Objective: The objective of this study was to investigate the association among adiposity, insulin resistance, and inflammatory markers [high‐sensitivity C‐reactive protein (hs‐CRP), interleukin (IL)‐6, and tumor necrosis factor (TNF)‐α] and adiponectin and to study the effects of exercise training on adiposity, insulin resistance, and inflammatory markers among obese male Korean adolescents. Research Methods and Procedures: Twenty‐six obese and 14 lean age‐matched male adolescents were studied. We divided the obese subjects into two groups: obese exercise group (N = 14) and obese control group (N = 12). The obese exercise group underwent 6 weeks of jump rope exercise training (40 min/d, 5 d/wk). Adiposity, insulin resistance, lipid profile, hs‐CRP, IL‐6, TNF‐α, and adiponectin were measured before and after the completion of exercise training. Results: The current study demonstrated higher insulin resistance, total cholesterol, LDL‐C levels, triglyceride, and inflammatory markers and lower adiponectin and HDL‐C in obese Korean male adolescents. Six weeks of increased physical activity improved body composition, insulin sensitivity, and adiponectin levels in obese Korean male adolescents without changes in TNF‐α, IL‐6, and hs‐CRP. Discussion: Obese Korean male adolescents showed reduced adiponectin levels and increased inflammatory cytokines. Six weeks of jump rope exercise improved triglyceride and insulin sensitivity and increased adiponectin levels.

The dramatic increase in the prevalence of obesity and its accompanying comorbidities are major health concerns in Korea. Obesity is defined as a body mass index ≥25 kg/m2 in Korea. Current estimates are that 32.8% of adults are obese: 36.1% of men and 29.7% of women. The prevalence of being overweight and obese in national surveys is increasing steadily. Early detection and the proper management of obesity are urgently needed. Weight loss of 5% to 10% is the standard goal. In obese patients, control of cardiovascular risk factors deserves the same emphasis as weight-loss therapy. Since obesity is multifactorial, proper care of obesity requires a coordinated multidisciplinary treatment team, as a single intervention is unlikely to modify the incidence or natural history of obesity.

The human body is in a constant state of turnover, that is, being synthesized, broken down and/or converted to different compounds. The dynamic nature of in vivo kinetics of human metabolism at rest and in stressed conditions such as exercise and pathophysiological conditions such as diabetes and cancer can be quantitatively assessed with stable, nonradioactive isotope tracers in conjunction with gas or liquid chromatography mass spectrometry and modeling. Although measurements of metabolite concentrations have been useful as general indicators of one's health status, critical information on in vivo kinetics of metabolites such as rates of production, appearance or disappearance of metabolites are not provided. Over the past decades, stable, nonradioactive isotope tracers have been used to provide information on dynamics of specific metabolites. Stable isotope tracers can be used in conjunction with molecular and cellular biology tools, thereby providing an in-depth dynamic assessment of metabolic changes, as well as simultaneous investigation of the molecular basis for the observed kinetic responses. In this review, we will introduce basic principles of stable isotope methodology for tracing in vivo kinetics of human or animal metabolism with examples of quantifying certain aspects of in vivo kinetics of carbohydrate, lipid and protein metabolism.

To evaluate the hypothesis that precursor supply limits gluconeogenesis (GNG) during exercise, we examined training-induced changes in glucose kinetics [rates of appearance (R a) and disappearance (Rd)], oxidation (R ox), and recycling (Rr) with an exogenous lactate infusion to 3.5-4.0 mM during rest and to pretraining 65% peak O 2 consumption (V O2 peak) levels during exercise. Control and clamped trials (LC) were performed at rest pre-(P RR, PRR-LC) and posttraining (POR, POR-LC) and during exercise pre-(P REX) and posttraining at absolute (POAB, P OAB-LC) and relative (PORL, PORL-LC) intensities. Glucose R r was not different in any rest or exercise condition. Glucose R a did not differ as a result of LC. Glucose Rox was significantly decreased with LC at P OR (0.38 Ϯ 0.03 vs. 0.56 Ϯ 0.04 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 ) and POAB (3.82 Ϯ 0.51 vs. 5.0 Ϯ 0.62 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 ). Percent glucose Rd oxidized decreased with all LC except P ORL-LC (PRR, 32%; PRR-LC, 22%; POR, 27%; P OR-LC, 20%; POAB, 95%; POAB-LC, 77%), which resulted in a significant increase in oxidation from alternative carbohydrate (CHO) sources at rest and P OAB. We conclude that 1) increased arterial [lactate] did not increase glucose R r measured during rest or exercise after training, 2) glucose disposal or production did not change with increased precursor supply, and 3) infusion of exogenous CHO in the form of lactate resulted in the decrease of glucose R ox. lactate; glucose kinetics; glucose recycling; training MAINTENANCE of blood [glucose] homeostasis requires coordination of delivery and utilization, or else hypo-or hyperglycemia results. Prolonged exercise and disease states, such as type 2 diabetes, represent situations in which glucose homeostasis is challenged. During postabsorptive rest (40) and exercise (3, 40), hepatic and renal gluconeogenesis (GNG) can increase to maintain glucose production (GP) and spare finite hepatic glycogen stores. Regular exercise training is accompanied, in part, by beneficial adaptations pertaining to glucose homeostasis (17). Donovan and Brooks (12) measured glucose recycling (R r ), an indirect measure of gluconeogenesis (GNG), and lactate incorporation into glucose and demonstrated that training increased lactate disposal and GNG in rats. Subsequently, Turcotte and Brooks (39) demonstrated that pharmacological blockade of GNG decreased run time to exhaustion and blood [glucose] during submaximal exercise in both untrained and trained rats. Together, these reports indicate that GNG capacity can increase with exercise training and that GNG is necessary to sustain blood [glucose] during exercise. Subsequent studies have demonstrated a training-induced increase in GNG in fasted rats (15) and in lactate-perfused (14) or alanine-perfused (8) livers in situ. Those reports were inconsistent with previous reports that training does not increase GNG enzyme concentrations in rats (19). Whereas there seems to be a training-induced increase in GNG capacity in rats, data on humans are less clear. The few longitudina...