Changes in circulating satiety hormones in obese children: a randomized controlled physical activity-based intervention study. Fasting gut hormone levels change with modest weight loss in obese adolescents. Relationship between adiponectin levels, acylated ghrelin levels, and short-term body mass index changes in children with diabetes mellitus type 1 at diagnosis and after insulin therapy. Long-term persistence of hormonal adaptations to weight loss. EFFECT OF EXERCISE ON APPETITE-REGULATING HORMONES IN OVERWEIGHT WOMEN Adipokines and biochemical changes in Egyptian obese subjects: possible variation with sex and degree of obesity Reduction in saturated fat intake improves cardiovascular risks in obese adolescents during interdisciplinary therapy. Circulating adipokines and mRNA expression in adipose tissue and the placenta in women with gestational diabetes mellitus Appetite-regulating hormone changes in patients with craniopharyngioma. A one-year school-based diet/exercise intervention improves non-traditional disease biomarkers in Mexican-American children. Serum leptin concentrations during short-term administration of growth hormone and triiodothyronine in healthy adults: a randomised, double-blind placebo-controlled study. Effects of Growth Hormone on Growth, Insulin Resistance and Related Hormones (Ghrelin, Leptin and Adiponectin) in Turner Syndrome Reversal of obesity-related hypoadiponectinemia by lifestyle intervention: a controlled, randomized study in obese adolescents. Circulating cytokines as determinants of weight loss-induced improvements in insulin sensitivity The influence of very-low-calorie-diet on serum leptin, soluble leptin receptor, adiponectin and resistin levels in obese women. Effect of obesity intervention programs on adipokines, insulin resistance, lipid profile, and low-grade inflammation in 3- to 5-y-old children The Effect of Laparoscopic Gastric Banding Surgery on Plasma Levels of Appetite-Control, Insulinotropic, and Digestive Hormones
The aims of this study are to examine in children : ( i ) obesity-related alterations in satiety factors such as leptin , ghrelin , and obestatin ; ( ii ) the link between satiety factors and cardiometabolic risk factors ; and ( iii ) the impact of a physical activity-based lifestyle intervention on the levels of these satiety factors in the obese . We studied a total of 21 adolescents ( BMI percentile , 99.0 + /- 0.6 for 15 obese and 56.2 + /- 1.1 for 6 lean ) . The obese subjects underwent a 3-month r and omized controlled physical activity-based lifestyle intervention .  Leptin , soluble leptin receptor ( sOB-R ) , ghrelin , and obestatin levels were determined as the primary outcome measures . Other markers of cardiometabolic disease such as inflammation and insulin resistance were also determined . Body composition was measured by dual-energy X-ray absorptiometry . The concentrations of ghrelin , obestatin , and sOB-R were significantly lower in the obese children compared to the lean controls , whereas that of leptin was higher ( all P < 0.05 ) . Although intervention led to a net increase in obestatin ( P < 0.01 ) and no change in ghrelin levels , the balance between ghrelin and obestatin ( ratio of ghrelin to obestatin , G/O ) decreased ( P < 0.02 ) . Intervention reduced leptin and increased sOB-R ( P < 0.01 for both ) . Significant associations between satiety factors and other cardiometabolic risk factors were also observed . Taken together , alterations in the levels of satiety factors are evident early in the clinical course of obesity , but physical activity-based lifestyle intervention either prevented their continued increase or normalized their levels . These beneficial effects appear to aid in the maintenance of body weight and reduction in cardiovascular risk BACKGROUND Gut hormones change with weight loss in adults but are not well studied in obese youth . OBJECTIVE The primary aim was to evaluate how gut hormones and subjective appetite measure change with dietary weight loss in obese adolescents . METHODS Participants were a subset of those taking part in the ' Eat Smart Study ' . They were aged 10 - 17 years with body mass index ( BMI ) > 90th centile and were r and omized to one of three groups :  wait-listed control , structured reduced carbohydrate or structured low-fat dietary intervention for 12 weeks . Outcomes were fasting glucose , insulin , leptin , adiponectin , total amylin , acylated ghrelin , active glucagon-like peptide-1 , glucose-dependent insulinotropic polypeptide ( GIP ) , pancreatic polypeptide ( PP ) and total peptide tyrosine-tyrosine . Pre- and postpr and ial subjective sensations of appetite were assessed using visual analogue scales . RESULTS Of 87 ' Eat Smart ' participants , 74 participated in this sub- study . The mean ( st and ard deviation ) BMI z-score was 2.1 ( 0.4 ) in the intervention groups at week 12 compared with 2.2 ( 0.4 ) in the control group . Fasting insulin ( P = 0.05 ) and leptin ( P = 0.03 ) levels decreased , while adiponectin levels increased ( P = 0.05 ) in the intervention groups compared with control . The intervention groups were not significantly different from each other . A decrease in BMI z-score at week 12 was associated with decreased fasting insulin ( P < 0.001 ) , homeostatic model of assessment -insulin resistance ( P < 0.001 ) , leptin ( P < 0.001 ) , total amylin ( P = 0.03 ) , GIP ( P = 0.01 ) , PP ( P = 0.02 ) and increased adiponectin ( P < 0.001 ) . There was no significant difference in appetite sensations . CONCLUSIONS Modest weight loss in obese adolescents leads to changes in some adipokines and gut hormones that may favour weight regain OBJECTIVE To determine the effect of the initial metabolic imbalance and its restoration after insulin therapy on adiponectin and acylated ghrelin levels in children with type 1 diabetes mellitus ( T1DM ) . STUDY DESIGN Twenty prepubertal children with newly diagnosed T1DM were prospect ively studied at diagnosis and after 1 and 4 months of therapy .  Body mass index ( BMI ) and serum levels of adiponectin , resistin , total and acylated ghrelin , leptin , tumor necrosis factor alpha ( TNF-alpha ) , and interleukin-6 ( IL-6 ) were determined . The control group comprised 40 healthy prepubertal children . RESULTS BMI was decreased at diagnosis , normalized at 1 month , and remained so thereafter . Adiponectin levels at diagnosis were similar to controls , increasing significantly after 1 month and normalizing at 4 months . Acylated ghrelin levels were lower at diagnosis , with a significant increase at 1 month and normalizing at 4 months . Resistin levels were normal at all time points . Leptin levels were decreased , while TNF-alpha and IL-6 were increased at diagnosis and normalized at 1 month . CONCLUSIONS These findings suggest that BMI is not the main predictor of acylated ghrelin or adiponectin levels in newly diagnosed T1DM subjects and that these peptides may play an important role in the metabolic adaptation in this disease BACKGROUND After weight loss , changes in the circulating levels of several peripheral hormones involved in the homeostatic regulation of body weight occur . Whether these changes are transient or persist over time may be important for an underst and ing of the reasons behind the high rate of weight regain after diet-induced weight loss . METHODS We enrolled 50 overweight or obese patients without diabetes in a 10-week weight-loss program  for which a very-low-energy diet was prescribed . At baseline ( before weight loss ) , at 10 weeks ( after program completion ) , and at 62 weeks , we examined circulating levels of leptin , ghrelin , peptide YY , gastric inhibitory polypeptide , glucagon-like peptide 1 , amylin , pancreatic polypeptide , cholecystokinin , and insulin and subjective ratings of appetite . RESULTS Weight loss ( mean [ ±SE ] , 13.5±0.5 kg ) led to significant reductions in levels of leptin , peptide YY , cholecystokinin , insulin ( P<0.001 for all comparisons ) , and amylin ( P=0.002 ) and to increases in levels of ghrelin ( P<0.001 ) , gastric inhibitory polypeptide ( P=0.004 ) , and pancreatic polypeptide ( P=0.008 ) . There was also a significant increase in subjective appetite ( P<0.001 ) . One year after the initial weight loss , there were still significant differences from baseline in the mean levels of leptin ( P<0.001 ) , peptide YY ( P<0.001 ) , cholecystokinin ( P=0.04 ) , insulin ( P=0.01 ) , ghrelin ( P<0.001 ) , gastric inhibitory polypeptide ( P<0.001 ) , and pancreatic polypeptide ( P=0.002 ) , as well as hunger ( P<0.001 ) . CONCLUSIONS One year after initial weight reduction , levels of the circulating mediators of appetite that encourage weight regain after diet-induced weight loss do not revert to the levels recorded before weight loss . Long-term strategies to counteract this change may be needed to prevent obesity relapse . ( Funded by the National Health and Medical Research Council and others ; Clinical Trials.gov number , NCT00870259 . ) Over the past decade , our knowledge of how homeostatic systems regulate food intake and body weight has increased with the discovery of circulating peptides such as leptin , acyl ghrelin , des-acyl ghrelin and obestatin . These hormones regulate the appetite and food intake by sending signals to the brain regarding the body 's nutritional status . The purpose of this study was to investigate the response of appetite-regulating hormones to exercise .  Nine overweight women undertook two 2 h trials in a r and omized crossover design . In the exercise trial , subjects ran for 60 min at 50 % of maximal oxygen uptake followed by a 60 min rest period . In the control trial , subjects rested for 2 h.  Obestatin , acyl ghrelin , des-acyl ghrelin and leptin concentrations were measured at baseline and at 20 , 40 , 60 , 90 and 120 min after baseline . A two-way ANOVA revealed a significant ( P < 0.05 ) interaction effect for leptin and acyl ghrelin . However , changes in obestatin and des-acyl ghrelin concentration were statistically insignificant ( P > 0.05 ) . The data indicated that although acute treadmill exercise result ed in a significant change in acyl ghrelin and leptin levels , it had no effect on plasma obestatin and des-acyl ghrelin levels The purpose of this study was firstly to evaluate the adipokines and biochemical changes in obese subjects in relation to different grade s of obesity and in relation to gender difference ( males versus females ) and secondly to evaluate the role of TNF-α in obesity . From January 2013 to February 2014 , a total number of 120 non-diabetic subjects of both sexes were recruited and r and omly selected from Dr. Abd-Elhamid Elsheikh center for physiotherapy and weight control , El-menofia-Egypt . Those subjects were classified according to their sex into two main groups ; the female group and the male group . The female group ( 60 women ) was distributed according to BMI into group 1 ( 15 lean women ) , group 2 ( 15 class I obese women ) , group 3 ( 15 class II obese women ) , and group 4 ( 15 class III obese women ) . The male group ( 60 men ) was also distributed according to the BMI into group 1 ( 15 lean men ) , group 2 ( 15 class I obese men ) , group 3 ( 15 class II obese men ) , and group 4 ( 15 class III obese men ) . All individuals enrolled in the study were su bmi tted to weight and height measurements with subsequent calculation of body mass index . Fasting blood sample s were collected from all participants for quantitative determination of blood glucose , serum lipid , TNF-α , leptin , and adiponectin levels . One-way analysis of variance followed by LSD post hoc test was used for comparison of variables . In obese subjects of both sexes , it was found that circulating leptin and TNF-α levels were significantly high ( P < 0.05 ) and positively correlated to BMI . In contrast to leptin , adiponectin concentrations were significantly low ( P < 0.05 ) and inversely correlated to BMI . Regarding gender difference , although serum leptin and adiponectin levels were higher in women than men , men showed higher atherogenic parameters . We conclude that leptin , TNF-α , and adiponectin were related to both BMI and grade s of obesity . Furthermore , TNF-α may play a role in obesity BACKGROUND / OBJECTIVES Obesity is related to inflammation and cardiovascular disease . The increase in saturated fatty acid intake ( SFA ) can potentiate cardiovascular risks . The aim of this study was to assess the influence of change in SFA on carotid intima-media thickness ( cIMT ) , metabolic profile and anti/pro-inflammatory adipokines in obese adolescents . METHODS Sixty obese adolescents were subjected to 1 year of interdisciplinary intervention ( nutrition , psychology , physical exercise and clinical therapy ) .  Blood glucose , insulin , lipid profile , leptin and adiponectin were analysed . Insulin resistance was estimated by HOMA-IR and HOMA-AD . cIMT was measured by ultrasonography . Dietetic intake was calculated by 3-day dietary record . Volunteers were analysed according to tertiles of change ( Δ ) in SFA intake : Low-SFA reduction<3.68 g ; Moderate-SFA reduction 3.68 - 13.67 g ; and High-SFA reduction>13.67 g. RESULTS Moderate and High-SFA tertiles presented reduction in insulin , leptin/adiponectin ratio , cIMT and increase in adiponectin and adiponectin/leptin ratio . Adiponectin/leptin ratio was predictor of cIMT . HOMA-IR , total cholesterol and LDL-cholesterol reduced only in High-SFA tertile , and was associated with SFA independent of visceral fat . Negative correlations between Δ of SFA and adiponectin and adiponectin/leptin ratio were observed . CONCLUSION Obese adolescents with moderate and high reduction in SFA presented improvements on pro/anti-inflammatory biomarkers and cIMT , leading to reduction in cardiovascular risks HighlightsChemerin and leptin are increased , omentin‐1 and visfatin are decreased in at term GDM‐obese women .  Chemerin and omentin‐1 are expressed mainly by the maternal VAT . Leptin is expressed mainly in maternal SAT.Circulating chemerin and leptin in at term pregnancy correlate with BMI and HOMA‐IR.Chemerin and leptin could contribute to insulin resistance and low grade inflammation that characterizes GDM women complicated by obesity . Weight control during pregnancy is necessary to avoid adverse metabolic complications for the mother and the offspring . & NA ; Maternal adipose tissue and the placenta secrete various molecules commonly called adipokines such as chemerin , omentin‐1 , visfatin , adiponectin , and leptin that are important players in the pathogenesis of insulin resistance . Gestational diabetes mellitus ( GDM ) is defined as a state of glucose intolerance characterized by & bgr;‐cell dysfunction and insulin resistance . To examine whether circulating adipokines and their mRNA expression in the adipose tissue and the placenta are altered in GDM pregnancy , we compared 15 GDM women [ obese ( BMI > 30 ) and non‐obese ( BMI < 30 ) ] to 23 NGT ( normal glucose tolerance ) women [ obese and non‐obese ] , at the time of the Cesarean section .  Circulating chemerin and leptin were higher ( p = 0.009 and p = 0.005 , respectively ) and circulating omentin‐1 , visfatin , as well as the adiponectin/leptin ratio were lower ( p = 0.039 , p = 0.007 and p = 0.011 , respectively ) in GDM‐obese compared to NGT‐non‐obese women . Chemerin and leptin correlated positively with BMI and HOMA‐IR and omentin‐1 correlated negatively with BMI . Serum TNF‐&agr ; was significantly elevated in all obese compared to non‐obese pregnant women and correlated positively with BMI . Adiponectin levels were reduced ‐although not significantly‐ in GDM‐ and NGT‐obese women compared to their non‐obese counterparts . Resistin , RPB4 and IL‐6 levels did not differ significantly between groups . Chemerin mRNA expression in subcutaneous adipose tissue ( SAT ) and visceral adipose tissue ( VAT ) was significantly higher compared to placenta in all women ( 6‐to 24‐times , p < 0.05 ) . Chemerin‐VAT mRNA expression in GDM‐obese tended to be significantly higher compared to NGT‐non‐obese women ( 3‐times , p = 0.005 ) . Omentin‐1 mRNA expression was significantly higher in VAT compared to SAT ( 50‐ to 100‐times , p < 0.01 ) and its expression in placenta was negligible in all women . Although , leptin was expressed significantly higher in SAT compared to VAT and the placenta in all women ( 5‐ to 46‐times , p < 0.05 ) , only its mRNA expression in VAT of obese ( GDM and NGT ) differed significantly when compared to NGT‐non‐obese women ( 3‐times higher , p < 0.02 ) . Visfatin mRNA expression was comparable in all tissues . In conclusion , chemerin and leptin are elevated and omentin‐1 and visfatin levels are decreased in GDM women complicated by obesity . This finding together with the positive association of chemerin and leptin with markers of insulin resistance , suggests that these adipokines and more especially chemerin and leptin accompanied by their adipose tissue expression could contribute to the increased insulin resistance and low grade inflammation that characterizes GDM‐obese women Patients with craniopharyngioma ( CP ) , an embryological tumor located in the hypothalamic and /or pituitary region , often suffer from uncontrolled eating and severe obesity . We aim ed to compare peripherally secreted hormones involved in controlling food intake in normal weight and obese children and adolescents with CP vs. controls .  Plasma insulin , glucose , total ghrelin , and peptide-YY ( PYY ) levels were assessed under fasting conditions as well as 60 min after liquid mixed meal in four groups : Normal weight ( n = 12 ) and obese ( n = 15 ) CP patients , and 12 normal weight and 15 obese otherwise healthy BMI - , gender- and age-matched controls .  Homeostasis model assessment of insulin resistance ( HOMA(IR ) ) , as well as quantitative insulin sensitivity check index ( QUICKI ) were calculated . Obese CP subjects had significantly higher HOMA(IR ) , higher baseline and postmeal insulin but lower ghrelin levels , weaker postmeal changes for PYY , and lower QUICKI compared to obese controls . QUICKI data from all CP patients correlated positively with ghrelin and PYY % postmeal changes ( ghrelin : r = 0.38 , P = 0.023 ; PYY r = 0.40 , P = 0.017 ) and negatively with st and ard deviation score- BMI ( SDS- BMI : r = -0.49 , P = 0.002 ) . Tumor growth of 87 % obese and 58 % of normal weight CP patients affected the hypothalamic area which was associated with higher SDS- BMI and weaker % postmeal ghrelin changes ( P = 0.014 ) compared to CP patients without hypothalamic tumor involvement . Blunted postmeal ghrelin and PYY responses in obese CP subjects are likely due to their higher degree of insulin resistance and lower insulin sensitivity compared to matched obese controls . Thus , insulin resistance in CP patients seems to affect eating behavior by affecting meal responses of gut peptides School-based interventions are an effective way to treat  childhood obesity . The purpose of the present study was to biologically vali date an established school-based intervention design ed to reduce st and ardised body mass index ( z BMI ) over a period of 12 months . This intervention focused on a subset of Mexican-American children who were participating in a larger clinical weight loss study . Plasma sample s were analysed from self-identified Mexican-American children ( 12 - 14 years ) who were r and omised to either a school-based intervention ( IN , n = 152 ) or self-help control ( CN , n = 69 ) . Treatment was 4 days week⁻¹ of exercise ( 45 min day⁻¹ ) and 1 day week⁻¹ of nutritional counselling for 6 months . Fasting ( > 8 h ) blood sample s were collected at baseline , 6 months ( end of active intervention ) and 12 months ( 6 months after the end of the active intervention ) . Plasma resistin , adiponectin and leptin concentration were measured using a multiplex assay . Separate linear mixed models and a P < 0.05 were used to test for significance . Significant group × time interactions were found for resistin ( P < 0.0001 ) , adiponectin ( P = 0.001 ) and leptin ( P = 0.013 ) . For resistin , IN was 12 % lower at 6 months than CN . Adiponectin concentration in IN was greater at 6 months ( 26 % ) and 12 months ( 8 % ) than CN . Leptin concentration was 22 % lower for IN at 12 months than CN . We have previously reported that our school-based intervention reduced z BMI and now reported alterations in biologically relevant disease biomarkers . Some of the observed changes were only present at the end of the active intervention ( resistin ) , while others persisted until 12 months ( leptin and adiponectin ) . These changes underscore the effectiveness of our school-based intervention at not only improving z BMI but also at reducing disease risk The regulation of adipose tissue mass and energy expenditure is currently subject to intensive research , which primarily relates to the discovery of leptin . Leptin is a peptide , which is the product of the obese ( ob ) gene expressed in adipose tissue of several species icluding humans . Leptin is supposed to serve both as an index of fat mass and as a sensor of energy balance . Administration of recombinant murine leptin in ob/ob-mice , which do not produce leptin , decreases food intake and increases thermogenesis both of which result in a reduction in body weight and adipose tissue mass . The calorigenic effect of leptin presumably acts through an increase in sympathetic outflow which in turn activates the beta3 adrenergic receptor in brown adipose tissue . The regulation and action of endogenous leptin in humans are less well understood , and clinical grade recombinant human leptin is so far not available . Serum leptin correlates logarithmically with total body fat in both normal weight and obese subjects , which suggest insensitivity to leptin in obese patients . Furthermore , more rapid excursions in serum leptin have been reported following short-term changes in caloric intake and administration of insulin . Growth hormone ( GH ) exerts pronounced effects on lipid metabolism and resting energy expenditure . The lipolytic actions of GH appear to involve both increased sensitivity to the beta-adrenergic pathway , and a suppression of adipose tissue lipoprotein lipase activity . The calorigenic effects of GH have been shown not only to be secondary to changes in lean body mass . Growth hormone administration furthermore increases the peripheral conversion of thyroxine to triiodothyronine , which may contribute to the overall actions of GH on fuel and energy metabolism . So far , little is known about the effects of GH and iodothyronines on serum leptin levels in humans . We therefore measured serum leptin levels and energy expenditure before and after the administration of GH and triiodothyronine , alone and in combinaion , in a r and omized double-blind placebo-controlled study in healthy young male adults . The dose of triiodothyronine was selected to obtain serum levels comparable to those seen after GH administration Background : Concomitant evaluation of the metabolic and growth-promoting effects of growth hormone ( GH ) therapy in Turner syndrome ( TS ) may be used in the prediction of the growth response to GH therapy . Aim : To evaluate the metabolic effects of GH therapy  in TS and correlation with the short-term growth response . Patients : 24 prepubertal children with TS , aged 9.4 ± 2.6 years were followed for auxology and IGF-I , IGFBP-3 , leptin , ghrelin , adiponectin , lipids and OGTT results in a prospect i ve multicenter study . Intervention : GH ( Genotropin ® ) in a dose of 50 µg/kg/day for 1 year . Results : Height st and ard deviation score ( SDS ) increased from –3.9 ± 1.5 to –3.5 ± 1.4 ( p = 0.000 ) on therapy . BMI did not change . IGF-I SDS increased from –2.3 ± 0.4 to –1.6 ± 1.1 at 3 and 6 months ( p = 0.001 ) and decreased thereafter . Serum leptin decreased significantly from 2.3 ± 3.9 to 1.7 ± 5.3 ng/ml ( p = 0.022 ) at 3 months and increased afterwards . Serum ghrelin decreased from 1.2 ± 0.8 to 0.9 ± 0.4 ng/ml ( p = 0.005 ) with no change in adiponectin . Basal and stimulated insulin levels also increased significantly . Δ height SDS over 1 year showed a significant correlation with Δ IGF-I0–3 months ( r = 0.450 , p = 0.027 ) . Conclusion : IGF-I may be considered as a marker of growth response in TS at short term . Leptin shows a decrease at short term but does not have a correlation with growth response . The decrease in ghrelin in face of unchanged weight seems to be associated with increase in IGF-I and insulin levels . The unchanged adiponectin levels in spite of an increase in insulin levels indicates that adiponectin is mainly affected by weight , not insulin CONTEXT Hypoadiponectinemia and chronic sub clinical inflammation in adults are associated with the development of diabetes and cardiovascular disease . The potential relationship between adiponectin and inflammation and its modulation by lifestyle intervention in the pediatric obese population remain unclear . OBJECTIVES The objectives were to investigate in adolescents 1 ) the relationship between adiponectin and obesity-related inflammatory factors , C-reactive protein , and IL-6 ; and 2 ) the effect of a lifestyle intervention on adiponectin and whether these effects are related to changes in inflammatory factors . RESEARCH METHODS AND PROCEDURES Twenty-one obese and age-matched lean adolescents ( age , 14 - 18 yr ; Tanner stage , > or = IV ) were studied cross-sectionally . Fifteen obese adolescents also underwent a r and omized , controlled physical activity-behavior-diet-based lifestyle intervention for 3 months . Associations among adiponectin , fat mass , insulin resistance , and inflammatory factors at baseline as well as after the intervention were assessed . RESULTS Plasma adiponectin concentration was lower ( P < 0.001 ) in the obese vs. age-matched lean adolescents . Significant inverse relationships were observed between adiponectin and inflammatory factors , insulinemia , insulin resistance , and fat mass . Intervention produced a 34 % increase in adiponectin concentration ( P = 0.0004 ) despite negligible weight loss but with reductions in fat mass , hyperinsulinemia , insulin resistance , and inflammatory factors ( all P < 0.01 ) . CONCLUSIONS The data suggest that in adolescents , obesity-related hypoadiponectinemia is associated with sub clinical inflammation , and a short-term lifestyle intervention augments adiponectin concentrations . These effects appear to be related to reductions in fat mass and inflammatory factors . Based on our current underst and ing of adiponectin physiology , reversal of hypoadiponectinemia in obese adolescents may protect against risks for cardiovascular disease and diabetes Dietary calorie restriction and exercise promote weight loss and may have additive effects for improving insulin sensitivity , independent of weight loss . It is not known if these effects are attributable to changes in circulating cytokines . We evaluated the hypothesis that modest , matched weight loss induced by calorie restriction and exercise have additive effects on circulating cytokines and these changes correlate with improvements in insulin sensitivity . Overweight and sedentary women and men ( n = 52 , 45–65 years ) were r and omized to undergo 7 % weight loss by using 3–6 months of calorie restriction , exercise , or a combination of both calorie restriction and exercise . Concentrations of cytokines and hormones were measured in fasting and oral glucose tolerance test blood sample s. Insulin sensitivity was estimated based on oral glucose tolerance test for glucose and insulin . With all groups combined , fasting leptin ( p < 0.0001 ) and high molecular weight adiponectin ( p = 0.04 ) decreased and pentraxin-3 increased ( p < 0.0001 ) , in a manner that correlated with improvements in insulin sensitivity ( all p ≤ 0.0002 ) . These changes , combined with decreases in glucose-dependent insulinotropic polypeptide from the oral glucose tolerance test , explained 63 % of the variance ( p < 0.0001 ) in insulin sensitivity improvements . Exercise and calorie restriction had additive effects on leptin , with a similar trend for high molecular weight adiponectin . Monocyte chemoattractant protein-1 and C-reactive protein concentrations did not change . Calorie restriction and exercise had opposite effects on soluble tumor necrosis factor receptor-1 .  Modest weight loss in overweight adults  decreases serum leptin and high molecular weight adiponectin , and increases pentraxin-3 concentrations in a manner that correlates with increased insulin sensitivity . Exercise has additive effects to those induced by calorie restriction for reductions in leptin and possibly adiponectin . These changes may contribute to the additive effects of calorie restriction and exercise for improving insulin sensitivity The aim of our study was to determine whether adipocyte-derived hormones leptin , adiponectin and resistin contribute to the improvement of insulin sensitivity after very-low calorie diet ( VLCD ) . Therefore , serum levels of these hormones were measured in fourteen obese females before and after three weeks VLCD and in seventeen age- and sex-matched healthy controls .  Body mass index , HOMA index , serum insulin and leptin levels in obese women before VLCD were significantly higher than in control group ( BMI 48.01+/-2.02 vs. 21.38+/-0.42 kg/m(2 ) , HOMA 10.72+/-2.03 vs. 4.69+/-0.42 , insulin 38.63+/-5.10 vs. 18.76+/-1.90 microIU/ml , leptin 77.87+/-8.98 vs. 8.82+/-1.52 ng/ml ) . In contrast , serum adiponectin and soluble leptin receptors levels were significantly lower in obese women before VLCD than in the control group . No differences were found in serum glucose and resistin levels between the obese group before VLCD and the control group . VLCD significantly decreased BMI , HOMA index , serum glucose , insulin and leptin levels and increased soluble leptin receptor levels . The changes in serum adiponectin and resistin levels in obese women after VLCD did not reach statistical significance . We conclude that leptin and soluble leptin receptor levels were affected by VLCD while adiponectin and resistin concentrations were not . Therefore , other mechanisms rather than changes in the endocrine function of the adipose tissue are probably involved in the VLCD-induced improvement of insulin sensitivity Background : Childhood obesity can cause the development of cardiovascular risk factors . We assessed the effect of a multidisciplinary intervention program on cardiovascular risk factors and compared this effect with a usual-care program in 3- to 5-y-old overweight or obese children . Methods : Seventy-five children were r and omly assigned to a multidisciplinary intervention or a usual-care program . Anthropometry , body composition , and abdominal adipose tissue were assessed at the start and end of a 16-wk program . Concurrently , fasting concentrations of serum lipids , glucose , insulin , HbA1c , leptin , adiponectin , high-sensitive C-reactive protein ( hsCRP ) , tumor necrosis factor (TNF)-α , and interleukin (IL)-6 were determined . Results : In both groups , insulin sensitivity improved , demonstrated by decreased insulin concentrations and a decreased HOMA2-IR . In the multidisciplinary intervention group , there was also a decrease of HbA1c and TNF-α . In the usual-care group , an increase in glucose concentrations was found . Comparing both groups , changes over time were not different , besides trends in the decrease in total cholesterol and TNF-α , in favor of the multidisciplinary intervention group . Combining the results of both groups , a correlation was found between the decrease in body fat percentage ( BF% ) , and both HOMA2-IR and triglyceride ( TG ) concentrations . Conclusion : In 3- to 5-y-old children , both obesity intervention programs improved insulin sensitivity , in parallel with a reduced BF% Background We hypothesized that  laparoscopic adjustable gastric b and ing ( LAGB )  reduces weight and modulates ghrelin production , but largely spares gastrointestinal endocrine function . To examine this hypothesis , we determined plasma concentrations of appetite-control , insulinotropic , and digestive hormones in relation to LAGB . Methods Twenty-four patients undergoing LAGB were prospect ively enrolled .  Body mass index ( BMI ) was measured and blood sample s obtained at baseline and 6 and 12 months post-surgery . Plasma concentrations of leptin , acylated and total ghrelin , pancreatic polypeptide ( PP ) , insulin , glucose-dependent insulinotropic peptide ( GIP ) , active glucagon-like peptide-1 ( GLP-1 ) , gastrin , and pepsinogens I and II were measured using enzyme-linked immunoassays . Results Median percent excess weight loss ( % EWL ) over 12 months was 45.7 % with median BMI decreasing from 43.2 at baseline to 33.8 at 12 months post-surgery ( p < 0.001 ) . Median leptin levels decreased from 19.7 ng/ml at baseline to 6.9 ng/ml at 12 months post-surgery ( p < 0.001 ) . In contrast , plasma levels of acylated and total ghrelin , PP , insulin , GIP , GLP-1 , gastrin , and pepsinogen I did not change in relation to surgery ( p > 0.05 ) . Pepsinogen II levels were significantly lower 6 months after LAGB but returned to baseline levels by 12 months . Conclusions LAGB yielded substantial % EWL and a proportional decrease in plasma leptin . Our results support the hypothesis that LAGB works in part by suppressing the rise in ghrelin that normally accompanies weight loss . Unchanged concentrations of insulinotropic and digestive hormones suggest that gastrointestinal endocrine function is largely maintained in the long term
Leptin levels decreased as BMI decreased .
Evidence regarding the relationships of ghrelin and adiponectin with BMI was inconclusive .
Conclusions : Despite known effects of maturation on hormones , studies did not consistently differentiate findings by maturational stage .
BMI and leptin levels have a positive relationship , but evidence on ghrelin and adiponectin was inconclusive
Problem : To address the complex phenomenon of pediatric obesity , one must underst and the physiological mechanisms regulating energy intake and inflammation .
The peptide hormones leptin , ghrelin , and adiponectin are involved in both , but their functions are dysregulated in obesity .
The purpose of this systematic review is ( 1 ) to characterize studies of nutrition interventions for weight management in children who measure these peptides as outcomes , ( 2 ) to assess risk of bias in the studies , and ( 3 ) to determine the relationships between these peptides and body mass index ( BMI ) .