Anthropometric and leptin changes in women following different dietary approaches to weight loss

Leptin may favorably respond to fat mass (FM) losses induced by a low-carbohydrate (LC) diet, although this is unclear. We examined serum leptin concentrations in women in midlife undergoing different dietary approaches to body weight (BW) loss. Women followed either a LC, high-protein (LCHP; n = 13) or high-carbohydrate, low-fat (HCLF; n = 12) diet for 12 weeks. Changes in anthropometric and soft-tissue mass measurements and leptin concentrations were assessed. Women in both diet groups had reductions in BW, BMI, fat-free soft-tissue mass, FM, body fat percentage, and central abdominal fat (CAF) (P < 0.001 for all variables) over the 12-week intervention. These changes were not significantly different between diet groups. Serum leptin concentrations decreased by 41.8% (P < 0.001) in the LCHP group and by 44.3% (P < 0.001) in the HCLF group from baseline to week 12, with no significant difference between groups. The association of CAF (r = 0.73) and FM (r = 0.83) change with leptin change was strong in the HCLF group. Leptin change did not relate to change in any variable in the LCHP group. Both LCHP and HCLF diets favorably lower FM, CAF, and leptin in women, suggesting that beneficial changes in leptin can be similarly achieved through different dietary approaches to BW loss.     

Longitudinal changes in energy expenditure and body composition in obese women with normal and impaired glucose tolerance

Our primary objective was to evaluate changes in energy expenditure and body composition in women with normal glucose tolerance (NGT) and gestational diabetes mellitus (GDM). A secondary objective was to examine the relationship between maternal leptin and nutrient metabolism. Fifteen obese women, eight with NGT and seven with GDM, were evaluated before conception (P), at 12-14 wk (E), and at 34-36 wk (L). Energy expenditure and glucose and fat metabolism were measured using indirect calorimetry. Basal hepatic glucose production was measured using [6,6-2H2]glucose and insulin sensitivity by euglycemic clamp. There was a significant increase (6.6 kg, P = 0.0001) in fat mass from P to L. There was a 30% (P = 0.0001) increase in basal O2 consumption (VO2, ml/min). There were no significant changes in carbohydrate oxidation during fasting or storage from P to L. There was, however, a significant (P = 0.0001) 150% increase in basal fat oxidation (mg/min) from P to L. Under hyperinsulinemic conditions, there were similar 25% increases in VO2 (P = 0.0001) from P to L in both groups. Because of the significant increases in insulin resistance from P to L, there was a significant (P = 0.0001) decrease in carbohydrate oxidation and storage. There was a net change from lipogenesis to lipolysis, i.e., fat oxidation (30-40 mg/min, P = 0.0001) from P to L. Serum leptin concentrations had a significant positive correlation with fat oxidation at E (r = 0.76, P = 0.005) and L (r = 0.72, P = 0.009). Pregnancy in obese women is associated with significant increases in fat mass and basal metabolic rate and an increased reliance on lipids both in the basal state and during the clamp. These modifications are similar in women with NGT and GDM. The increased reliance on fat metabolism is accompanied by a concomitant decrease in carbohydrate metabolism during hyperinsulinemia. The increase in fat oxidation may be related to increased maternal serum leptin.     

Gender Differences in the Response of Plasma Leptin Concentrations to Weight Loss in Obese Older Individuals

Plasma leptin concentration is directly related to the degree of obesity and is higher in women than in men of the same body mass index (BMI). We hypothesized that fasting plasma leptin concentrations and the response of leptin to weight loss would differ in older men and women of a similar fat mass. Plasma leptin concentrations (radioimmunoassay) and fat mass (DXA) were measured in 47 older, obese (BMI=30 ± 4 kg/m²) women and 23 older, obese (BMI=31 ± 3 kg/m²) men after a 2 to 4 week period of weight and dietary stabilization, and then in 22 of the women and 18 of the men after a 6-month weight loss intervention (250–350 kcal/d deficit). Leptin correlated with fat mass in men and women (r=0.75 and r=0.77, respectively; p values<0.0001), but women had 3-fold higher leptin levels for a given fat mass than men (p=0.01). In response to the 6-month hypocaloric diet, men and women lost a similar percentage of fat mass (?13% and ?16%, respectively), but the relative decline in circulating leptin was greater in women than men (-45% and ?21%, respectively; p<0.0001). In addition, when leptin was normalized for fat mass using the ratio method, the decrease in leptin per kilogram of fat mass was greater in women than men (-0.37 ± 0.34 vs. ?0.04 ± 0.06 ng/mL/kg; p<0.01). After weight loss, the change in leptin concentrations correlated positively with the change in fat mass in men (r=0.60; p<0.01), but not in women (r=0.31; p=0.17). Furthermore, the loss in fat mass correlated negatively with baseline leptin levels in women (r=-0.47; p<0.05), but not in men (r=0.03, p=NS). These results indicate that the decline in leptin concentration with weight loss correlates with the loss in fat mass in men; but, in women, other factors affect the decrease in leptin concentration. This suggests that the role of leptin in the regulation of obesity is gender-specific and may account for gender differences in response to hypocaloric treatment and maintenance of lost weight.     

自愿转轮运动对雄性长爪沙鼠体重和能量代谢的影响

运动是影响动物能量平衡和体重变化的重要因素之一。为研究自愿转轮运动对体重和能量代谢的影响,我们监测了8 周自愿转轮运动过程中,雄性长爪沙鼠的体重、能量摄入、消化率、静止代谢率(RMR) 和非颤抖性产热(NST)的变化,以及8 周后的体脂含量、血清甲状腺激素(T3、T4 )和瘦素(leptin)水平的变化等。结果发现,8 周自愿转轮运动增加了长爪沙鼠的体重和能量摄入以及血清瘦素水平(血清瘦素浓度比对照组高27% ),但对消化率、RMR 和褐色脂肪组织的线粒体蛋白浓度等没有明显影响。尽管体脂含量和血清T₃ 和T₄ 没有显著差异,但运动组体脂含量比对照组高33%,血清T₃ 和T₄ 水平分别比对照组低10% 和38%。血清瘦素浓度与体脂重量呈正相关。因此,自动转轮运动并没有降低动物的体重和体脂含量,但瘦素和甲状腺素在雄性长爪沙鼠能量代谢和能量平衡中的作用尚需进一步确定。     

Leptin predicts bone and fat mass after accounting for the effects of diet and glucocorticoid treatment in piglets

The role of leptin in neonatal growth and bone metabolism has been investigated, but not simultaneously. The objectives of this study were to determine if leptin relates to bone mass during rapid growth; if consumption of maternal milk is related to elevated circulating concentrations of leptin resulting in higher fat mass; and if glucocorticoids result in higher fat mass and reduced bone mass due to elevated leptin. Thirty-two piglets were randomized to either a suckling or milk substitute plus either dexamethasone (DEX) or placebo injection for 15 days beginning at 5 days of age. Milk and blood samples were obtained at baseline, and after 15 days, blood was sampled again for measurement of leptin and bone biochemistry. Weight at baseline plus weight and length after 15 days were recorded, followed by measurement of whole body bone mineral content, bone area, and fat mass using dual energy x-ray absorptiometry. At baseline, plasma leptin was elevated in suckled piglets. Piglets that suckled had elevated fat mass as did those who received DEX. However, DEX resulted in suppressed weight and length, bone mass, and bone metabolism. Leptin was similar among groups after the 15 days. After accounting for body size and treatment effects, piglet plasma leptin was predictive of bone and fat mass. Leptin circulating early postnatally is linked to body composition, specifically fat and bone mass. Elevations in fat mass and reductions in bone mass observed after 15 days of DEX treatment are not related to leptin metabolism. Both human and porcine neonates share similar characteristics with respect to relationships of leptin with fat and bone mass.     

Relationship Between Circulating Leptin and Energy Expenditure in Adult Men and Women Aged 18 Years to 81 Years

SUSAN B. ROBERTS, MARGERY NICHOLSON, MYRLENE STATEN, GERALD E. DALLAL, ANA L. SAWAYA, MELVIN B. HEYMAN, PAUL FUSS, ANDREW S. GREENBERG. Relationship between circulating leptin and energy expenditure in adult men and women aged 18 years to 81 years. Recent studies suggest that leptin may be an important metabolic signal for energy regulation in rodents, but the role of leptin in human energy regulation remains uncertain. Because adaptive variations in energy expenditure play an important role in human energy regulation, we investigated the relationship between leptin and energy expenditure parameters in 61 weight-stable men and women aged 18 years to 81 years who were not obese. Measurements were made of circulating leptin in the fasting state, body fat and fat free mass, resting metabolic rate (n=61), free-living total energy expenditure (n=52), and the thermic effect of feeding (n=33). After statistically accounting for age, body fat, and fat free mass, there was no association between leptin and any measured energy expenditure parameter. In addition, there was no effect of age on the relationship between circulating leptin and body fat mass. These results indicate that physiological variations in circulating leptin are not linked with adaptive variations in energy expenditure in humans, in contrast to indications of this phenomenon in the ob/ob mouse.     

Leptin concentrations and their relation to body fat distribution and weight loss--a prospective study in individuals with impaired glucose tolerance. DPS-study group.

Leptin is proposed to be involved in regulation of body weight. Only little information is available on leptin concentrations in individuals with impaired glucose tolerance (IGT). The aim of the present study was to assess the effect of body fat distribution and weight reduction on serum leptin levels in a prospective setting in IGT subjects. Sixty-nine individuals with impaired glucose tolerance aged 45-64 years participated in this prospective study. Serum leptin levels were about 300% higher among females than among males, despite an only 30% higher fat percentage in females. A close association between degree of obesity and leptin concentrations was observed in both sexes. The correlation coefficient between fat mass and leptin concentration ranged between r = 0.467- 0.817 (p< 0.001 - 0.01). A close correlation between degree of weight loss and decrease in leptin concentrations was observed in both sexes. A 10.1 kg (9.6%) decrease in body weight among females was associated with a 32% decrease in leptin concentrations. The corresponding value among males for an 8.0 kg (8.6%) decrease was 29%. Changes in leptin concentrations were best explained by changes in fat mass among both males and females. Body fat distribution was also of importance, especially among females. Gender associated differences in leptin concentrations appear to be largely influenced by gender differences in body fat distribution.     

Serum leptin levels and anthropometric correlates in Ache Amerindians of eastern Paraguay

Leptin is a recently discovered peptide hormone secreted primarily from adipocytes in humans and other mammals; it is a reflection of fat stores, and has been associated with reproductive function. However, few leptin measurements are available from nonindustrialized populations, including contemporary hunter/gatherer communities undergoing the transition to sedentary agriculture. This investigation reports single-sample serum leptin measurements in healthy Ache Amerindian males (n = 21; average age, 32.8 +/- 3.4 SE) and females (n = 12; average age, 31.3 +/- 4.3) in eastern Paraguay. Ache leptin concentrations were much lower than in industrialized populations, although significant sexual dimorphism was evident (female 5.64 ng/ml +/- 0.91 SE vs. male 1.13 ng/ml +/- 0.08; P < 0.0001). Indeed, female leptin levels were similar to those of anorexic women, despite apparently adequate adiposity. Controlling for fat percentage, no significant sex difference was evident, suggesting that adiposity was the primary source of leptin variation. Body fat percentage was highly correlated with leptin in females (r2 = 0.72; P < 0.0005) but not males, who exhibited a modest negative correlation (r2 = 0.25; P < 0.03). Weight (r2 = 0.45; P = 0.02) and BMI (kg/m2) (r2 = 0.81; P < 0.0001) were also significantly correlated in females but not males. These results suggest that: 1) clinical leptin norms based on industrialized populations may represent the highest range of human variation and may not be representative of most human populations; 2) hormonal priming may underlie population variation in leptin profiles; and 3) the relative importance of leptin as a proximate mechanism regulating reproductive effort during human evolution may have been modest.     

Characterization of leptin pulse dynamics and relationship to fat mass,growth hormone,cortisol, and insulin

To investigate the regulation of leptin secretion and pulsatility by fat mass, we performed overnight leptin sampling every 20 min for 12 h and compared leptin dynamics with total body and regional fat measurements in 20 healthy male subjects. Simultaneous growth hormone (GH), cortisol, and insulin levels were assessed to determine relatedness and synchronicity during overnight fasting. Deconvolution analyses were performed to determine simultaneous hormonal dynamics, synchronicity, and interrelatedness using cross-correlation and cross-approximate entropy (X-ApEn) analyses. Subjects demonstrated 4.7 +/- 0.4 leptin pulses/12 h. Leptin secretion correlated highly with total body fat (r = 0.78, P < 0.001) and regional fat depots. In contrast, leptin pulsatility did not correlate with total fat (r = 0.07, P = 0.785) or other measures of fat. There was synchronicity between GH and leptin (lag -39 minutes), cortisol and leptin (lag -211 min), and leptin and insulin, with leptin following insulin by 275 min. The mean random X-ApEn was significant between leptin and GH (0.854 +/- 0.030), cortisol (0.891 +/- 0.023), and insulin (0.868 +/- 0.034), demonstrating a high degree of regularity and pattern frequency. These data demonstrate differential regulation of leptin secretion and pulsatility in adipocytes and suggest that the leptin pulse generator is extrinsic to fat, whereas fat mass acts as an amplifier to modulate secretion and amplitude for a given pulsatility. We demonstrate synchronicity between leptin and GH, cortisol, and insulin. The directionality of the cross correlation suggests a temporal construct in which changes in leptin follow those of insulin but precede those of GH and cortisol during overnight fasting.     

Effect of prolonged training period on plasma adiponectin in elite male rowers.

Adiponectin is secreted by adipocytes and has been implicated in the regulation of energy homeostasis. Vigorous training program represents a physical stress condition in which heavy changes in energy expenditure might increase adiponectin concentration in athletes. Therefore, the aim of the present study was to investigate if there are changes in fasting adiponectin concentration during preparatory period in elite male rowers. Twelve rowers (mean and SD; age: 20.8+/-3.0 years; height: 192.9+/-4.7 cm; body mass: 91.9+/-5.3 kg; body fat percentage: 11.9+/-1.4%) were tested seven times over a 24-week training season. In addition to adiponectin, leptin, insulin, growth hormone, and glucose values were evaluated. Maximal oxygen consumption (VO (2 max)) and aerobic power (Pa (max)) were determined before and after the training period. Training was mainly organized as low-intensity prolonged training. Significant increases in VO (2 max) (by 3.2+/-1.8%; from 6.2+/-0.5 to 6.4+/-0.4 l/min), VO (2 max/kg) (by 2.2+/-2.0%; from 67.9+/-3.0 to 69.4+/-3.0 ml/min/kg) and Pa (max) (by 4.6+/-6.3%; from 444.6+/-39.1 to 465.8+/-25.0 W) were observed after the 24-week period. All measured body compositional values were similar to pretraining values after the training period. Fasting adiponectin did not change during the preparatory period. Likewise, leptin, insulin, growth hormone, and glucose values were not significantly changed after the training period. Adiponectin concentration was significantly correlated (all p<0.05) with body mass (r=-0.40), body fat mass (r=-0.33), body fat free mass (r=0.38), and leptin (r=-0.31) values. In conclusion, fasting adiponectin does not change throughout the prolonged training period in elite male rowers despite substantial changes in training volume. Further studies are needed to clarify possible mechanisms by which adiponectin might influence energy homeostasis during heavy training in elite athletes.     

Leptin and exercise

Short-term exercise (<60 min) studies suggest that leptin concentrations are not acutely affected in healthy males and females. Most reports of reductions in serum leptin may be attributed to circadian rhythms or hemoconcentration. For long-term (> or =60 min) exercise, a reduction in leptin concentrations reported from 1 to 3 hr of running or cycling has been attributed to diurnal reduction in circulating leptin, independent of exercise. Exercise that produces a sufficient energy imbalance (kilocalorie intake versus kilocalorie expenditure) suppresses 24-hr mean and amplitude of the diurnal rhythm of leptin in women. Suppression of leptin concentrations may be counterbalanced by feeding and may explain consistent reports of reductions in leptin concentrations following extreme bouts of exercise such as marathons or ultramarathons. In addition, leptin concentrations are reduced 48 hr after long-term aerobic exercise and long-term resistance exercise is associated with delayed leptin reduction 9 hr postexercise. Training studies have documented that short-term exercise training (< or =12 weeks) does not affect leptin levels, with the exception of patients with type 2 diabetes. Exercise training protocols that result in reduced fat mass will lower leptin concentrations, thus, most investigators have reported leptin concentrations after accounting for fat loss. There are disparate findings concerning long-term (>12 weeks) training studies, with a number of studies finding no effect of training on leptin concentrations other than effects induced by fat loss, and other studies finding reductions in leptin concentrations after accounting for fat loss. Exercise training-induced reductions in leptin levels have been attributed to alterations in energy balance, improvements in insulin sensitivity, alterations in lipid metabolism, and unknown factors. Hormone replacement does not seem to affect leptin adaptations to training. Patients with type 2 diabetes show delayed effects of short-term resistance exercise on leptin concentrations, reduced leptin levels with long-term training, and appear to be more sensitive to training-induced leptin adaptations than other populations.     

Effect of Training Judo in the Competition Period on the Plasmatic Levels of Leptin and Pro-inflammatory Cytokines in High-Performance Male Athletes

The purpose this study was to evaluate the effect of training judo in the competition period on the plasmatic levels of bioactive molecules in high-performance male athletes. The subjects were divided into two groups, a trained group with 11 judokas and a nontrained group also with 11 subjects. Blood samples obtained 60 h after training to measure plasma tumor necrosis factor (TNF-α), interleukin-6 (IL-6), monocyte chemotactic protein 1 (MCP-1), and leptin levels. The trained group presented a significant reduction in the percentage of fat and fat mass and an increase in the lumbar and lower limbs traction forces and the maximum VO₂ when compared to the nontrained group. There was no significant difference in the serum concentrations of TNF-α and IL-6 between the two groups. The trained group presented a lower concentration of leptin, both as absolute values as well as relative to the percentage of fat, and a higher concentration of MCP-1, in relation to the nontrained group. Our results suggest an adaptation in the capacity of synthesizing and secreting leptin in response to chronic stress in judo, what suggests a neuro-hormonal adjustment that guarantees the efficiency of metabolism. The changes of MCP-1 indicated a possible inflammatory state.     

Fat and energy partitioning: longitudinal observations in leptin-treated adults homozygous for a Lep mutation

Objective: Partitioning of body energy content in the aleptinemic ob/ob mouse differs from that in wild‐type mice, but it is not known whether parallel differences exist between humans with leptin (Lep) gene mutations and healthy adults. The objective of this study was to evaluate body composition in three leptin‐treated Turkish adults homozygous for a missense mutation (C→T substitution at codon 105 resulting in Arg→Trp) of Lep. Research Methods and Procedures: Subjects, one male and two female Turkish family members, were evaluated at baseline and treated for 18 months with r‐MetHuLeptin. Patient data (fat mass, energy content) were compared with adult sex‐specific predicted values (adjusted for weight, height, and age) derived in healthy control subjects. Results: Weight loss with leptin treatment was substantial, ranging from 43.9% to 52.1%. At baseline and with leptin treatment, the two women had a fat mass and energy content similar (±12%) to predicted values. Baseline fat and energy content in the male patient was high compared with predicted values (e.g., fat +33%) but approached and reached normal values (e.g., fat, +2%) after 18 months of leptin therapy. Discussion: Adult women with Lep mutations had body composition similar to normal women at baseline and with leptin treatment. In contrast, the man with a Lep mutation had high body fat in the untreated state but a normal male phenotype with leptin administration, possibly secondary to androgenic fat partitioning effects. Fat and energy partitioning can, thus, be quantitatively assessed and linked with potential hormonal mechanisms in humans with inherited disturbances in energy regulation.     

PLTP activity decreases with weight loss: changes in PLTP are associated with changes in subcutaneous fat and FFA but not IAF or insulin sensitivity

Phospholipid transfer protein (PLTP) activity is elevated in obese and diabetic subjects. No prospective studies have examined the effect of weight loss on PLTP activity and assessed whether the resultant changes in activity are related to changes in body weight, insulin resistance, or both. PLTP activity was measured at baseline in 46 subjects (body mass index = 19-64 kg/m2) and after diet-induced weight loss in 19 of the obese subjects. Total body fat mass (FM) by dual-energy X-ray absorptiometry, intraabdominal fat (IAF), and abdominal subcutaneous fat (SQF) by CT scan, insulin sensitivity (SI) by frequently sampled intravenous glucose tolerance test, leptin, and lipids were determined. At baseline, PLTP activity correlated with FM (r = 0.36, P = 0.02) and SQF (r = 0.31, P = 0.045), but not with IAF (r = 0.16, P = 0.32) or SI (r = 0.10, P = 0.52). With diet-induced weight loss (16 +/- 7.3 kg), PLTP activity significantly decreased 9.1% (P = 0.002). The change in PLTP activity correlated with the change in SQF (r = 0.55, P = 0.014) (33.6% decrease), but not with IAF (r = 0.09, P = 0.73) or SI (r = 0.18, P = 0.44), and was highly correlated with the change in nonesterified fatty acid (NEFA) (r = 0.71, P < 0.001). In conclusion, elevated PLTP activity in obese subjects is likely a result of increased body fat, reflected by SQF, and is influenced by NEFAs but is not directly related to insulin resistance.     

Associations between Metabolic Risk Factors and the Hypothalamic Volume in Childhood Leukemia Survivors Treated with Cranial Radiotherapy

Metabolic complications are prevalent in individuals treated with cranial radiotherapy (CRT) for childhood acute lymphoblastic leukemia (ALL). The hypothalamus is a master regulator of endocrine and metabolic control. The aim of this study was to investigate whether the hypothalamic volume would be associated to metabolic parameters in ALL survivors. Thirty-eight (21 women) survivors participated in this study 34 years after diagnosis and with a median age of 38 (27–46) years. All were treated with a median CRT dose of 24 Gy and 11 years (3–13) of complete hormone supplementation. Comparisons were made to 31 matched controls. We performed analyses of fat mass, fat free mass, plasma (p)-glucose, p-insulin, Homa-Index (a measure of insulin resistance), serum (s)-leptin, s-ghrelin and of the hypothalamic volume in scans obtained by magnetic resonance imaging (MRI) at 3 Tesla. Serum leptin/kg fat mass (r = -0.4, P = 0.04) and fat mass (r = -0.4, P = 0.01) were negatively correlated with the HT volume among ALL survivors, but not among controls. We also detected significantly higher BMI, waist, fat mass, p-insulin, Homa-Index, leptin/kg fat mass and s-ghrelin and significantly lower fat free mass specifically among female ALL survivors (all P<0.01). Interestingly, s-ghrelin levels increased with time since diagnosis and with low age at diagnosis for childhood ALL. Our results showed that leptin/kg fat mass and fat mass were associated with a reduced HT volume 34 years after ALL diagnosis and that women treated with CRT after ALL are at high risk of metabolic abnormalities. Taken together our data suggest that the hypothalamus is involved in the metabolic consequences after CRT in ALL survivors.     

Effects of dietary fat type and energy restriction on adipose tissue fatty acid composition and leptin production in rats

To investigate whether dietary fatty acid (FA) composition and energy restriction (ER) interactively influence obese (ob) gene expression, rats consumed diets containing beef tallow, safflower, or fish oil ad libitum (AL) or at 60% AL intake. Circulating leptin concentrations were higher (P < 0.0001) after AL feeding, but were not influenced by dietary fat. ER decreased (P < 0.0001) weight gain and visceral adipose weight, which were positively correlated (r = 0.40 P < 0.001, r = 0.58 P < 0.0001) with circulating leptin levels. Visceral adipose ob mRNA levels were greater in animals fed unsaturated fats, particularly safflower oil, which had the highest ob mRNA levels. Circulating leptin levels did not parallel ob mRNA levels, except for the greater abundance detected in AL adipose in comparison to ER animals. In addition, visceral FA profiles reflected dietary fat source and were influenced by an interaction of dietary fat and energy. These data demonstrate that dietary fat, particularly from a plant or marine source, and ER interactively influence ob mRNA levels; however, alterations in ob mRNA do not confer changes in circulating leptin, with the exception of ER, which is a key determinant. Thus, dietary intake is an important regulator of leptin production; however, the significance of these modest changes in diet-induced obese animals requires further study.     

Plasma leptin levels of elite endurance runners after heavy endurance training

A decrease in testosterone levels and an increase in cortisol levels are observed in male athletes with the overtraining syndrome (OTS). Cortisol causes blood leptin levels to rise and testosterone has an inverse relationship with blood leptin levels. Therefore, we hypothesized that the hormonal changes as a result of OTS induce an increase in leptin. To test this hypothesis, we examined the relationship among changes in leptin, testosterone and cortisol in thirteen male collegiate distance runners (aged 20.3+/-1.1 years) before and after an 8-day strenuous training camp. Runners ran 284.1+/-48.2 km during the training camp. Body fat percentages and plasma glucose concentrations decreased significantly after the training. Non-ester fatty acids and total cholesterol concentrations in blood were unchanged. Serum cortisol concentrations showed a significant increase after the training camp (from 11.82+/-2.00 microg/dl to 16.78+/-3.99 microg/dl), and serum testosterone decreased significantly (from 408.0+/-127.6 ng/dl to 265.2+/-97.6 ng/dl). The ratio of testosterone to cortisol (TCR) dropped by 50% after training (from 35.62+/-13.69 to 16.94+/-8.47). These results suggest that the subjects reached a state of the OTS. Contrary to our hypothesis, plasma leptin was not significantly changed (from 1.34+/-0.29 ng/ml to 1.49+/-0.18 ng/ml). Delta Plasma leptin was not significantly correlated with delta serum cortisol, delta TCR or delta fat percentage. However, delta serum testosterone was positively correlated with delta plasma leptin (r=596, p<0.05). Plasma leptin concentrations might modulate the secretion of testosterone in overtraining conditions. In conclusion, the change in blood leptin level is independent of the changes in cortisol, TCR and fat percentage in highly trained male athletes in the state of the OTS.     

Collection and Interpretation of Plasma Leptin Concentration Data in Humans

JENSEN, MICHAEL D, DONALD HENSRUD, PETER C. O'BRIEN, AND SØREN NIELSEN. Collection and interpretation of plasma leptin concentration data in humans. Obes Res. Objective: To reassess the relationship between body fat and plasma leptin concentrations when a) replicate measures of leptin are made; b) energy intake is controlled at isoenergetic levels before the study; and c) body fat and percent body fat are measured with dual energy X-ray absorptiometry (DXA). Research Methods and Procedures: Two separate studies were conducted. In the first study, four plasma samples were collected for measurement of leptin over 30 minutes on a single day in 43 lean and obese men and women. For the second study, plasma samples were collected on four consecutive days from a group of 50 lean and obese men and women. Percent body fat (and body fat mass) was related to log-transformed mean plasma leptin concentrations using linear regression analysis; multiple linear regression analysis was used to determine whether there was an effect of gender on this relationship, and the analysis of Choi was used to examine whether percent body fat or body fat mass better predicts plasma leptin concentrations. Results: For the first study, percent body fat was highly correlated (r = 0. 96, p<O. OOOl) with log-transformed mean leptin concentrations. No difference in the relationship between leptin and percent body fat in men and women was detected. The second study confirmed this observation; the relationship between In leptin and percent body fat was virtually identical (r = 0. 93, p<0. 001). Analysis of the pooled data suggests that percent body fat is a better predictor of plasma leptin concentration than body fat mass. The use of multiple (as opposed to a single) leptin measurements did not significantly improve the leptinhody fat relationship. Discussion: When robust body composition techniques and diet control measures are taken into consideration, the relationship between In plasma leptin concentrations and percent body fat is not different in men and women.     

Slower gastric emptying in high-fat diet induced obese rats is associated with attenuated plasma ghrelin and elevated plasma leptin and cholecystokinin concentrations

Gastrointestinal (GI) motility and gut hormones have been considered to be involved in the development and maintenance of obesity. Our aim was to assess the relationships between gastric emptying (GE), GI transit and gut hormones and leptin concentrations in diet-induced obese rat model. Male 6-week-old Sprague-Dawley rats were fed with a high-fat (HF) diet for 8weeks to generate diet-induced obesity (DIO) and diet resistant (DR) rats. GE, GI transit and plasma ghrelin, cholecystokinin (CCK), PYY and leptin concentrations were determined in DIO, DR and control (CON) rats. The DIO rats had slower GE, higher plasma leptin and CCK concentrations, and lower plasma ghrelin concentration compared with CON and DR rats. GE was correlated with plasma ghrelin (r=0.402, P=0.028), CCK (r=-0.518, P=0.003) and leptin concentration (r=-0.514, P=0.004). The slower GE, which can be considered as an adaptive response aimed at HF diet induced obesity, may be mediated by changes of plasma ghrelin, CCK and leptin concentrations.