Iranian Journal of

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Background: Leptin is an adipocyte- derived hormone that plays an important role in the pathogenesis of obesity. Obesity is associated with insulin resistance and hyperinsulinemia. Insulin resistance is one of the factors which have been suggested to affect leptin serum levels. There are few studies evaluating the relation between leptin level and insulin resistance in childhood and adolescence obesity. The aim of the present study is to investigate this relationship in Iranian obese children. Methods: We screened 13089 primary school students aged 7-12 years. Children were divided to overweight and normal based on the recently published National Center for Health Statistics growth charts. The number of children which were overweight was 498, of whom 347 subjects particiated in the study. Fasting blood glucose, insulin and leptin levels were measured and homeostasis model assessment (HOMA) of insulin resistance (HOMA-IR) and fasting glucose to insulin ratio (FGIR) were calculated and compared between two groups. Results: Serum leptin levels were significantly higher in overweight compared to normal group. (11.58±8.1 and 8.1±5.2 respectively p<0.05). Before adjustment for BMI, there was a significant correlation between leptin and fasting insulin, HOMA –IR index and FGIR. (r=0.1, p< 0.05, r=0.1 , p<0.01, r=0.07, p<0.05 respectively). After adjustment for BMI, no significant correlation was found (r=0.097, p=0.20). Conclusion: The relation between leptin and insulin resistance was weak and disappeared after adjustment for BMI. It seems that many other factors including BMI and total fat amount may affect this relationship. Further studies in this field are required.

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Leptin is a 16-kD protein which is secreted from white adipocytes and, its discovery has generated enormous interest in the regulation of energy balance. Leptin has been implicated in the regulation of food intake, energy expenditure, and whole-body energy balance in animals and human. Plasma leptin levels correlate with fat storages and respond to changes in energy balance. It was initially proposed that leptin serves a primary role as an anti-obesity hormone, but this role is commonly thwarted by leptin resistance. The profound effects of leptin on regulating body energy balance, make it as a prime candidate for drug therapies of obesity in humans and animals. Despite the recent achievements in unearthing the role of leptin in the pathophysiology of obesity, many important questions still remained that must be responded. More studies with follow-up designs and genetic evaluations are warranted to understand the comprehensive role of leptin in human. In this letter we have a review of known effects of leptin on human obesity up to now.

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Background: It is well recognized that an increased body weight is often associated with increased blood pressure. Moreover, leptin an adipocyte-derived hormone is strongly suggested to have an important role in pathogenesis of the obesity. We aimed to evaluate the levels of serum leptin in association with obesity and hypertension in a sample of Iranian obese children.
Methods: Children from all the primary schools of a distinct of Tehran were screened for obesity. Children with a waist circumference equal to or above 90th percentile for their age and height were invited for the study. Anthropometric measurements were done and blood samples for fasting serum leptin levels were collected from 563 enrolled obese children. Multivariate linear regression analysis was used to evaluate relationship of various factors with obesity.
Results: Mean Serum leptin levels were 8.65 ±2.18 (ng/ml). Serum Leptin levels were higher in girls than boys (P=0.009). There were significant correlations between body mass index (BMI) and serum Leptin levels, child age, systolic and diastolic blood pressure. Systolic blood pressure and diastolic blood pressure lost their association with serum Leptin level in multivariate linear regression analysis.
Conclusion: BMI is independently associated with Leptin levels among obese children. This may affirm a role for this hormone in the pathogenesis of childhood obesity. It seems unlikely that plasma Leptin be a major mediator of association between obesity and hypertension. However, severe hyperleptinemia may act as a risk factor for increased blood pressure.

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Background: Leptin, a peptide hormone, is the product of "ob" Gene. Leptin regulate body weight and composition through reducing appetite and energy expenditure in rodents and humans. The aim of this study was to evaluate differences in expression of Leptin Gene in different tissues of streptozotocin induced diabetic rats.
Methods: 40 Sprague Dawely rat were selected. Intra peritoneal injection was carried out in 20 rats and another 20 rats were used as control. After injection of 60mg/kg Streptozotocin, animals were transformed into diabetic. Glucose was measured by glucose oxidase method. Leptin and insulin were measure by commercially available immunoassay kits. After one week treatment, different tissues including adipose tissues, Spleen, epidydimis, and Liver of both control and experimental animals were dissected. For investigation of any changes of the Leptin gene expression in different tissues, RNA was extracted using Trizo1 method. By using RT-PCR technique, Leptin cDNA and β-actin cDNA as internal control were constructed and PCR was carried out. The RT-PCR products were detected on 2% agarose gel using electrophoresis.
Results: Mean serum levels of Leptin was 5.23± 0.45 ng/ml before injection of streptozotocin and markedly decreased in STZ induced diabetic rats to 0.79±0.25 ng/ml. This decrease was statistically significant P<0.05). There was a direct and significant correlation between leptin and insulin in streptozotocin-induced diabetic rats (r=0.37, P<0.05 ) while, this was reverse in control rats ( r= -0.28, P<0.05). Using RT-PCR method, Leptin gene expression in different tissues including fat epidydimis, liver, and spleen showed that the intensity of leptin band with 452 bp was decreased in diabetic rats in comparison to normal rats. Actin Gene expression was identified in PCR products having 403 bp and the intensity was constant in both groups. The reduction rates of "ob" mRNA in fat epidydimis tissue in STZ diabetic rats was remarkable in comparison to Spleen and Liver.
Conclusion: It is speculated that Leptin gene could be under regulation of insulin dependent mechanism in diabetic rats and by modulating Leptin gene expression in diabetic patients, it may be useful in clinical practices.

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Background: Diabetes is a common endocrine disease in human kind. In most type II diabetic patients, obesity and overweight status account as the serious health problems worldwide and variety of endocrine factors well known that have regulatory role in weight balance and body composition including Leptin and IGF-I factor. The aim of this study was to examine the correlation between Leptin and IGF-I in type II diabetics and controls.
Methods: As a case- control study, 38 type 2 diabetics (20 males and 18 female with mean age 49.22) and 46 healthy controls (16 males and 30 females with mean age 49.52) are recruited. We measured the concentrations of FPG, IGF-I, HbA1C and IGFBP-3 in both groups. FPG was measured by enzymatic glucose oxidase method and Hb Gold analyzer HPLC was used to measure HbA1C. Determination of Leptin, IGF-I, IGFBP-3 and Insulin concentrations were carried out using ELIZA method. P< 0.05 was considered as statistically significant.
Results: The mean of BMI and age were not significantly different in both groups. The mean serum levels of IGF-I, Leptin, Insulin, FPG and HbA1c concentrations in type II diabetics were significantly higher than controls (P< 0.05). In males, the mean serum levels of Leptin were statistically lower than in females in both groups. There was a strong correlation between IGF-I and IGFBP-3, Leptin and insulin, IGF-I and age, and BMI with FPG in both patients and controls (P< 0.05). A reverse correlation was observed between IGF-I and HbA1c in patients and controls (P< 0.05).
Conclusion: It is speculated that based on this findings, Leptin and IGF-I system could have regulatory roles in body composition and fat content particularly in obese and overweight diabetic patients and have significant correlation with Insulin, glucose, BMI and age.

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Background: Adiponectin and leptin are hormones which are related to body fat tissues and body weight. In pregnant women, conflicting associations have been reported between the role of serum concentrations of adiponectin and leptin with infant birth weight. The aim of this study was to determine the association between maternal and cord blood adiponectin and leptin concentrations with birth weight. Methods: As a cross-sectional study 86 pregnant women referred to university hospital clinics were recruited. Maternal and umbilical cord blood samples were obtained in delivery room just after birth. The maternal and umbilical cord serum samples were analyzed for adiponectin and leptin. Their birth weight and height were measured at labor.
Results: The mean of maternal BMI, birth weight, and gestational age was 23.8±4.8 kg/m2, 3.13±0.14 kg, and 38.15±2.6 week, respectively. No correlation between adiponectin and birth weight were found. Birth weight positively correlates with leptin.
Conclusion: leptin concentrations in cord blood may be reflected the alternation of body fat tissue in infant and independently associated with infant birth weight.

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Background: Leptin is a peptide strongly correlated with adiposity and is a potential determinant of obesity and its complications. The aim of this study was to evaluate the correlation between serum leptin levels and different anthropometric indices among obese women.

Methods: This analytical descriptive study consisted of 106 women with different grade of obesity (BMI ³ 25 kg/m²) and 38 women with normal weight (BMI ≤ 25 kg/m²).serum leptin and glucose levels were measured via enzyme immunoassay and glucose oxidase methods respectively.

Results: The mean (± SE) serum leptin concentrations  in apparently healthy women with normal weight ,overweight, obese grade I, and obese grade II were 6.88 ± 0.56, 39.30 ± 1.73, 46.60 ±1.04, and 48.22± 3.31 ng/ml respectively. There was a dramatic increase in serum Leptin concentration when the BMI was increased. There was statistically significant differences between all groups in serum leptin concentration (P<0.001). There was a direct and significant correlation between serum leptin concentration and BMI in obese subjects (r= 0.736, P< 0.001). There was no significant correlation between leptin with age, and leptin with WHR neither in normal weight group nor in different grades of obesity groups.

 Conclusion: Our findings showed that the serum leptin levels continuously raised with increasing degree of obesity and among different anthropometric indices serum leptin concentration has significant correlation with BMI. 

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It is estimated that up to 40-70% of obesities is attributable to genetic factors.  Monogenic forms of obesity are uncommon.  We present the first such reported case in Iran. The patient presented with a history of severe hyperphagia, rapid weight gain and recurrent infections.  He was born after a normal pregnancy in a highly consanguineous marriage.  His birth weight had been normal.  At age of 18 months he weighted 28 kg.  Apart from obesity and syndactyly of second/third digits in both feet there were no other abnormalities on physical examination.    His fasting serum leptin was 45 ng/ml.  Genotyping revealed 66-bp deletion in codon 514 of leptin receptor gene.

Unfortunately he developed another respiratory infection which was unresponsive to intensive treatment and died following a cardiorespiratory arrest. Genetic assessment is recommended in morbid obese patients especially those with a childhood onset.  Leptin receptor mutations can be associated with immune system deficiency and recurrent infections.

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Background: The possibility that childhood obesity is a chronic disease in adulthood becomes enormous. The incidence and spread of obesity has increased substantially over the past two decades. The importance of personal health and quality of life has prompted researchers to study in this field. The aim of this study was to investigate the changes of serum levels of leptin, insulin, lipid profile, and body mass index after a period of sprint interval training in obese children. Methods: In this study, 30 obese children aged 9 to 11 years were randomly targeted placed in two groups (Training and control group). Sprint interval training was conducted for 8 weeks. Before and after training, measurements of leptin, insulin, lipid profile, and body mass index were measured. Data were analyzed using independent t-test (p<0.05). Results: Data analysis showed that after training, leptin, insulin and cholesterol levels were significantly reduced (p=0.001). Also, a significant decrease in BMI was seen (p=0.01). Conclusion: Sprint interval training on leptin, insulin and cholesterol in obese children has a significant impact and this exercise improve body mass index in these individuals.

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Background: Imbalanced production of adipokines as leptin and adiponectin in diabetic patients may lead to the development of metabolic complications. Therefore, the aim of this study was to determine the effects of 2-month of caffeine ingestion along with aerobic training on changes in serum leptin and adiponectin levels and leptin/adiponectin ratio (LAR) in type 2 diabetic men.
Methods: Thirty-two diabetic men participated in a quasi-experimental designs in the four groups for two-months period of a aerobic training (treadmill walking 3 times/week, 1.5 hour/session, 65-85% HRR) with and without caffeine ingestion (3 mg.kg^-1.day). Serum changes in leptin and adiponectin were measured during two phases (baseline and 24-hours after completing of the training program). Data were analyzed by one-way ANOVA and bonferroni's post-hoc test at level P≤0.05.
Results: Administration of two-months caffeine (CA) alone and combination with aerobic training (AT) were significantly could reduced and increased in leptin and adiponectin level, respectively (P=0.001). Thus, the combined group (AT+CA) effect were far more appropriate intervention in changing the studied indices (P=0.001). Also, the LAR method was notable reduced in all study groups, although these effects were more significantly in the combined group (AT+CA) (P=0.001).
Conclusion: It seems administration of caffeine supplementation and aerobic training for two-months have a positive effects on the improved relative of leptin and adiponectin levels as well as their ratio in diabetics, although the combination of these two variables has been shown to have far more dual effects.

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Background: Leptin and adiponectin are adipokines produced by fat cells and play an important role in obesity. The purpose of this study was to compare the effect of low-calorie diet (LCD) and exercise (Exe) on leptin and adiponectin in middle-aged and elderly adults with overweight and obesity.
Methods: A systematic search was conducted in PubMed, Web of Science, SID, Magiran, and Google scholar databases for English and Persian articles published until August 2023. The effect size and 95% confidence interval (CI) were calculated using the random effect model.
Results: The results of 25 studies with 2063 middle-aged and elderly people with overweight and obesity showed that the combination of exercise and diet compared to exercise alone causes a significant decrease in serum leptin [SMD=-0.4, P=0.001], and a significant increase in serum adiponectin [SMD=0.17, P=0.02] in middle-aged and elderly adults with overweight and obesity. Also, findings showed that the diet compared to exercise alone causes a decrease in serum leptin [SMD=-0.16, P=0.1], and a significant increase in serum adiponectin [SMD=0.05, P=0.7] in middle-aged and elderly adults with overweight and obesity. Also, diet compared to exercise alone does not cause a significant change in serum leptin [SMD=-0.11, P=0.2], and serum adiponectin [SMD=0.02, P=0.8] in middle-aged and elderly adults with overweight and obesity. Conclusion: It is suggested that middle-aged and elderly people to achieve hypoleptinemia and hyperadiponectinemia, use a combination Include exercise training and low-calorie diet in your lifestyle.

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Background: This review aims to investigate and analyze recent studies related to the effects of various exercise training on adipokines secreted from adipose tissue in patients with type 2 diabetes.
Methods: Search in Persian and Latin databases PubMed, ScienceDirect, Google Scholar, Magiran, and SID with the keywords aerobic exercise, resistance training, High-intensity interval training, diabetes, Adipokine, Leptin, Adiponectin, and Resistin, resistance training, intense interval training, aerobic exercise, combined exercise, adipokine, leptin, adiponectin and resistin were performed to retrieve articles published in the period from 2010 to 2023.
Results: The results obtained from the study showed that aerobic exercise with moderate intensity (60 to 80%) reduces the leptin levels of diabetic patients, however, the effect of combined exercises (aerobic and resistance) is much greater than other types of exercises. In addition, aerobic exercises with moderate intensity (50 to 70%) lead to an increase in adiponectin levels in diabetic patients, however, high-intensity interval training (HIIT) had a greater effect in increasing adiponectin levels than other exercises. Also, studies showed that all three types of activities, aerobic exercise (50-70% intensity), intense intermittent exercise, and resistance exercise (30-70% 1RM) have the same effects in reducing the resistance levels of diabetic patients.
Conclusion: Aerobic exercises with medium and high intensity and especially combined exercises (aerobic and resistance) while improving adipokines, decreasing leptin and resistin levels, and also increasing adiponectin in diabetic patients.