Regulation of lipid metabolism in adipose tissue

Abstract

Adipose tissue is a major source of metabolic fuel. This metabolic fuel is stored in the form of triacylglycerol. Lipolysis of triacylglycerol yields non-esterified fatty acids and glycerol. In human subjects in vivo studies of the regulation of lipid metabolism in adipose tissue have been difficult because of the heterogeneous nature of the tissue and lack of a vascular pedicle. In the last decade the methodology of study of adipose tissue has improved with the advent of the anterior abdominal wall adipose tissue preparation technique and microdialysis. These techniques have demonstrated that lipid metabolism in adipose tissue is finely coordinated during feeding and fasting cycles, in order to provide metabolic fuel when required. Lipolysis takes place both in extracellular and intracellular space. The extracellular lipolysis is regulated by lipoprotein lipase and the intracellular lipolysis is regulated by hormone-sensitive lipase. In pathophysiological conditions such as trauma, sepsis and starvation profound changes are induced in the regulation of lipid metabolism. The increased mobilization of lipid fuel is brought about by the differential actions of various counter-regulatory hormones on adipose tissue blood flow and adipose tissue lipolysis through lipoprotein lipase and hormone-sensitive lipase, resulting in increased availability of non-esterified fatty acids as a source of fuel. In recent years, it has been demonstrated that adipose tissue produces various cytokines and these cytokines can have paracrine and endocrine effects. It would appear that adipose tissue has the ability to regulate lipid metabolism locally as well as at distant sites such as liver, muscle and brain. In future, it is likely that the mechanisms that lead to the secondary effects of lipid metabolism on atheroma, immunity and carcinogenesis will be demonstrated.

Role of nuclear receptor SHP in metabolism and cancer

“…Energy intake is mainly dependent on food ingestion and energy expenditure depends on several factors, including exercise and heat production, or so-called adaptive thermogenesis. Brown adipose tissue (BAT) is the major site for adrenergic mediated adaptive thermogenesis involving the uncoupling protein-1 (UCP1), whereas white adipose tissue (WAT) is mostly implicated in the regulation of lipid storage and catabolism [118, 119]. Previous study showed that basal gene expression of UCP1 and PGC-1α was increased in BAT of SHP −/− mice and this was associated with increased oxygen consumption, heat production and decreased obesity, indicating that SHP may be a negative regulator of energy utilization [120].…”

Developmental Origins of Obesity: Programmed Adipogenesis

“…SREBP1 facilitates lipogenesis by induction of extracellular lipolytic enzyme (lipoprotein lipase) and lipogenic enzyme (fatty acid synthase) that in turn, lead to an increase in fatty acid uptake and synthesis, promoting lipid accumulation within the adipocyte [58,59]. The release of free fatty acid from adipocytes is facilitated by an intracellular lipolytic enzyme, hormone-sensitive lipase [60]. …”

Overexpression of nuclear receptor SHP in adipose tissues affects diet-induced obesity and adaptive thermogenesis

“…Whereas energy intake is solely dependent on food ingestion, energy expenditure depends on several factors, such as exercise and heat production, or so-called adaptive thermogenesis. Despite extensive research focused on the understanding of obesity, the molecular mechanisms underlying increased adiposity are not fully understood.Brown adipose tissue (BAT) is the major site for adrenergic mediated adaptive thermogenesis involving the uncoupling protein-1 (UCP1), whereas white adipose tissue (WAT) is mostly implicated in the regulation of lipid storage and catabolism (8,13,15,26). Adaptive thermogenesis allows rodents to slow the development of obesity when overfed and maintain body temperature when exposed to a cold environment.…”