Antonio Carlos Lerario

Effect of zinc supplementation on serum leptin levels and insulin resistance of obese women

Leptin is thought to be a lipostatic signal that contributes to body weight regulation. Zinc might play an important role in appetite regulation and its administration stimulates leptin production. However, there are few reports in the literature on its role on leptin levels in the obese population. The present work asseses the effect of zinc supplementation on serum leptin levels in insulin resistance (IR). A prospective double-blind, randomized, clinical, placebo-controlled study was conducted. Fifty-six normal glucose-tolerant obese women (age: 25–45 yr, body mass index [BMI]=36.2 ±2.3 kg/m2) were randomized for treatment with 30 mg zinc daily for 4 wk. Baseline values of both groups were similar for age, BMI, caloric intake, insulin concentration, insulin resistance, and zinc concentration in diet, plasma, urine, and erythrocytes. Insulin and leptin were measured by radioimmunoassay and IR was estimated by the homeostasis model assessment (HOMA). The determinations of zinc in plasma, erythrocytes, and 24-h urine were performed by using atomic absorption spectrophotometry. After 4 wk, BMI, fasting glucose, and zinc concentration in plasma and erythrocyte did not change in either group, although zinc concentration in the urine increased from 385.9±259.3 to 470.2±241.2±μg/24 h in the group with zinc supplementation (p<0.05). Insulin did not change in the placebo group, whereas there was a significant decrease of this hormone in the supplemented group. HOMA also decreased from 5.8±2.6 to 4.3±1.7 (p<0.05) in the zinc-supplemented group but did not change in the placebo group. Leptin did not change in the placebo group. In the zinc group, leptin was 23.6±12.3 μg/L and did not change. More human data from a unique population of obese individuals with documented insulin resistance would be useful in guiding future studies on zinc supplementation (with higher doses or longer intervals) or different measures.

Diabetes mellitus do tipo 2, síndrome metabólica e modificação no estilo de vida

Type 2 diabetes mellitus promotes increased morbidity and mortality from cardiovascular diseases. These diseases have the same genetic components and environmental antecedents and insulin resistance is considered one of the main possible antecedents. The metabolic syndrome is a complex disorder represented by a set of cardiovascular risk factors that are commonly associated with central adiposity and insulin resistance. Changing inadequate feeding habits, losing weight and exercising regularly are considered first-choice therapies in treating the metabolic syndrome since they reduce waist circumference, visceral fat and plasma concentrations of glucose and triglycerides; they improve insulin sensitivity and increase HDL cholesterol; consequently, they reduce the risk factors for type 2 diabetes mellitus and cardiovascular diseases. Thus, the objective of this article was to describe and analyze some of the main studies published in the last decades which showed that adopting a healthy lifestyle promotes the primary prevention of type 2 diabetes mellitus. An educational intervention that focuses on proper nutrition and exercise and, therefore, reduces the risk factors associated with metabolic syndrome and cardiovascular diseases, can help change inadequate lifestyles.

Participação do zinco na resistência à insulina

This review reports the etiological aspects of insulin resistance as well as the participation of zinc in this process. Zinc participates in the metabolic pathways involving protein synthesis, and the metabolism of carbohydrate, lipid and nucleic acid. This element has been associated with the interaction between hormones and their receptors and to the improvement in the post-receptor stimulus. In vitro studies show that insulin may form a complex with zinc improving the solubility of this hormone in the pancreatic b cells and also increasing the binding ability of insulin to its receptor. Regarding obesity and insulin resistance, alterations in zinc concentration and distribution in tissues, as well as improvement in sensitivity to insulin after supplementation with this element, have been detected. Thus, the metabolic role of zinc in the insulin resistance syndrome should be further investigated having in mind that this element may contribute to the control of the usual metabolic alterations present in obese patients.This review reports the etiological aspects of insulin resistance as well as the participation of zinc in this process. Zinc participates in the metabolic pathways involving protein synthesis, and the metabolism of carbohydrate, lipid and nucleic acid. This element has been associated with the interaction between hormones and their receptors and to the improvement in the post-receptor stimulus. In vitro studies show that insulin may form a complex with zinc improving the solubility of this hormone in the pancreatic beta cells and also increasing the binding ability of insulin to its receptor. Regarding obesity and insulin resistance, alterations in zinc concentration and distribution in tissues, as well as improvement in sensitivity to insulin after supplementation with this element, have been detected. Thus, the metabolic role of zinc in the insulin resistance syndrome should be further investigated having in mind that this element may contribute to the control of the usual metabolic alterations present in obese patients.

ACANTHOSIS NIGRICANS, HIRSUTISM, INSULIN RESISTANCE AND INSULIN RECEPTOR DEFECT

A 24‐year‐old negress with the triad of acanthosis nigricans, hirsutism associated with polycystic ovaries and insulin resistance is reported. Metabolic studies were done 3 years after a bilateral ovarian wedge resection. Partial remission of the hirsutism and return of menstrual cycles occurred after surgery. Extreme resistance to endogenous and exogenous insulin was observed. Three studies of insulin receptors on circulating red blood cells (RBC) showed abnormal inhibition‐competition curves, characterized by increased percentage insulin binding at higher unlabelled insulin levels. Scatchard plots suggested an apparent increase in the number of low affinity receptors. Despite the changes in receptor‐insulin interaction, the defect does not seem to explain the insulin resistance since binding of insulin to a target tissue (RBC) appeared to be quantitatively normal at physiological insulin levels, suggesting a simultaneous post receptor defect.

Glycemia and cardiovascular disease in type 1 diabetes mellitus.

OBJECTIVE To evaluate the role of glycemic control in the development of cardiovascular disease (CVD) in type 1 diabetes mellitus (DM). METHODS We review the literature regarding coronary atherosclerosis, coronary artery calcification, and the epidemiologic studies related to the role of glycemia and the classic risk factors for coronary artery disease (CAD) in type 1 DM. RESULTS Four prospective studies (Wisconsin Epidemiologic Study of Diabetic Retinopathy, EURODIAB, Steno Diabetes Center Study of Adults With Type 1 DM, and Pittsburgh Epidemiology of Diabetes Complications study) do not show that glycemic control predicts CAD occurrence. Findings from the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications study show that compared with conventional insulin therapy, intensive insulin therapy reduces CVD among patients with type 1 DM and is associated with lower prevalence of coronary artery calcification. The discrepancies between the findings from the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications study and the Pittsburgh Epidemiology of Diabetes Complication study are likely due to differences between the study populations and the lower prevalence of renal disease in the former study. Besides duration of DM and albuminuria/overt nephropathy, insulin resistance is a major determinant of CAD associated with type 1 DM. CONCLUSIONS Discrepant study results regarding the relationship between glycemia and CAD/coronary artery calcification may be related to the prevalence of renal disease and the presence of the metabolic syndrome. Published data suggest that addressing traditional risk factors including albuminuria, the metabolic syndrome, and inflammatory markers is better for preventing and treating CAD than focusing exclusively on glycemic control, which is still necessary for preventing microvascular complications. Furthermore, there is a synergistic effect of glycemic control and albuminuria on the development of CVD.

Preparation of high-quality iodine-125-labelled pituitary human follicle-stimulating hormone (hFSH) for radioimmunoassay: Comparison of enzymatic and chloramine-T iodination

A method is described for the enzymatic radioiodination of human follicle-stimulating hormone (hFSH) by a system consisting of lactoperoxidase, hydrogen peroxide and Na125I. It was compared with the Chloramine-T modified technique. A satisfactory specific activity of the labelled hormone was obtained with the enzymatic iodination with much greater immunoreactivity was stability than after Chloramine-T.

Algorithm for the treatment of type 2 diabetes: a position statement of Brazilian Diabetes Society

The Brazilian Diabetes Society is starting an innovative project of quantitative assessment of medical arguments of and implementing a new way of elaborating SBD Position Statements. The final aim of this particular project is to propose a new Brazilian algorithm for the treatment of type 2 diabetes, based on the opinions of endocrinologists surveyed from a poll conducted on the Brazilian Diabetes Society website regarding the latest algorithm proposed by American Diabetes Association /European Association for the Study of Diabetes, published in January 2009.An additional source used, as a basis for the new algorithm, was to assess the acceptability of controversial arguments published in international literature, through a panel of renowned Brazilian specialists. Thirty controversial arguments in diabetes have been selected with their respective references, where each argument was assessed and scored according to its acceptability level and personal conviction of each member of the evaluation panel.This methodology was adapted using a similar approach to the one adopted in the recent position statement by the American College of Cardiology on coronary revascularization, of which not only cardiologists took part, but also specialists of other related areas.

Avaliação da prevalência do diabetes e da hiperglicemia de estresse no infarto agudo do miocárdio

OBJECTIVES: To evaluate in our population the real prevalence of diabetes (DM) and stress hyperglycemia (HE) in patients with myocardial infarction (IAM) admitted in a cardiologic emergency unit. METHODS: A retrospective analysis of 2262 patients with AMI evaluating the prevalence of DM (referred and diagnosed) and stress hyperglycemia. RESULTS: Besides 12,1% of subjects were previously referred to be diabetic (men: 10.7% and women: 15.8%), diabetes was effectively diagnosed in 24,8% (M: 22,9%, W: 29,7%) and stress hyperglycemia in 13,6% HE of the patients (M: 14,3%, W: 11,7%) indicating that glycemic alterations were effectively observed in 37.2.% of the patients with IAM (M: 37,2%, W: 41,4%). In DM subjects IAM events occurred earlier, total intra-hospital mortality was higher (DM: 20.7%, ND: 13,8%, HE: 13,4%) and less surgical procedures were performed (ND 33.8%, DM: 21.7%, HE: 18.0%). CONCLUSION: The elevated DM and stress hyperglycemia prevalence observed in our study indicates that glycemic alterations is one of the most important risk factors for IAM.

Doença cardiovascular no diabetes melito tipo 1

The association between type 1 diabetes and coronary heart disease has become very clear since the late 1970. It has been demonstrated that there is an important increased risk in morbidity and mortality caused by coronary artery disease in young adults with type 1 diabetes compared with the non diabetic population. The underlying pathogeneses is still poorly understood. While the role of glycemic control in the development of microvascular disease complication is well established its role in CVD in patients with DM1 remains unclear with epidemiologic studies reporting conflicting data. Recent findings from the DCCT/EDIC showed that prior intensive diabetes treatment during the DCCT was associated with less atherosclerosis, largely because of reduced level of HbA1c during the DCCT. The improvement of glycemic control itself appeared to be particularly effective in younger patients with shorter duration of the disease. Other analyses suggested the glycemia may have a stronger effect on CAD in patients without than in those with albuminúria. Other major determinants of coronary artery disease are the components of metabolic syndrome and the surrogate measure of insulin resistence: eGDR. It is proposed that patients with DM1 should have aggressive medical therapy, risk factor modification and careful monitoring not only of his blood sugar but also of the other processes involved in the atherosclerotic process, mostly the ones with family history of type 2 diabetes.

Insulin Resistance in Cushing's Disease: Evaluation by Studies of Insulin Binding to Erythrocytes

Studies of 125I-insulin binding to erythrocytes (RBC) from 5 patients with Cushings disease were performed in an attempt to evaluate the insulin resistance in this disease. Five obese, nondiabetic patients and six normal subjects served as controls. Insulin resistance was present in both the obese, nondiabetic subjects and in the patients with Cushings disease. Patients with Cushings disease showed insulin resistance out of proportion to obesity, and of greater severity than in the obese subjects. As in previous studies, the insulin resistance of the obese subjects could be at least partially ascribed to a reduced number of receptors. In contrast, in our patients with Cushings disease, no physiologically significant changes in the parameters of insulin-receptor interaction could be demonstrated. This suggests that the RBC insulin receptor is not involved in this type of insulin resistance.