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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 x kg(-1) x min(-1)), glucagon (0.65 ng x kg(-1) x min(-1)), and two-step insulin (0.25 mU x kg(-1) x min(-1) and 1.0 mU x kg(-1) x 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 [6,6(2)H(2)] glucose. Mean plasma insulin increased from 5.6 +/- 0.1 microU/mL at baseline to 15.1 +/- 1.5 microU/mL in the first stage, and to 80.7 +/- 0.5 microU/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.

Type 2 diabetes represents an epidemic disease that has become a widespread healthcare problem throughout the world. The prevalence of a sedentary lifestyle and excess caloric intake promotes the aetiology of insulin resistance that results in the development of the metabolic condition, Type 2 diabetes. Despite numerous investigations that have demonstrated the positive influence of aerobic exercise training on a reduction in the severity of insulin resistance, many of these exercise programmes yield benefits that are only short-lived and promote only modest reductions in the severity of the disease aetiology. Therefore, the efficacy of exercise training as a therapeutic intervention against the development of Type 2 diabetes rests on its ability to normalize insulin resistance in the liver and skeletal muscle using a progressive approach that combines the beneficial influences of exercise training and weight loss.

Purpose: The effect of different quantities of carbohydrate (CHO) intake on CHO metabolism during prolonged exercise was examined in endurance-trained females. Method: On four occasions, eight females performed 2 h of cycling at approximately 60% V?O2max with ingestion of beverages containing low (LOW, 0.5 g·min-1), moderate (MOD, 1.0 g·min-1), or high (HIGH, 1.5 g·min-1) amounts of CHO, or water only (WAT). Test solutions contained trace amounts of [U-13C] glucose. Indirect calorimetry combined with measurement of expired 13CO2 and plasma 13C enrichment enabled calculation of exogenous CHO, liver-derived glucose, and muscle glycogen oxidation during the last 30 min of exercise. Results: The highest rates of exogenous CHO oxidation were observed in MOD, with no further increases in HIGH (peak rates of 0.33 ± 0.02, 0.50 ± 0.03, and 0.48 ± 0.05 g·min-1 for LOW, MOD, and HIGH, respectively; P < 0.05 for LOW vs MOD and HIGH). Endogenous CHO oxidation was lowest in MOD (0.99 ± 0.06, 0.82 ± 0.08, 0.70 ± 0.07, and 0.89 ± 0.09 g·min-1; P < 0.05 for MOD vs all other trials). Compared with WAT, CHO ingestion reduced liver glucose oxidation during exercise by approximately 30% (P < 0.05 for WAT vs all CHO). Differential rates of muscle glycogen oxidation were observed with different CHO doses (0.57 ± 0.07, 0.53 ± 0.08, 0.41 ± 0.07, and 0.60 ± 0.09 g·min-1 for WAT, LOW, MOD, and HIGH respectively; P < 0.05 for MOD vs HIGH). Conclusion: In endurance-trained women, the highest rates of exogenous CHO oxidation and greatest endogenous CHO sparing was observed when CHO was ingested at moderate rates (1.0 g·min-1, 60 g·h-1) during exercise.

Both carbohydrate (CHO) and caffeine have been used as ergogenic aids during exercise. It has been suggested that caffeine increases intestinal glucose absorption, but there are also suggestions that it may decrease muscle glucose uptake. The purpose of the study was to investigate the effect of caffeine on exogenous CHO oxidation. In a randomized crossover design, eight male cyclists (age 27 ± 2 yr, body mass 71.2 ± 2.3 kg, maximal oxygen uptake 65.7 ± 2.2 ml·kg−1·min−1) exercised at 64 ± 3% of maximal oxygen uptake for 120 min on three occasions. During exercise subjects ingested either a 5.8% glucose solution (Glu; 48 g/h), glucose with caffeine (Glu+Caf, 48 g/h + 5 mg·kg−1·h−1), or plain water (Wat). The glucose solution contained trace amounts of [U-13C]glucose so that exogenous CHO oxidation could be calculated. CHO and fat oxidation were measured by indirect calorimetry, and13C appearance in the expired gases was measured by continuous-flow IRMS. Average exogenous CHO oxidation over the 90- to 120-min period was 26% higher ( P < 0.05) in Glu+Caf (0.72 ± 0.04 g/min) compared with Glu (0.57 ± 0.04 g/min). Total CHO oxidation rates were higher ( P < 0.05) in the CHO ingestion trials compared with Wat, but they were highest when Glu+Caf was ingested (1.21 ± 0.37, 1.84 ± 0.14, and 2.47 ± 0.23 g/min for Wat, Glu, and Glu+Caf, respectively; P < 0.05). There was also a trend ( P = 0.082) toward an increased endogenous CHO oxidation with Glu+Caf (1.81 ± 0.22 g/min vs. 1.27 ± 0.13 g/min for Glu and 1.12 ± 0.37 g/min for Wat). In conclusion, compared with glucose alone, 5 mg·kg−1·h−1of caffeine coingested with glucose increases exogenous CHO oxidation, possibly as a result of an enhanced intestinal absorption.

It has been difficult to distinguish the independent effects of caloric restriction versus exercise training on insulin resistance.Utilizing metabolic feeding and supervised exercise training, we examined the influence of caloric restriction vs. exercise training with and without weight loss on hepatic and peripheral insulin resistance.Thirty-four obese, older subjects were randomized to: caloric restriction with weight loss (CR), exercise training with weight loss (EWL), exercise training without weight loss (EX), or controls. Based on an equivalent caloric deficit in EWL and CR, we induced matched weight loss. Subjects in the EX group received caloric compensation. Combined with [6,6(2)H(2)]glucose, an octreotide, glucagon, multistage insulin infusion was performed to determine suppression of glucose production (SGP) and insulin-stimulated glucose disposal (ISGD). Computed tomography scans were performed to assess changes in fat distribution.Body weight decreased similarly in EWL and CR, and did not change in EX and controls. The reduction in visceral fat was significantly greater in EWL (-71 +/- 15 cm(2)) compared to CR and EX. The increase in SGP was also almost 3-fold greater (27 +/- 2%) in EWL. EWL and CR promoted similar improvements in ISGD [+2.5 +/- 0.4 and 2.4 +/- 0.9 mg x kg fat-free mass (FFM)(-1) x min(-1)], respectively.EWL promoted the most significant reduction in visceral fat and the greatest improvement in SGP. Equivalent increases in ISGD were noted in EWL and CR, whereas EX provided a modest improvement. Based on our results, EWL promoted the optimal intervention-based changes in body fat distribution and systemic insulin resistance.

Background. Previous studies have identified relationships between subcutaneous abdominal fat (SAF), visceral fat (VF), and insulin resistance. In addition, lower muscle attenuation and decreased adiponectin have also been associated with insulin resistance. Methods. In order to define these relationships within a group of older, obese adults, we studied 48 individuals (20 men; 71 ± 1 years and 28 women; 65 ± 1 years) who underwent a single, hyperinsulinemic, euglycemic clamp procedure, computed tomography scan at the L4-L5 level, and whole-body plethysmography or dual energy x-ray absorptiometry. Endogenous glucose production (basal glucose R a ) was also measured at baseline and during the clamp procedure using an infusion of [6,6 2 H 2 ] glucose. Results. Mean body mass index (BMI; 31 ± 1 kg/m 2 ) and glycosylated hemoglobin A1c (HbAlc; 5.7 ± 0.1%) levels were not significantly different between men and women. In men, there was an inverse relationship between SAF and insulin-stimulated glucose disposal (ISGD) (r = -.60, p = .01). In addition, there was a trend between thigh muscle attenuation and ISGD in men (r = .41, p = .07). Adiponectin was associated with ISGD in men (r =.46, p = .04) and women (r = .48, p = .01). There were no significant relationships between body fat distribution and basal glucose R a in men or women, and no relationships between triglycerides and glucose metabolism. Conclusions. Our results indicate that (i) SAF was negatively associated with ISGD in men, (ii) thigh muscle attenuation demonstrated a trend toward ISGD in men, and (iii) adiponectin was associated with ISGD in men and women.