differentiation remain to be investigated.

Potential Benefits of Acupuncture and Herbs for Obesity-Related Chronic Inflammation by Adipokines.

The adipose tissue is an organ that stores energy in the form of fats. It also has been known as an endocrine playing an integral role in metabolic homeostasis by secreting various adipokines. In obesity, the adipokine components and secretion patterns are altered toward proinflammation with weight gain, causing low chronic inflammation, which is closely linked to various metabolic diseases.