[대학원 생명과학과 세미나 안내]
연사 : Sheila Collins 교수(Vanderbilt University Medical Center)
연제 : Integration of Receptor Signaling Mechanisms for Brown Adipose Thermogenesis and Physiology
일시 : 2018년 4월 23일 (월) 오후 4시
장소 : 하나과학관 A동 207호
초청교수 : 백자현 교수
Abstract
Brown adipose tissue (BAT) evolved as a means of generating heat from stored calories, an adaptation termed non-shivering thermogenesis (NST); it was particularly important to early humans before the advent of houses and clothing. Brown adipocytes are highly enriched in mitochondria and express uncoupling protein-1 (UCP1), a unique protein that serves to ‘uncouple’ the mitochondrial proton gradient from ATP production. These cells are avid consumers of the glucose and fatty acids to support this activity, the net result being energy expenditure. Active brown fat is now appreciated to be present in humans throughout the lifespan. Moreover, its amount, as in rodents, significantly correlates with lower body fat and greater insulin sensitivity. Therefore an increase in humans of brown fat cells and their metabolic activity could target obesity and its comorbidities. β-adrenergic receptors (βARs) and protein kinase A convey the signal from catecholamines to increase lipolysis in adipocytes and to promote the ‘browning’ of adipocytes within white fat depots. The cardiac natriuretic peptides ANP and BNP also increase lipolysis and adipose ‘browning’ through a parallel pathway via protein kinase G. An important component of adipose browning is the expansion of mitochondrial density and capacity to consume glucose and fatty acids. By understanding the components in the network of signals and their regulation we may identify new targets for clinical intervention in metabolic disease. This presentation will focus on novel mechanisms driving mitochondrial biogenesis and adipose browning and their contribution to whole body fuel homeostasis.