Effects of zinc supplementation on serum zinc and leptin levels, BMI, and body composition in hemodialysis patients

This study was carried out to evaluate the relationship between dietary and serum zinc and leptin levels with protein-energy wasting (PEW) in haemodialysis patients. The study was conducted on 80 volunteer patients aged 19-65years who received haemodialysis treatment three times a week for at least 1year. Anthropometric measurements and body composition analyses were performed. Blood samples were collected for serum zinc and leptin and other biochemical parameters. Food consumption of the patients was recorded for 3 days. Malnutrition-inflammation score (MIS) was calculated for all patients. PEW was assessed according to the criteria recommended by the International Society of Renal Nutrition and Metabolism (ISRNM). According to the ISRNM criteria, 38.1% of male patients and 36.8% of female patients were diagnosed with PEW. The median serum leptin levels of patients with PEW [9.0 (16.9) ng/mL] were significantly lower than those without PEW [20.7 (38.5) ng/mL] (p < 0.05). Dietary zinc intake in patients with PEW was significantly lower than that in patients without PEW (p < 0.05). However, there was no significant difference in serum zinc levels between the patients with and without PEW. In the multivariate analyses, dietary and serum zinc and leptin was associated with PEW. After controlling for several confounding factors these associations disappeared. Dietary zinc intake and serum leptin levels were inversely correlated with MİS. There was no relationship between serum leptin and dietary and serum zinc in these patients. Dietary zinc intake and serum zinc and leptin concentration were not associated with PEW. Low serum leptin levels might be the outcome rather than the cause of PEW in haemodialysis patients.

Objective The aim of this study was to determine the effect of zinc supplementation on serum levels of zinc and leptin in pediatric patients on hemodialysis (HD). Background Zinc is an essential trace element for human nutrition, and its deficiency which could result in anorexia, poor nutritional status, high rates of infections, and growth retardation. Many patients on maintenance HD exhibit zinc deficiency. Leptin may offer a tool for making clear the physiology of zinc deficiency–induced anorexia based on a relationship between zinc and leptin levels. Patient and methods The study was carried out on 42 children divided into two groups: group I included 22 children on HD who received 50-mg zinc gluconate twice daily for 90 days, and group II included healthy children as controls. Anthropometric measurements were taken, and serum zinc and leptin levels were determined the day before supplementation and at day 90 of the study. Results Serum level of zinc is decreased and serum leptin level is increased in children on regular HD. There is an increase in zinc level and a decrease in serum leptin level after zinc supplementation. Conclusion Zinc supplementation increased serum zinc level and decreased serum leptin level among males and females in the studied patients. Enhancement of serum zinc level improves appetite and stimulate food intake.

IntroductionZinc is an essential trace element for human nutrition, and its deficiency is associated with anorexia, poor food efficiency, growth retardation, and impaired neurological and immune systems. The zinc-deficiency rate is particularly high in many disease states, such as with end-stage renal disease patients undertaking hemodialysis. The aim of this study was to determine the effect of zinc supplementation on body mass index (BMI) and serum levels of zinc and leptin in pediatric hemodialysis patients.Patients and methodsThis was a prospective clinical trial study in which 60 hemodialysis patients were randomly divided into two groups: group I received 50–100 mg zinc sulfate (equivalent to 11–22 mg elemental zinc) according to age, sex, and nutritional status of the child; and group II received placebo (cornstarch) twice daily for 90 days. Anthropometric measurements were taken, and serum zinc and leptin levels were determined by colorimetric test with 5-Br-3′-phosphoadenosine-5′-phosphosulfate and enzyme-linked immunosorbent assay, respectively, at days 0 and 90 of the study.ResultsZinc supplementation resulted in a significant increase in mean serum zinc level and BMI. Serum leptin decreased significantly after supplementation in children under hemodialysis. A significant negative correlation was observed between serum zinc and leptin levels as a result of zinc supplementation.ConclusionThere was an increase in serum zinc level and BMI and decreased serum leptin after zinc supplementation in children under hemodialysis.

P-28: The utility of serum leptin and follicular fluid leptin, estradiol, and progesterone concentrations in infertility patients undergoing in vitro fertilization

Serum leptin and lipoprotein levels in women with PCOS.

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This study aimed to investigate the possible changes in serum leptin concentration caused by acute exercise and the effects of zinc deficiency on these changes. Forty male rats were divided into control-control, control-exercise, zinc-deficient-control, and zinc-deficient-exercise groups (10 rats in each). Control-exercise and zinc-deficient-exercise groups performed exercise at 6 m/min speed on a rodent treadmill for 60 min or until exhaustion. All rats were decapitated 48 h after the exercise, and blood samples were collected to determine serum leptin and zinc levels. Serum leptin levels in the exercise groups were lower than in the control groups. Leptin levels in the zinc-deficient-control group were lower than in the control-control group. The mean exercise time of control-exercise group was significantly longer than the zinc-deficient-exercise group. We conclude that serum leptin levels significantly decrease both 48 h after strenuous exercise and in the zinc-deficient rats, and there is a further decrease in leptin levels when rats fed on a zinc-deficient diet performed exercise.

Chronic inflammation is prevalent in dialysis patients. We investigated the relationship between inflammation and newly identified adipokines: leptin and adiponectin in this population. A total of 129 chronic hemodialysis patients were collected. Serum high sensitivity C-reactive protein (CRP), interleukin-6 (IL-6), leptin and adiponectin levels were determined as well as other metabolic variables. Correlation studies and multiple regression analysis were performed among variables. Our results showed that hemodialysis patients had elevated levels of inflammatory markers, leptin and adiponectin. Diabetic subjects had higher serum CRP and lower albumin levels than non-diabetics. Serum CRP levels were positively correlated with IL-6 levels and negatively correlated with albumin levels. Serum leptin levels were directly related to CRP levels while adiponectin levels were inversely related to CRP levels. A significant negative correlation was observed between serum leptin and adiponectin levels. Serum IL-6 levels were the single independent factor affecting CRP levels. Body mass index can predict both serum leptin and adiponectin levels. We conclude that hemodialysis patients are at an increased risk of chronic inflammation and diabetes patients are even more susceptible to this status. Both serum leptin and adiponectin levels are associated with inflammatory markers. As adipose tissue is the major secreting site of these adipokines, our results suggest that adipose tissue plays an important role in the pathogenesis of chronic inflammation in dialysis patients.

Secretion of insulin is compromised in type 2 diabetes (T2DM) individuals and inadequate to accommodate for insulin resistance (IR) in peripheral tissue. Hyperleptinemia reflects leptin resistance, which is a key factor in the production of IR in T2DM patients, making leptin a potential biomarker for evaluating IR levels. The objective of the study was to assess the association of serum leptin and insulin levels among T2DM patients. This case-control research was carried out on T2DM patients. A total of 73 patients diagnosed with T2DM (the case group) and 40 healthy participants (control; group 3) were enrolled according to the American Diabetes Association (ADA) criteria. In the case group, T2DM patients were enrolled with metabolic syndrome (group 1, n = 38) or without metabolic syndrome (group 2, n = 35) according to the WHO criteria. Metabolic profiles of T2DM patients with or without metabolic syndrome were evaluated, and compare these two groups with healthy controls. The subjects of all groups were age- and gender-matched. Body mass index (BMI, P < .01), fasting (P = .0133) and postprandial (P < .01) blood sugar levels, % glycated hemoglobin (HbA1c, P < .01), and lipid profile (P < .01) were found significantly different and higher in group 1 as compared to groups 2 and 3. Serum leptin and insulin levels were found higher and significant in patients with metabolic syndrome (P < .01 for both). The values of serum leptin levels were 10.01 ± 2.7 ng/mL, 6.9 ± 2.4 ng/mL, and 4.11 ± 1.8 ng/mL, and those of serum insulin 120 ± 40.7 µIU/mL, 20.43 ± 5.2 µIU/mL, and 11.4 ± 2.5 µIU/mL in groups 1, 2, and 3, respectively. There was a positive linear correlation between BMI, blood sugar, HbA1c, serum cholesterol (TC), and triglycerides (TG) with serum insulin and leptin levels in the case group. An extremely significant correlation (R = 0.74, P < .001) was found in BMI and serum leptin level in the case group. Serum leptin and insulin levels have a positive association, with serum leptin being a significant predictor of IR syndrome (Evidence Level: 5; Technical Efficacy: Stage 3).

Leptin may contribute to renal pathology in some situations by stimulating transforming growth factor-beta1 (TGF-beta1) synthesis. The soluble leptin receptor (sOb-R) is a transport protein contributing to binding and activation of circulating leptin. We investigated the interaction between serum and urinary leptin, TGF-beta1, and serum sOb-R levels in 38 patients with minimal change nephrotic syndrome (MCNS) aged between 6 and 12 years and 10 age- and sex-matched healthy controls (group III). Patients were divided into two groups: group I, proteinuria exceeding >40 mg/m(2) per hour and group II, patients in remission. Serum leptin levels in group I were significantly lower than those in group II and group III ( P=0.011, P=0.007, respectively). There was a negative correlation between serum leptin levels and proteinuria ( r=-0.52, P=0.02) as well as between serum leptin and sOb-R levels ( r=-0.82, P=0.000) in group I. Urine leptin and sOb-R levels in group I were significantly higher than in group II ( P=0.0021, P=0.001, respectively) and group III ( P=0.07, P=0.009, respectively). Serum TGF-beta1 levels in healthy controls (406+/-424 pg/ml) were significantly lower than those in groups I and II ( P=0.004, P=0.000, respectively). However, no significant correlation was found between the serum TGF-beta1 and leptin levels in MCNS patients. In conclusion, low serum leptin, high serum TGF-beta1 and sOb-R levels, and elevated urine leptin concentrations were observed at the onset of MCNS. Since long-term proteinuria and leptinuria might be associated with the progression of renal damage, future in vivo and in vitro studies are needed to explain the interaction between these parameters in different types of nephrotic syndrome.

The enigma of increasing serum leptin levels during peritoneal dialysis.

Weight gain is a common adverse effect associated with the use of most antipsychotic drugs. Leptin has been reported to be associated with antipsychotic-induced weight gain. Previous studies have demonstrated a relationship between the atypical antipsychotics clozapine and olanzapine and serum leptin levels. We planned to comparatively investigate the effects of the atypical antipsychotics quetiapine, olanzapine, risperidone, and clozapine on leptin and triglyceride levels and weight gain. The study population comprised 56 patients with DSM-IV schizophrenia, who were divided into 4 treatment groups: quetiapine (N = 14), olanzapine (N = 14), risperidone (N = 14), or clozapine (N = 14) monotherapy, and a control group of 11 patients receiving no psychopharmacologic treatment. The patients were evaluated at baseline and at the sixth week according to the Positive and Negative Syndrome Scale (PANSS), body mass index (BMI), weight, and fasting serum leptin and triglyceride levels. Data were gathered in 2001 and 2002. Olanzapine and clozapine caused a marked increase in weight and serum triglyceride and leptin levels, though increases in these variables were modest in the patients receiving quetiapine and minimal in those receiving risperidone. There were positive correlations between serum leptin levels and BMI and triglyceride levels. Clinical efficacy, as indicated by decrease in total PANSS scores, was associated with leptin levels in all atypical antipsychotic groups. Our results suggest that leptin may be associated with olanzapine- and clozapine-induced weight gain and that quetiapine appears to have modest influence and risperidone appears to have minimal influence on leptin and triglyceride levels and weight gain compared with olanzapine and clozapine.

Adipocytokines are thought to be associated with inflammatory disorders and autoimmune diseases. However, limited information is available on the relationship between serum adipocytokine levels, Graves' disease (GD), and Graves' ophthalmopathy (GO). The present study examined the relationship between serum adipocytokine levels and GD and GO. A total of 80 patients with GD participated in this study. The medical records of patients were reviewed retrospectively. GO activity was assessed using the clinical activity score (CAS). GO severity was assessed by the modified NOSPECS classification and included soft tissue involvement, proptosis, and extraocular muscle involvement. Serum adiponectin, leptin, resistin, and retinol-binding protein 4 (RBP-4) levels were measured using commercially available enzyme-linked immunosorbent assays. The prevalence of GO was 36.3%. Serum adiponectin, leptin, and resistin levels were significantly higher in patients with GO than in those without GO. The CAS was positively correlated with serum adiponectin and leptin levels. The total eye score was positively correlated with serum adiponectin, leptin, resistin, and RBP-4 levels. A multivariate analysis revealed that serum leptin and resistin levels were associated with the presence of GO after adjusting for clinical factors. Free thyroxine was negatively correlated with serum leptin level. These results suggest that adipocytokines, such as leptin and resistin, may play a role in inflammatory and autoimmune processes of GD and GO. Future studies with larger numbers of patients are required to establish relationships between serum adipocytokines levels and GO and ascertain the role of adipocytokines in GD and GO.

Obesity is considered as a major health problem. Angiogenic vessels by providing oxygen, nutrients and growth factors trigger growth and survival signals in adipocytes. We aimed to investigate the effect of high-fat diet (HFD) on serum angiogenic biomarkers including vascular endothelial growth factor (VEGF), soluble VEGF receptor 1 (sVEGFR1), nitric oxide (NO) concentrations and their correlations with serum leptin level in obese and control groups. Twenty male C57BL/6 mice were randomly assigned into the control and obese groups. Obese group received HFD for 15 weeks. At the end of experiment, blood samples were collected for blood glucose, serum insulin, VEGF, sVEGFR1, NO and leptin level measurements and correlation between serum angiogenic factors and leptin levels were analyzed. HFD induced higher serum NO and leptin levels compared to the control group, while, it did not affect serum VEGF and sVEGFR1 concentrations. There was a strong positive correlation between serum leptin and NO levels (r=0.78), however, a weak correlation was found between serum leptin and VEGF and VEGFR-1 concentrations. It seems that the angiogenic activities in obese mice are through the mechanisms that were not regulated by VEGF or VEGF receptors rather; other factors such as leptin and NO are involved (Tab. 1, Fig. 4, Ref. 32).

Ghrelin and leptin are two hormones that possess multiple functions, including appetite regulation, maintenance of the tissue homeostasis and regulation of proinflammatory cytokines. A few studies on serum ghrelin and leptin levels in autoimmune diseases have exhibited conflicting results. Therefore, the present study aimed to investigate the relationship between the two energy balance hormones and autoimmune diseases. Serum ghrelin and leptin levels were assessed in 94 adult patients, 61 females and 33 males, with various autoimmune diseases (celiac disease, type 1 diabetes mellitus and rheumatoid arthritis) as well as in 35 healthy people as controls, using commercially available ELISA kits. Statistically important distinctions (P &lt; 0.05) were found between the patients and controls with regard to serum ghrelin and leptin levels. Moreover, females had higher mean serum ghrelin and leptin levels than males. On the other hand, serum ghrelin level was positively correlated with serum leptin levels (r = 0.399, P &lt; 0.05) in the RA group. Whereas no significant correlation (P &gt; 0.05) was found between serum ghrelin and leptin levels in both CD and T1DM groups. As well as the correlation of the diseases biomarkers (tissue transglutaminase antibodies, anti-tTG; glutamic acid decarboxylase antibodies, anti-GAD; and cyclic citrullinated peptide antibodies, anti-CCP) with ghrelin/leptin levels revealed that anti-CCP was the only marker that significantly (P &lt; 0.05) associated with ghrelin and leptin in patients with RA. The current study indicates a linkage between the immune system and metabolic hormones depending on response to different autoimmune conditions. Additional studies are required to understand whether changes in ghrelin-leptin levels influence the emergence of autoimmune diseases or vice versa.