Nutritional regulation of lipid metabolism in human adipose tissue.

Pfeiffer and colleagues years ago pointed out that different distributions and amounts of adipose tissue are associated with abnormalities of lipolysis and lipoprotein metabolism. Adipose tissue has several crucial roles including (i) mobilization from stores of fatty acids as an energy source, (ii) catabolism of lipoproteins such as very-low-density lipoprotein and (iii) synthesis and release of hormonal signals such as leptin and interleukin-6. These adipose tissue actions are crucially regulated by nutrition. The review considers the existence of metabolic pathways and modes of regulation within adipose tissue, and how such metabolic activity can be quantitated in humans. Nutrition can influence adipose tissue at several 'levels'. Firstly the level of obesity or malnutrition has important effects on many aspects of adipose tissue metabolism. Secondly short-term overfeeding, underfeeding and exercise have major impacts on adipose tissue behaviour. Lastly, specific nutrients are capable of regulating adipose tissue metabolism. Recently there have been considerable advances in understanding adipose tissue metabolism and in particular its regulation. This review discusses the behaviour of adipose tissue under various nutritional conditions. There is then a review of recent work examining the ways in which nutritional influences act via intra-cellular mechanisms, insulin and the sympathetic innervation of adipose tissue.

The endocrine function of the fat cell-regulation by the sympathetic nervous system.

The landmark discovery of leptin established beyond question the fact that adipose tissue is a crucial active regulator of body weight, an endocrine organ in its own right and part of a feedback circuit possessing both afferent and efferent loops. This is in addition to its more established roles as a receiver of incoming endocrine signals and modulator of circulating hormones such as sex steroids. Since this discovery, much has been learned about the role of leptin in the afferent loop of the hypothalamic regulation of body weight and indeed about some of the neuro-endocrine circuitry involved in the regulation of appetite and weight. Much less, however, is known about the efferent limb of the circuit, specifically relating to how the hypothalamus is able to influence adipocyte behaviour and how this link may itself be influenced by endocrine and paracrine signals, both acting on and emanating from adipocytes themselves, acting at multiple levels. This review will focus on the role of the sympathetic nervous system (SNS) and adreno-medullary system in relation to the regulation of adipose tissue physiology and endocrine function. The evidence in support of the hypothesis that the SNS is a crucial mediator of the efferent loop of this feedback circuit will be considered.

Immunosuppressive activity of BCG: effects of adjuvant disease, lymphocyte subpopulations, and homing of thoracic duct cells in rats.

Administration of BCG by various dosage schedules suppressed adjuvant disease in rats. BCG administration produced an initial increase, followed by a depression, of the phytohemagglutinin response of purified blood lymphocytes. An increase in absolute and relative numbers of bursa-equivalent (B)-cells followed BCG administration, concurrent with a decrease in the phytohemagglutinin responsiveness. With adjuvant alone, there was a diminution in phytohemagglutinin response and an increase in number of B-cells; the latter occurred immediately after adjuvant injection and also when the generalized disease appeared. When both BCG and adjvant were present, parallel increases of phytohemagglutinin responsiveness and B-cell numbers resulted. The pattern of tissue localization of radioactively labeled thoracic duct cells from normal or BCG-treated donors given to normal, BCG-treated, adjuvant-injected, and BCG-treated + adjuvant-injected syngeneic recipients indicated significantly greater homing to the thymus and decreased localization to the bone marrow when BCG had been given to either donors or recipients. When labeled thymus cells were used, only the decreased bone marrow localization was noted. These observations suggest that the suppressive effect of BCG may be mediated through modification of the lymphocyte recirculation pattern, possibly resulting from alterations in lymphocyte recognition sites.