Brown adipose tissue-derived metabolites and their role in regulating metabolism

Adults with metabolically healthy overweight or obesity present more brown adipose tissue and higher thermogenesis than their metabolically unhealthy counterparts

“… 67 These batokines can regulate whole-body metabolism through autocrine, paracrine, and endocrine functions and act in different organs and tissues (e.g., WAT, heart, skeletal muscle). 68 Indeed, the batokines' endocrine function might underlie the association between BAT volume and activity and a healthy cardiometabolic profile. 68 Batokines enhance peripheral insulin sensitivity and lower blood lipids improving systemic glucose and lipid homeostasis and protecting against cardiometabolic diseases in mice.…”

“… 68 Indeed, the batokines' endocrine function might underlie the association between BAT volume and activity and a healthy cardiometabolic profile. 68 Batokines enhance peripheral insulin sensitivity and lower blood lipids improving systemic glucose and lipid homeostasis and protecting against cardiometabolic diseases in mice. 67 Indeed, humans with detectable BAT showed lower glucose and triglyceride levels and higher HDL-C levels than those without detectable BAT.…”

Adiponectin stimulates Sca1+CD34−-adipocyte precursor cells associated with hyperplastic expansion and beiging of brown and white adipose tissue

“…A high capacity for hyperplastic expansion of subcutaneous adipose tissue protects against metabolic disturbances in obesity [1]. Moreover, brown and beige adipocytes play also a protective role -these cell types regulate metabolism and energy expenditure through non-shivering thermogenesis and the release of metabolism-regulatory factors [2,3]. Brown/beige adipocytes may also act as a metabolic sink for circulating nutrients and thereby prevent deleterious ectopic lipid deposition [4].…”

Potential regulatory role of PGC-1α within the skeletal muscle during metabolic adaptations in response to high-fat diet feeding in animal models

“…We have previously reviewed evidence on the implications of lipid overload and its potential contribution to the development of skeletal muscle insulin resistance and pathological changes in mitochondrial oxidative capacity [ 60 ], without focusing on the molecular mechanisms that could be involved in this process. Therefore, because of its significant role in controlling energy metabolism and involvement in insulin signaling [ 23 , 73 , 86 ], it remains important to establish how HFD affects skeletal muscle function in preclinical models of obesity. Special attention falls on the causal relationship between regulation of PGC-1α in connection with the development of mitochondrial dysfunction and insulin resistance within the skeletal muscle.…”