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Although the pineal gland influences several physiological systems, only a few studies have investigated its role in the intermediary metabolism. In the present study, male Wistar rats, pinealectomized or sham-operated 6 wk before the experiment, were submitted to both intravenous glucose tolerance tests (IVGTT) and insulin binding as well as glucose transport assays in isolated adipocytes. The insulin receptor tyrosine kinase activity was assessed in liver and muscle. The insulin secretory response during the IVGTT was impaired, particularly in the afternoon, and the glucose transport responsiveness was 33% lower in pinealectomized rats. However, no difference was observed in the insulin receptor number of adipocytes between groups as well as in insulin-stimulated tyrosine kinase activity, indicating that the initial steps in the insulin signaling were well conserved. Conversely, a 40% reduction in adipose tissue GLUT-4 content was detected. In conclusion, pinealectomy is responsible for both impaired insulin secretion and action, emphasizing the influence of the pineal gland on glucose metabolism.

Numerous studies address the physiology of adipose tissue (AT). The interest surrounding the physiology of AT is primarily the result of the epidemic outburst of obesity in various contemporary societies. Briefly, the two primary metabolic activities of white AT include lipogenesis and lipolysis. Throughout the last two decades, a new model of AT physiology has emerged. Although AT was considered to be primarily an abundant energy source, it is currently considered to be a prolific producer of biologically active substances, and, consequently, is now recognized as an endocrine organ. In addition to leptin, other biologically active substances secreted by AT, generally classified as cytokines, include adiponectin, interleukin-6, tumor necrosis factor-alpha, resistin, vaspin, visfatin, and many others now collectively referred to as adipokines. The secretion of such biologically active substances by AT indicates its importance as a metabolic regulator. Cell turnover of AT has also recently been investigated in terms of its biological role in adipogenesis. Consequently, the objective of this review is to provide a comprehensive critical review of the current literature concerning the metabolic (lipolysis, lipogenesis) and endocrine actions of AT.

Objectives: To describe the advances in research into the physiological role of white adipose tissue, with emphasis on its endocrinal role in inflammatory processes, feeding behavior, insulin sensitization and modulation of the atherogenetic process. To deal with the potential role of adipose tissue as a source of stem cells for regeneration of tissues, with special emphasis on adipogenesis and its consequences for development of obesity.Sources: Important information was compiled from the scientific literature in order that this analysis contains an explanatory synthesis of the aspects mentioned above. Summary of the findingsIn addition to its classical functions as primary metabolic energy store, meeting energy requirements during periods of deprivation by means of lypolisis, adipose tissue also has the capacity to synthesize and secrete a variety of hormones -the adipokines. These are active in a range of processes, such as control of nutritional intake (leptin) and control of sensitivity to insulin and inflammatory processes (TNF-α, IL-6, resistin, visfatin, adiponectin). Furthermore, since adipose tissue also contains undifferentiated cells, it has the ability to generate new adipocytes, regenerating its own tissue (adipogenesis), and also the ability to give rise to other cells (myoblasts, chondroblasts, osteoblasts), which has great therapeutic potential in the not-too-distant future. Conclusions:The range of functional possibilities of adipose tissue has widened. An understanding of these potentials could make this tissue a great ally in the fight against conditions that are currently assuming epidemic proportions (obesity, diabetes mellitus, arterial hypertension and arteriosclerosis) and in which adipose tissue is still seen as the enemy.J Pediatr (Rio J). 2007;83(5 Suppl):S192-203: Adipocyte, lipogenesis, lypolisis, adipokines adipogenesis.

All of the adaptations acquired through physical training are reversible with inactivity. Although significant reductions in maximal oxygen uptake (Vo2max) can be observed within 2 to 4 wk of detraining, the consequences of detraining on the physiology of adipose tissue are poorly known. Our aim was therefore to investigate the effects of discontinuing training (physical detraining) on the metabolism and adipocyte cellularity of rat periepididymal (PE) adipose tissue. Male Wistar rats, aged 6 wk, were divided into three groups and studied for 12 wk under the following conditions: 1) trained (T) throughout the period; 2) detrained (D), trained during the first 8 wk and detrained during the remaining 4 wk; and 3) age-matched sedentary (S). Training consisted of treadmill running sessions (1 h/day, 5 days/wk, 50-60% Vo2max). The PE adipocyte size analysis revealed significant differences between the groups. The adipocyte cross-sectional area (in μm(2)) was significantly larger in D than in the T and S groups (3,474 ± 68.8; 1,945.7 ± 45.6; 2,492.4 ± 49.08, respectively, P < 0.05). Compared with T, the isolated adipose cells (of the D rats) showed a 48% increase in the ability to perform lipogenesis (both basal and maximally insulin-stimulated) and isoproterenol-stimulated lipolysis. No changes were observed with respect to unstimulated lipolysis. A 15% reduction in the proportion of apoptotic adipocytes was observed in groups T and D compared with group S. The gene expression levels of adiponectin and PPAR-gamma were upregulated by factors of 3 and 2 in D vs. S, respectively. PREF-1 gene expression was 3-fold higher in T vs. S. From these results, we hypothesize that adipogenesis was stimulated in group D and accompanied by significant adipocyte hypertrophy and an increase in the lipogenic capacity of the adipocytes. The occurrence of apoptotic nuclei in PE fat cells was reduced in the D and T rats; these results raise the possibility that the adipose tissue changes after detraining are obesogenic.

ResumoA obesidade é um dos principais problemas de saúde pública. Indivíduos obesos são mais suscetíveis a desenvolver doenças cardiovasculares e diabetes melito tipo 2. A obesidade resulta do aumento no tamanho e no número de adipócitos. O balanço entre adipogênese e adiposidade determina o grau de obesidade do indivíduo. Adipócitos maduros secretam adipocinas, tais como TNFα, IL-6, leptina e adiponectina, e lipocina, o ácido palmitoleico ω-7. A produção de adipocinas é maior na obesidade, o que contribui para o estabelecimento de resistência periférica à insulina. O conhecimento dos eventos moleculares que regulam a diferenciação dos pré-adipócitos e de células-tronco mesenquimais em adipócitos (adipogênese) é importante para o entendimento da gênese da obesidade. A ativação do fator de transcrição PPARγ é essencial na adipogênese. Certos ácidos graxos são ligantes de PPARγ e podem, assim, controlar a adipogênese. Além disso, alguns ácidos graxos atuam como moléculas sinalizadoras em adipócitos, regulando sua diferenciação ou morte. Dessa forma, a composição lipídica da dieta e os agonistas de PPARγ podem regular o balanço entre adipogênese e morte de adipócitos e, portanto, a obesidade. Arq Bras Endocrinol Metab. 2009;53(5):582-94. DescritoresAdipogênese; tecido adiposo; ácidos graxos; obesidade; PPAR gama; C/EBP-α AbstRActObesity is one of the major Public Health problems. Obese individuals are more susceptible to develop cardiovascular diseases and type 2 diabetes mellitus. The obesity results from the increase in size and number of the adipocytes. The balance between adipogenesis and adiposity determines the degree of obesity. Mature adipocytes secrete adipokines, such as TNFα, IL-6, leptine and adiponectin, and lipokine, the palmitoleic acid ω-7. The production of adipokines is increased in obesity, contributing to the onset of peripheral insulin resistance. The knowledge about the molecular events that regulate the differentiation of pre-adipocytes and mesenchymal stem cells into adipocytes (adipogenesis) is important for the comprehension of the genesis of obesity. Activation of transcription factor PPARγ plays an essential role in the adipogenesis. Certain fatty acids are PPARγ ligands and can control adipogenesis. Moreover, some fatty acids act as signaling molecules regulating their differentiation into adipocytes or death. Accordingly, the lipid composition of the diet and PPARγ agonists can regulate the balance between adipogenesis and death of adipocytes and, therefore, the obesity. Arq Bras Endocrinol Metab. 2009;53(5):582-94.

The effect of sodium chloride salt restriction and overload on insulin sensitivity is still an open question. Some authors have shown that NaCl salt restriction increases insulin resistance, whereas others have reported the opposite. In the present study, the objective was to get some more insight on this issue by studying the influence of dietary salt content on glucose uptake in isolated adipocytes. Male Wistar rats were fed from weaning either low (0.15%) or high (7.94%) salt diets. On the 12th week of age, weight and tail-cuff blood pressure were measured, followed 10 days later by an intravenous glucose tolerance test with concomitant insulin determinations. One week later, the rats were killed by decapitation and epididymal adipocytes were obtained for glucose metabolism evaluation. No weight differences were observed between both groups of animals. Blood pressure was significantly higher (P < .001) on salt overloaded rats (146 +/- 11 mm Hg) than on salt restricted ones (115 +/- 5 mm Hg). Dietary salt content did not influence the area under the curve of plasma glucose. Area under the curve of insulin levels was lower (P = .023) on the high than on the low salt diet. A higher (P < .001) glucose uptake in the absence and in the presence of insulin was observed in adipocytes from rats on the high salt diet. The median effective concentration (EC50) from the dose-response curves of glucose uptake was the same on both groups of animals. Glucose oxidation and incorporation into lipids was also enhanced by salt overload. High salt increased insulin receptor density (P < .001). In conclusion, salt overload increased blood pressure, and high and low salt dietary content did not influence insulin sensitivity based on the unchanged EC50 from the in vitro studies. However, insulin-independent glucose uptake, oxidation, and incorporation into lipids were enhanced in adipocytes from rats on the high salt diet. The lower levels of insulin during the glucose tolerance test on salt-loaded animals may be a consequence of the higher insulin-independent glucose uptake in that group.

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