AGRP neurons integrate environmental food-related cues with internal metabolic signals to modulate interscapular brown adipose tissue thermogenesis and energy expenditure, at least in part, via mTORC1 signalling.

Sulforaphane through NRF2-dependent and -independent cellular and molecular pathways alleviates leptin resistance to reverse the diet-induced obesity.

Intracellular and interorgan skeletal crosstalk highlights integrative skeletal physiology.

T3 regulates BAT thermogenesis by controlling the expression of genes involved in the management of metabolic fuels as well as tissue plasticity.

In sensory neurons, the receptors LXRα and LXRβ sense dietary-derived molecules to regulate whole body energy expenditure, and present a possible target for new anti-obesity agents.

NFATc1 is identified as a molecular marker of articular cartilage progenitor cells and a transcriptional repressor of chondrocyte differentiation, providing fundamental insights into the origin and differentiation mechanism of articular chondrocytes.

Diet-induced obesity in mice led to a duration of diet-dependent bone marrow adipocyte whitening, which drove monocyte expansion and skewing towards a tissue-invasive phenotype, likely contributing to ensuing tissue infiltration that accompanies obesity and diabetes.

A newly identified adipose lineage cell population, MALP, regulates marrow vasculature and osteogenesis in bone.