Adipose tissue is a complex, essential, and highly active metabolic and endocrine organ. Besides adipocytes, adipose tissue contains connective tissue matrix, nerve tissue, stromovascular cells, and immune cells. Together these components function as an integrated unit. Adipose tissue not only responds to afferent signals from traditional hormone systems and the central nervous system but also expresses and secretes factors with important endocrine functions. These factors include leptin, other cytokines, adiponectin, complement components, plasminogen activator inhibitor-1, proteins of the renin-angiotensin system, and resistin. Adipose tissue is also a major site for metabolism of sex steroids and glucocorticoids. The important endocrine function of adipose tissue is emphasized by the adverse metabolic consequences of both adipose tissue excess and deficiency. A better understanding of the endocrine function of adipose tissue will likely lead to more rational therapy for these increasingly prevalent disorders. This review presents an overview of the endocrine functions of adipose tissue.

/pdf/adipose-tissue-as-an-endocrine-organ-18h86uxhhc.pdf

Adipose Tissue as an Endocrine Organ

Methods for assessment, e.g., anthropometric indicators and imaging techniques, of several phenotypes of human obesity, with special reference to abdominal fat content, have been evaluated. The correlation of fat distribution with age, gender, total body fat, energy balance, adipose tissue lipoprotein lipase and lipolytic activity, adipose tissue receptors, and genetic characteristics are discussed. Several secreted or expressed factors in the adipocyte are evaluated in the context of fat tissue localization. The body fat distribution and the metabolic profile in nonobese and obese individuals is discussed relative to lipolysis, antilypolysis and lipogenesis, insulin sensitivity, and glucose, lipid, and protein metabolism. Finally, the endocrine regulation of abdominal visceral fat in comparison with the adipose tissue localized in other areas is presented.

/pdf/subcutaneous-and-visceral-adipose-tissue-their-relation-to-5crse4rslq.pdf

Subcutaneous and visceral adipose tissue : Their relation to the metabolic syndrome

Obesity is a heterogeneous disorder. Obese individuals vary in their body fat distribution, their metabolic profile and degree of associated cardiovascular and metabolic risk. Abdominal obesity carries greater risk of developing diabetes and future cardiovascular events than peripheral or gluteofemoral obesity. There are differences between adipose tissue present in subcutaneous areas (SCAT) and visceral adipose tissue (VAT) present in the abdominal cavity. These include anatomical, cellular, molecular, physiological, clinical and prognostic differences. Anatomically, VAT is present mainly in the mesentery and omentum, and drains directly through the portal circulaion to the liver. VAT compared with SCAT is more cellular, vascular, innervated and contains a larger number of inflammatory and immune cells, lesser preadipocyte differentiating capacity and a greater percentage of large adipocytes. There are more glucocorticoid and androgen receptors in VAT than in SCAT. VAT adipocytes are more metabolically active, more sensitive to lipolysis and more insulin-resistant than SCAT adipocytes. VAT has a greater capacity to generate free fatty acids and to uptake glucose than SCAT and is more sensitive to adrenergic stimulation, while SCAT is more avid in absorption of circulating free fatty acids and triglycerides. VAT carries a greater prediction of mortality than SCAT.

/pdf/subcutaneous-and-visceral-adipose-tissue-structural-and-1v45i8x6iq.pdf

Subcutaneous and visceral adipose tissue: structural and functional differences

Accumulating evidence indicates that obesity is closely associated with an increased risk of metabolic diseases such as insulin resistance, type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease. Obesity results from an imbalance between food intake and energy expenditure, which leads to an excessive accumulation of adipose tissue. Adipose tissue is now recognized not only as a main site of storage of excess energy derived from food intake but also as an endocrine organ. The expansion of adipose tissue produces a number of bioactive substances, known as adipocytokines or adipokines, which trigger chronic low-grade inflammation and interact with a range of processes in many different organs. Although the precise mechanisms are still unclear, dysregulated production or secretion of these adipokines caused by excess adipose tissue and adipose tissue dysfunction can contribute to the development of obesity-related metabolic diseases. In this review, we focus on the role of several adipokines associated with obesity and the potential impact on obesity-related metabolic diseases. Multiple lines evidence provides valuable insights into the roles of adipokines in the development of obesity and its metabolic complications. Further research is still required to fully understand the mechanisms underlying the metabolic actions of a few newly identified adipokines.

Obesity and Its Metabolic Complications: The Role of Adipokines and the Relationship between Obesity, Inflammation, Insulin Resistance, Dyslipidemia and Nonalcoholic Fatty Liver Disease

This paper presents the 12th update of the human obesity gene map, which incorporates published results up to the end of October 2005. Evidence from single-gene mutation obesity cases, Mendelian disorders exhibiting obesity as a clinical feature, transgenic and knockout murine models relevant to obesity, quantitative trait loci (QTL) from animal cross-breeding experiments, association studies with candidate genes, and linkages from genome scans is reviewed. As of October 2005, 176 human obesity cases due to single-gene mutations in 11 different genes have been reported, 50 loci related to Mendelian syndromes relevant to human obesity have been mapped to a genomic region, and causal genes or strong candidates have been identified for most of these syndromes. There are 244 genes that, when mutated or expressed as transgenes in the mouse, result in phenotypes that affect body weight and adiposity. The number of QTLs reported from animal models currently reaches 408. The number of human obesity QTLs derived from genome scans continues to grow, and we now have 253 QTLs for obesity-related phenotypes from 61 genome-wide scans. A total of 52 genomic regions harbor QTLs supported by two or more studies. The number of studies reporting associations between DNA sequence variation in specific genes and obesity phenotypes has also increased considerably, with 426 findings of positive associations with 127 candidate genes. A promising observation is that 22 genes are each supported by at least five positive studies. The obesity gene map shows putative loci on all chromosomes except Y. The electronic version of the map with links to useful publications and relevant sites can be found at http://obesitygene.pbrc.edu.

/pdf/the-human-obesity-gene-map-the-2005-update-3zvtci1u6f.pdf

The human obesity gene map: the 2005 update.

Aims/hypothesis Tumour necrosis factor alpha (TNFα) is a candidate gene for the development of obesity, which in turn is a major risk factor for diabetes mellitus The aim of our study was to investigate whether a previously known NcoI-sensitive polymorphism (–308 G/A) in the promoter region of the TNFα gene was related to body weight¶Methods Genotyping was done in 239 male and 342 female non-diabetic subjects with a marked variation in body mass index (BMI)¶Results We found three genotypes; AA (n = 13), AG (n = 158) and GG (n = 410) When the material was divided according to sex, allele specific phenotypic differences were confined to women The female subjects carrying the AA genotype were markedly more obese than both the AG and GG carriers (mean BMI = 414 vs 323 and 317 kg/m2, respectively, p = 002) The body fat content of female AA carriers was increased by one-third compared with AG/GG carriers (p = 002) We found no differences between genotypes with respect to waist-to-hip ratio, blood pressure or metabolic variables Among obese female subjects (BMI > 27 kg/m2), we also found that the BMI and body fat content of AA carriers (n = 7) were also higher than for AG/GG carriers¶Conclusion/interpretation The AA-variant at position –308 in the promoter region of the TNFα gene could be an important genetic factor behind excessive fat accumulation in women [Diabetologia (2000) 43: 117–120]

https://link.springer.com/content/pdf/10.1007%2Fs001250050015.pdf

Excessive fat accumulation is associated with the TNFα -308 G/A promoter polymorphism in women but not in men.

OBJECTIVE : To investigate the influence of four weeks treatment with a strictly defined very low calorie diet (VLCD) on the regulation of adipocyte metabolism in vitro in subcutaneous fat cells of obese subjects. DESIGN : Prospective study. SUBJECTS : Nine obese, but otherwise healthy and drug-free women aged 26-48 years with BMI 36.4-51.9 kg/m 2 were investigated before and during the fourth week on a calorie restricted diet. MEASUREMENTS : A subcutaneous adipose tissue biopsy was obtained from the abdominal area. Isolated fat cells were prepared and incubated in vitro with different agents acting on lipolysis at defined steps in the lipolytic cascade. Glycerol (lipolytic index), hormone-sensitive lipase activity and incorporation of glucose into lipids were measured. RESULTS : VLCD caused a two-fold rise in basal lipolysis (p < 0.005). In spite of this, the maximal lipolytic response of noradrenaline, isoprenaline (non-selective beta-adrenoceptor agonist), dobutamine (beta-adrenoceptor agonist), terbutaline (beta 2 -adrenoceptor agonist), CGP 12177 (beta 3 -adrenoceptor agonist), forskolin (stimulating adenylyl cyclase), dibuturyl cyclic AMP and 8-bromo cyclic AMP (cyclic AMP analogues resistant or sensitive to phosphodiesterase, respectively) were maintained. No differences were found in the hormone-sensitive lipase activity before or during VLCD. The specific alpha 2 -adrenoceptor agonist UK 14304 was equally effective in inducing antilipolysis both before and during calorie restriction. However, during VLCD, the sensitivity and maximal antilipolytic effect of insulin were significantly reduced (p < 0.05) and the ability of insulin to stimulate lipogenesis was almost completely blunted. CONCLUSIONS : Four weeks of VLCD induced elevated basal lipolysis, a resistance to the ability of insulin to induce antilipolysis and lipogenesis in subcutaneous fat cells, but preserved lipolytic catecholamine action. These are factors that together promote fat mobilization and thereby weight reduction during long-term calorie restriction.

Regulation of lipolysis in fat cells of obese women during long-term hypocaloric diet.

Increased lipid mobilization in thyrotoxicosis is attributed to amplification of catecholamine action in fat cells by thyroid hormones. We investigated the adrenergic regulation of lipolysis in isolated sc abdominal fat cells obtained from 14 patients with thyrotoxicosis and 18 control subjects. Ten of the hyperthyroid subjects were also reinvestigated after antithyroid treatment. The thyrotoxic state was associated with a 3-fold increase in maximum norepinephrine-induced lipolysis (P < 0.005), unaltered sensitivity to dobutamine (selective beta 1-adrenoceptor agonist) and clonidine (selective alpha 2-adrenoceptor agonist), but 15 times enhanced sensitivity to terbutaline (selective beta 2-adrenoceptor agonist; P < 0.01). Moreover, thyrotoxicosis was accompanied by a 3-fold increase in beta 2-adrenoceptor number (P < 0.005), but unchanged beta 1-adrenoceptor levels. Further, the lipolytic effects of dibutyryl cAMP (activating protein kinase A and thereby hormone-sensitive lipase) and forskolin (activating adenylate cyclase) were about 60% enhanced (P < 0.005). No change in the maximum activity of the hormone-sensitive lipase could be demonstrated in the hyperthyroid state compared to that in the euthyroid state. The observed abnormalities in lipolysis and beta 2-adrenoceptor number were normalized after antithyroid treatment. It is concluded that in human hyperthyroidism, the interactions between thyroid hormone and catecholamines in adipocytes involve abnormalities at both receptor and postreceptor levels. The former mechanism seems to be a selective increase in the expression of the beta 2-adrenoceptors. The latter mechanism involves increased ability of cAMP to activate hormone-sensitive lipase, but not a change in maximum enzyme capacity.

/pdf/catecholamine-induced-adipocyte-lipolysis-in-human-2qh8qam4hh.pdf

Catecholamine-induced adipocyte lipolysis in human hyperthyroidism.

Lipolytic catecholamine resistance linked to α 2 -adrenoceptor sensitivity—a metabolic predictor of weight loss in obese subjects

Lipolytic catecholamine resistance linked to alpha 2-adrenoceptor sensitivity--a metabolic predictor of weight loss in obese subjects.

OBJECTIVE: To evaluate a possible influence of a hereditary trait for obesity on the regulation of adipocyte metabolism in vitro in subcutaneous fat cells in obese and non-obese subjects. DESIGN: A biopsy from abdominal subcutaneous fat was obtained from consecutive subjects with or without a family trait for obesity. A positive family history of obesity was considered present if one or more of the first degree relatives had a BMI of 27 kg/m2 or more. SUBJECTS: 67 non-obese and 60 obese subjects, age 19–60 y. A family trait for overweight was present in 42 of the lean subjects and in 50 of the obese subjects. MEASUREMENTS: Fat cells were isolated and incubated in vitro with isoprenaline (a non-selective beta-adrenoceptor agonist), forskolin (activates the adenylyl cyclase) and dibutyryl cyclic AMP (stimulates the protein kinase hormone-sensitive lipase complex). Glycerol release was measured and used as lipolytic index. RESULTS: Maximal lipolytic response per g triglycerides was about 50% lower in obese subjects both with and without a positive heredity and in non-obese subjects with a family trait for obesity as compared to non-obese subjects without such trait (P=0.0001). Fat cell volume was twice as high in obese as compared to lean subjects. Drug-induced maximal glycerol release per fat cell in the obese subjects, regardless of family history of obesity, reached a similar level, but did not exceed that of the lean group without heredity. CONCLUSIONS: Obesity is associated with catecholamine resistance with a relatively ineffective lipolysis in fat cells, and presence of a family history of obesity was not associated with a further suppression of lipolysis. In the lean subjects, heredity for obesity significantly influenced lipolysis to similar low levels as in the obese subjects.

Influence of heredity for obesity on adipocyte lipolysis in lean and obese subjects

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