Does Visceral or Subcutaneous Fat Influence Peripheral Cortical Bone Strength During Adolescence? A Longitudinal Study

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Abstract

This study evaluated the longitudinal relationships among visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and peripheral bone strength during adolescence. Fat and lean mass, VAT and SAT area, and android/gynoid (A/G) ratio were estimated with DXA. Our main outcome was strength-strain index (SSI), an indicator of peripheral bone strength estimated by pQCT at the radius and tibia. Sex-specific analyses evaluated the longitudinal bone-fat relationship from ages 11 to 19 years with linear mixed models using biological age as the time variable and adjusted for limb length and lean mass in 182 girls and 167 boys. Variables were standardized (mean =0, SD =1) prior to model fitting and results shown are parameter estimates ± SE. Fat mass and SAT were positively associated with SSI (radius: 0.07 ± 0.02, p =0.003 and 0.05 ± 0.02, 0.041, respectively; tibia: 0.09 ± 0.02, p <0.001 and 0.08 ± 0.02, p <0.001, respectively) prior to, but not following adjustment for lean mass in girls. In contrast, fat mass and SAT were negatively associated with radial SSI, both before and after adjustment for lean mass in boys (fat mass: −0.05 ± 0.01, p =0.001; SAT: −0.04 ± 0.01, p =0.004). In full models, negative associations were limited to VAT in girls and included radial (−0.06 ± 0.02, p =0.001) and tibial SSI (−0.04 ± 0.02, p =0.033). For boys, there were no significant associations present between VAT and SSI at the radius or tibia. In analyses limited to obese participants, an A/G ratio was not significantly associated with SSI in girls, but was negatively associated with radial SSI regardless of adjustment for lean mass in boys (−0.06 ± 0.02, p =0.018). These results that show a negative relationship between peripheral bone strength and VAT in girls, but greater total and central adiposity in boys, suggest these factors play a role in adequate acquisition of bone strength during adolescence.

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Cloning of adiponectin receptors that mediate antidiabetic metabolic effects.

Toshimasa Yamauchi, Junji Kamon, Yusuke Ito … (2003)

Adiponectin (also known as 30-kDa adipocyte complement-related protein; Acrp30) is a hormone secreted by adipocytes that acts as an antidiabetic and anti-atherogenic adipokine. Levels of adiponectin in the blood are decreased under conditions of obesity, insulin resistance and type 2 diabetes. Administration of adiponectin causes glucose-lowering effects and ameliorates insulin resistance in mice. Conversely, adiponectin-deficient mice exhibit insulin resistance and diabetes. This insulin-sensitizing effect of adiponectin seems to be mediated by an increase in fatty-acid oxidation through activation of AMP kinase and PPAR-alpha. Here we report the cloning of complementary DNAs encoding adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2) by expression cloning. AdipoR1 is abundantly expressed in skeletal muscle, whereas AdipoR2 is predominantly expressed in the liver. These two adiponectin receptors are predicted to contain seven transmembrane domains, but to be structurally and functionally distinct from G-protein-coupled receptors. Expression of AdipoR1/R2 or suppression of AdipoR1/R2 expression by small-interfering RNA supports our conclusion that they serve as receptors for globular and full-length adiponectin, and that they mediate increased AMP kinase and PPAR-alpha ligand activities, as well as fatty-acid oxidation and glucose uptake by adiponectin.

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Visceral fat adipokine secretion is associated with systemic inflammation in obese humans.

Luigi Fontana, J. Eagon, Maria Trujillo … (2007)

Although excess visceral fat is associated with noninfectious inflammation, it is not clear whether visceral fat is simply associated with or actually causes metabolic disease in humans. To evaluate the hypothesis that visceral fat promotes systemic inflammation by secreting inflammatory adipokines into the portal circulation that drains visceral fat, we determined adipokine arteriovenous concentration differences across visceral fat, by obtaining portal vein and radial artery blood samples, in 25 extremely obese subjects (mean +/- SD BMI 54.7 +/- 12.6 kg/m(2)) during gastric bypass surgery at Barnes-Jewish Hospital in St. Louis, Missouri. Mean plasma interleukin (IL)-6 concentration was approximately 50% greater in the portal vein than in the radial artery in obese subjects (P = 0.007). Portal vein IL-6 concentration correlated directly with systemic C-reactive protein concentrations (r = 0.544, P = 0.005). Mean plasma leptin concentration was approximately 20% lower in the portal vein than in the radial artery in obese subjects (P = 0.0002). Plasma tumor necrosis factor-alpha, resistin, macrophage chemoattractant protein-1, and adiponectin concentrations were similar in the portal vein and radial artery in obese subjects. These data suggest that visceral fat is an important site for IL-6 secretion and provide a potential mechanistic link between visceral fat and systemic inflammation in people with abdominal obesity.

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Sex steroids and the construction and conservation of the adult skeleton.

Sundeep Khosla, L. Joseph Melton, B Riggs (2002)

Here we review and extend a new unitary model for the pathophysiology of involutional osteoporosis that identifies estrogen (E) as the key hormone for maintaining bone mass and E deficiency as the major cause of age-related bone loss in both sexes. Also, both E and testosterone (T) are key regulators of skeletal growth and maturation, and E, together with GH and IGF-I, initiate a 3- to 4-yr pubertal growth spurt that doubles skeletal mass. Although E is required for the attainment of maximal peak bone mass in both sexes, the additional action of T on stimulating periosteal apposition accounts for the larger size and thicker cortices of the adult male skeleton. Aging women undergo two phases of bone loss, whereas aging men undergo only one. In women, the menopause initiates an accelerated phase of predominantly cancellous bone loss that declines rapidly over 4-8 yr to become asymptotic with a subsequent slow phase that continues indefinitely. The accelerated phase results from the loss of the direct restraining effects of E on bone turnover, an action mediated by E receptors in both osteoblasts and osteoclasts. In the ensuing slow phase, the rate of cancellous bone loss is reduced, but the rate of cortical bone loss is unchanged or increased. This phase is mediated largely by secondary hyperparathyroidism that results from the loss of E actions on extraskeletal calcium metabolism. The resultant external calcium losses increase the level of dietary calcium intake that is required to maintain bone balance. Impaired osteoblast function due to E deficiency, aging, or both also contributes to the slow phase of bone loss. Although both serum bioavailable (Bio) E and Bio T decline in aging men, Bio E is the major predictor of their bone loss. Thus, both sex steroids are important for developing peak bone mass, but E deficiency is the major determinant of age-related bone loss in both sexes.