Brown Vs White Adipose Tissue, Or Together?

Wednesday, 15 April 2009 00:00

The worldwide increase of obesity rate (and its consequent increase in disability, life, and economic burdens) is causing increasingly more alarm among the authorities and more concern and attention among the scientists because of a lack of appropriate and adequate treatment. Increased energy intake and reduced consummation of energy is considered the basis of an algebraic interpretation of the appearance and development of adiposity. Increased adipose tissue in some areas of the body is the anatomical pattern of adiposity. We learned in the last decades once more that the adipose tissue is not just a fat repository such as an energetic store. For many years  anatomists have described two different types of adipose tissue: white adipose tissue and brown. During the last 40-50 years the white adipose tissue has been shown to be involved in several pathophysiologic mechanisms: from the metabolism of fatty acids and the production of cytokines (e.g. CRP, IL-6, IL-9, Il-18) and hormones (e.g. adypokine, leptine) (Curr Diab Rep 2003; 3:293-8), to insulin resistance, inflammation, endothelial dysfunction, and cardio-metabolic deregulation (Nature 2006, 444:847-853). Over the last ten years, the so-called metabolic syndrome (see definitions in the box below) attracted the attention of researchers and clinicians in the fields of diabetology, cardiology, internal medicine, gender medicine, pediatrics, geriatrics, etc. The most recent guidelines issued jointly by the ESH (European Society of Hypertension) and ESC (European Society of Cardiology) (EHJ 2007; 28: 1462-1536) on hypertension introduced the metabolic syndrome into the constellation of multiple risk factors for cardio- and cardiovascular diseases and stroke. The studies on, and the consequent pharmacologic approach to, the endocannabinoid system had raised hopes to find the right way to approach the metabolic syndrome or its synonym, the cardio-metabolic syndrome. These studies deserve further innovative pharmacologic approaches; however, they have paved the way to the development of a large amount of information on the physiology and metabolism of white adipose tissue. It is well established that this tissue is the primary site of energy storage and release of hormones and cytokines that modulate whole-body metabolism and insulin resistance (Clin Endocrinol (Oxf) 2006; 64:355-65).

While excess accumulation of white adipose tissue causes obesity, brown adipose tissue, on the other hand, is important for both basal and inducible energy expenditure in the form of thermogenesis mediated by the expression of the tissue-specific uncoupling protein 1 (UCP1). Brown adipose tissue is considered to affect the whole-body metabolism and may modify sensitivity to insulin and modify susceptibility to weight gain (NEJM 2009; 360:1509-1517).

The attention being paid to the pathophysiologic role of brown adipose tissue in thermogenesis and its correlation to obesity is not new: Arne Astrup (et al. Clin Sci 1984; 66:179-186 - Am J Physiol 1985; 248: E 507), Bradford B. Lowell (Nature 1993; 366: 740-742 - Nature 2000; 404:652-660), J.Enrique Silva (Nature 1983; 305:712-713) noted the thermogenesis induced by ephedrine, the adaptive thermogenesis, and the adrenergic activation of triiodothyronine production in brown adipose tissue. More recently three papers and one editorial have been issued by New England Journal of Medicine on the thermogenesis in humans by brown adipose tissue. Groups of researchers from Maastricht (NL), Boston (MA, US), Turku (FI) together with Goteborg (SE), have approached the topic from different point of view: the cold activation of brown adipose tissue in healthy men (NEJM 2009, 360:1500-8), the identification and importance of brown adipose tissue, in human adults (NEJM 2009; 360:1509-1517), and function of brown (and white) adipose tissue in healthy humans (NEJM 2009; 360:1518-25). More details on the comparison between the two adipose tissues are in the Focus on Science of this issue of HealthEurope. Comments by Francesco Celi from Boston deserve attention here. There is agreement that it is not easy to achieve an ideal fat mass in obese people simply through the right balance of energy intake and energy consumption. In fact evolutionary pressure has demanded for thousands of years that enough energy be stored to survive the lack of food due to climate and other reasons (Obes Rev 2008; 9:165-80). “Interventions designed to increase energy expenditure are relatively limited. An increase in physical activity, although effective, is not easy to sustain. The pharmacologic approach has also been disappointing. Supraphysiologic doses of thyroid hormones or adrenergic agonists result in an increase in energy expenditure, but their systemic adverse events preclude their use for the treatment of obesity….”  Taken together, these studies on brown adipose tissue point to a potential "natural" intervention to stimulate energy expenditure: turn down the heat and burn calories (and reduce the carbon footprint in the process). Obviously, this strategy is an oversimplification, and one should expect compensatory mechanisms aimed at maintaining the energy homeostasis — that is, an increase in energy intake in response to a loss of energy secondary to cold exposure. Nonetheless, these studies, by showing the presence and activity of brown adipose tissue in adult humans, are a powerful proof of concept that this tissue might be used as a target for  pharmacologic and environmental intervention, aimed at modulating energy expenditure (NEJM 2009, 360:1553-6).
 

15 April, 2009

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Adipobiology of NGF and BDNF George Chaldakov 2009-05-29 09:34:55 Adipobiology of NGF and BDNF: implication for cardiometabolic diseases Recently, adipobiology became a focus of numerous studies showing that the adipose tissue is the body’s largest endocrine and paracrine organ producing multiple signaling proteins collectively designated adipokines (Chaldakov et al. Curr Pharm Des 2003; 9: 1023-1031). However, studies on adipobiology of neurotrophins have recently emerged, nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) being examples of adipose-derived neurotrophins. Based on our own and other authors\' data, we suggest that both neurotrophic and metabotrophic potentials of NGF and BDNF may be involved in the pathogenesis of cardiometabolic diseases, including human coronary atherosclerosis and the metabolic syndrome (Chaldakov et al. Prog Brain Res 2004; 146: 279-289) and acute coronary syndromes (Manni et al. Int J Cardiol 2005; 102: 169-171). To what extend adipose tissue secretion may contribute to the alteration of plasma levels of NGF and BDNF remains to further be evaluated (Sornelli et al. Biomed Rev 2007; 18: 85-88).

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