During sustained cold exposure, lipid fuel is specifically directed towards brown adipose tissue, but not white adipose tissue, via cold-induced regulation of Angiopoietin-like 4 (ANGPTL4).

Integrative analysis of multi-tissue transcriptomics data of mice subjected to cold, mild warm or room temperature places the thermal adaptation of individual tissues in a whole-organism perspective.

Single-cell expression profiling and genetic lineage analysis show that aging impairs adipocyte differentiation from precursor cells and blocks the thermogenic activation of adipocytes during cold exposure.

The production of beige adipocytes following cold exposure is blocked as mice get older and leads to changes in the expression of metabolic genes.

The activation of beige adipocyte thermogenesis by cold temperatures and β3-adrenergic receptor agonists induce beige adipocyte formation, function and perdurance.

A single mutation in acetyl-CoA carboxylase blocking AMPK regulation inhibits food intake in mice in response to cold exposure or fasting causing them to lose weight.

A gene regulatory program regulating thermal stress response and organismic death.

A combination of neuroscience approaches and indirect calorimetry demonstrate a physiological role for AgRP neurons in cold-induced hyperphagia and strongly suggest temperature is an important regulator of AgRP neuron activity.

Crosstalk between IL10-producing immune cells and adipocytes within adipose tissue is an important determinant of thermogenesis and systemic energy balance.

Mitochondrial pyruvate transport is required for brown fat thermogenesis.