Bone marrow adipocyte lipolysis is required for maintaining bone mass under conditions of energy deficiency and is necessary for myelopoiesis following caloric restriction and irradiation.

The survival and growth of solid tumor cells in hypoxia is dependent on fatty acid storage in triglyceride lipid droplets promoted by HIG2.

SAA removes toxic products of lipolysis of the cell membrane by sPLA₂, indicating that SAA and sPLA₂ act synergistically to clear debris from injured sites, as required for tissue healing.

Reduced energy expenditure in obesity may result from reduced sensitivity to sympathetic activation due to inflammation-generated signals in adipose tissue.

A non-canonical p53 function in adipocyte plays a critical role in energy homeostasis and is involved in obesity-associated metabolic dysfunctions.

A novel transgenic lipid droplet reporter in transparent casper zebrafish allows direct visualization of individual lipid droplets in a living animal.

Specific human mitofusin 2 mutations induce selective upper body obesity with suppressed leptin expression and severe adipose mitochondrial dysfunction.

Celastrol covalently inhibited the chaperone activity of GRP78 and could disconnect the transduction of ER stress signal to downstream inflammatory response and lipid metabolism.

Intravascular triglyceride hydrolysis by lipoprotein lipase is crucial for delivering lipid nutrients to vital tissues, such as the heart, skeletal muscle, and adipose tissue.

Modulation of dermal adipocytes contributes to skin homeostasis and provides a promising new therapeutic strategy in the treatment of EGFRI-related skin disorders.