mRNA concentrations of MIF in subcutaneous abdominal adipose cells are associated with adipocyte size and insulin action

Objective To determine whether the mRNA concentrations of inflammation response genes in isolated adipocytes and in cultured preadipocytes are related to adipocyte size and in vivo insulin action in obese individuals. Design Cross-sectional inpatient study. Subjects Obese Pima Indians with normal glucose tolerance. Measurements Adipocyte diameter (by microscope technique; n=29), expression of candidate genes (by quantitative real-time PCR) in freshly isolated adipocytes (monocyte chemoattractant protein [MCP] 1 and MCP2, macrophage inflammatory protein [MIP] 1α, MIP1β and MIP2, macrophage migration inhibitory factor [MIF], tumor necrosis factor alpha, interleukin [IL] 6 and IL8; n=22) and cultured preadipocytes (MCP1, MIP1α, MIF, IL6 and matrix metalloproteinase 2; n=33) from subcutaneous abdominal adipose tissue (by aspiration biopsy, n=34), body fat by dual-energy X-ray absorptiometry, glucose tolerance by 75-gram oral glucose tolerance test, and insulin action by euglycemic-hyperinsulinemic clamp (insulin infusion rate 40 mU/m2.min)(all n=34). Results MIF was the only gene whose expression in both freshly isolated adipocytes and cultured preadipocytes was positively associated with adipocytes diameter and negatively associated with peripheral and hepatic insulin action (all P<0.05). In multivariate analysis, the association between adipocyte MIF mRNA concentrations and adipocytes diameter was independent of percent body fat (P=0.03), whereas adipocyte MIF mRNA concentrations but not adipocytes diameter independently predicted peripheral insulin action. The mRNA expression concentrations of MIF gene in adipocytes were not associated with plasma concentrations of MIF, but were negatively associated with plasma adiponectin concentrations (P=0.004). In multivariate analysis, adipocyte MIF RNA concentrations (P=0.03) but not plasma adiponectin concentrations (P=0.4) remained a significant predictor of insulin action. Conclusions Increased expression of MIF gene in adipose cells may be an important link between obesity characterized by enlarged adipocytes and insulin resistance in normal glucose tolerant people

Effects of competition of selected hormones in women field hockey and volleyball teams

Includes bibliographical references.The purposes of the study were: (1) to measure and compare selected menstrual and physical activity characteristics in 24 members, age 18-29. of the NIU women's intercollegiate field hockey (FH) or volleyball (VB) teams; (2) to measure and compare percent body fat values in the teams; (3) to compare the responses of cortisol, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) to competition based on team affiliation; and (4) to compare the responses of cortisol, FSH and LH to competition based on menstrual phase. Between group results of the questionnaire data, skinfold measurements and hormone levels were statistically analyzed with the non-parametric Mann-Whitney U test. The McNemar test was utilized for within group changes and a one-way analysis of variance was used to compare between group changes for each hormone. Comparisons of menstrual and physical activity histories showed that there were no significant differences between the two teams in terms of age of menarche (FH = 13.4 yrs., ±.31; VB = 13.6 yrs., ±.28), age at onset of training (FH = 12.15 yrs., ±.71; VB = 11.82 yrs., ±.66), total number of years of competition (FH = 7 yrs., ±.86; VB = 7.36 yrs., ±.64), and activity level (FH = 2.94 ±.37; VB = 2.91 ±.10) for the past year. None of the subjects, with the exception of two FH players, had a history of menstrual dysfunction. Every subject had begun training prior to menarche, yet this had no apparent effect on the present functioning of their menstrual cycles. Mean percent body fat measurements were similar between the teams (FH = 22.84%, ±2.08; VB = 21.35%, ±.89) with field hockey having a wider range. Cortisol levels were higher than the normal range prior to the games and increased by 3.74 µg% (±2.95) in the FH players and 3.8 µg% (±1.29) in the VB players. These increases, howevever, were not significant. FSH rose slightly in the VB players (+.45 mlU/ml, ±1.85) and decreased slightly in the FH players (-1.42 mlU/ml, ±.74) following competition. Although these responses were different, they were not significant. LH levels decreased by 4.5 mlU/ ml (±5.46) in the IH team and by 1.19 mlU/ml (±2.40) in the VB team, resulting in nonsignificant changes. Cortisol increased slightly more during the luteal phase (+5.7 µg% ±4.82) than the follicular phase (+2.97 µg% ±1.31) but it was not statistically different. While FSH levels were higher in the follicular phase (11.69 mlU/ml, ±1.39) than in the luteal phase (6.68 mlU/ml, ±.53) initially, the levels remained unchanged as a result of competition. LH levels remained unchanged in response to competition in the follicular phase and dropped during the luteal phase by 10.41 mlU/ml (±9.37). This decrease was not significant. As a result of these data it was concluded that training for and competing in intercollegiate volleyball and field hockey did not appear to affect the menstrual functioning of the athletes that were tested.M.S. (Master of Science

The Maximally Accumulated Oxygen Deficit as an Indicator of Anaerobic Capacity

The maximally accumulated oxygen deficit as an indicator of anerobic capacity. Med. Sci. Sports Exerc., Vol. 23, No. 5, pp. 618–624, 1991. Recently, a procedure has been established for the determination of the maximally accumulated oxygen deficit (MAOD) (Medbo et al., J. Appl. Physiol. 64:50–60, 1988) as an indicator of anaerobic capacity. We hypothesized that, if MAOD were a valid indicator of anaerobic capacity, it should distinguish between aerobically and anaerobically trained athletes and correlate with other existing anaerobic testing measures. Subjects were four distance and five middle distance runners, three sprinters, and four controls. The subjects ran for 2–3 min at 125–140% of VO2max until exhaustion, and the accumulated O2 deficit for that run was calculated by an extrapolation procedure. Subjects also performed the Wingate cycle ergometer test and runs of 300, 400, and 600 m. (Only atheletes performed the runs.) Post-exercise blood lactates were obtained following the supramaximal treadmill run. MAOD (in O2 equivalents–ml.kg-1) was higher for the sprinters (78) and middle distance runners (74) than for the long distance runners (56) and control subjects (56) (P ≤ 0.05), indicating a greater anaerobic capacity for the former two groups. Consequently, the relative anaerobic capacity for the former two groups. Consequently, the relative anaerogic contribution was larger for the sprinters (39%) and middle distance runners (37%) than for the long distance runners (30%; P ≤ 0.05). Significant correlations were found between MAOD and both Wingate power and treadmill work for all subjects and between Wingate power, Wingate capacity, treadmill work, and 300 m time for the atheletes, suggesting that relationships do exist among MAOD and other anaerobic test measures. Potential use of MAOD as an indicator of anaerobic capacity is therefore promising and should be further explored

Water intake, thirst, and copeptin responses to two dehydrating stimuli in lean men and men with obesity

Objective Physiological systems responsible for water homeostasis and energy metabolism are interconnected. This study hypothesized altered responses to dehydration including thirst, ad libitum water intake, and copeptin in men with obesity. Methods Forty-two men (22 lean and 20 with obesity) were stimulated by a 2-hour hypertonic saline infusion and a 24-hour water deprivation. In each dehydrating condition, thirst, ad libitum water intake after dehydration, and urinary and hormonal responses including copeptin were assessed. Results After each dehydration condition, ad libitum water intake was similar between both groups (p &gt; 0.05); however, those with obesity reported feeling less thirsty (p &lt; 0.05) and had decreased copeptin response and higher urinary sodium concentrations when stressed (p &lt; 0.05). Angiotensin II, aldosterone, atrial and brain natriuretic peptides, and apelin concentrations did not differ by adiposity group and did not explain the different thirst or copeptin responses in men with obesity. However, leptin was associated with copeptin response in lean individuals during the hypertonic saline infusion (p &lt; 0.05), but the relationship was diminished in those with obesity. Conclusions Diminished thirst and copeptin responses are part of the obesity phenotype and may be influenced by leptin. Adiposity may impact pathways regulating thirst and vasopressin release, warranting further investigation