9 research outputs found

    Influence of Exercise Intensity on Abdominal Fat and Adiponectin in Elderly Adults

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    To examine the influence of moderate-intensity (50% of VO2peak) exercise training (MI) versus high-intensity (75% of VO2peak) exercise training (HI) on regional fat distribution and plasma adiponectin, we randomized 18 overweight (body mass index [BMI] = 30 ± 1 kg/m2) elderly (71 ± 1 years) to HI, MI, or a control group (CON). Subjects enrolled in HI or MI completed a 12-week exercise training protocol designed to expend 1000 kcal/week. Body composition testing was completed prior to and following the exercise training using dual energy X-ray absorptiometry and a computed tomography scan. Plasma adiponectin was measured using enzyme-linked immunoassay (ELISA). VO2peak improved in HI and MI, whereas there was no change in VO2peak in CON. No significant change in body weight, BMI, and % fat occurred in MI, HI, or CON. Although there was a significant reduction in visceral fat with HI (−39 cm2), there was no change in the MI or CON groups. In addition, there was a significant increase in thigh muscle attenuation in the HI group. There were no changes in thigh muscle attenuation in the MI and CON groups. Also, there was no change in plasma adiponectin in the MI, HI, or CON groups. In summary, our direct comparison of exercise intensity without weight loss promotes the efficacy of HI in the reduction in visceral fat, even without changes in adiponectin

    Visceral Fat and Adiponectin: Associations with Insulin Resistance Are Tissue-Specific in Women

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    Body fatness and its distribution are strongly and independently associated with peripheral insulin action. However, these associations are limited in their ability to predict the independent nature of hepatic and peripheral insulin resistance, especially in obese women. To define the relationships more precisely between regional fat distribution and adiponectin, and hepatic and peripheral insulin resistance, we studied 22 obese (43 ± 0.1%) women who underwent a dual-energy X-ray absorptiometry scan and a computed tomography scan at the L4–L5 level. An octreotide (60 ng · kg−1 · min−1), glucagon (0.65 ng · kg−1 · min−1), and two-step insulin (0.25 mU · kg−1 · min−1 and 1.0 mU · kg−1 · min−1) infusion was performed to quantify insulin-mediated suppression of hepatic glucose production (SGP) and insulin-stimulated glucose disposal (ISGD) in a simultaneous fashion. Hepatic glucose production (HGP) was measured using a primed, constant infusion of [6,62H2] glucose. Mean plasma insulin increased from 5.6 ± 0.1 μU/mL at baseline to 15.1 ± 1.5 μU/mL in the first stage, and to 80.7 ± 0.5 μU/mL in the second stage. Although there was no significant relationship between visceral adipose tissue (VAT) and basal HGP (r = 0.34, p = 0.117), there was a significant inverse correlation (r = −0.67, p = 0.003) between VAT and SGP. There was a significant correlation (r = 0.55, p = 0.008) between adiponectin and ISGD. In conclusion, these data support: (1) the inability of basal glucose metabolism to accurately reflect hepatic insulin resistance, (2) the deleterious role of VAT in the development of insulin resistance in the liver, and (3) provide additional support for the positive influence of adiponectin against peripheral insulin resistance in obese, postmenopausal women
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