Diabetology & Metabolic Syndrome - Latest Articles

Metabolic syndrome in central Brazil: prevalence and correlates in the adult population

Eliane Said Dutra — 2012-05-14T00:00:00Z

Background: The prevalence of metabolic syndrome (MetS) has increased in developing countries inrecent decades. This syndrome, a clustering of metabolic abnormalities, has been correlatedto various socioeconomic and behavioral variables. We investigated the prevalence andprevalence ratios (PR) of MetS and related factors in an adult population of the FederalDistrict (FD) of Brazil, which is located in the central region of the country. Methods: A cross-sectional, population-based study conducted in 2007, with 2130 adults (aged 18 yearsor older) in the FD of Brazil. Metabolic syndrome was defined according to the recentlyharmonized criteria. The prevalence of MetS and PR were estimated for each sex accordingto the diagnostic components and the overall contribution of the selected correlates. Results: The overall prevalence of MetS was 32.0% (95%CI: 28.9-35.2), with no gender difference.The single component with the greatest contribution to the diagnosis of MetS washypertension in men (PR 5.10, 95%CI: 3.17-8.22) and high waist circumference in women(PR 5.02, 95%CI: 3.77-6.69). The prevalence of MetS increased significantly andprogressively with age and excess weight. In women, higher education was protective againstMetS (PR 0.66, 95%CI: 0.49-0.89) compared to 8 or less years of education. There was noassociation between the prevalence of MetS and behavioral variables studied. Conclusions: This study provides comprehensive and alarming data about the prevalence of MetS amongthe adult population of Brazil's FD. The results suggest that reducing education inequalitiesmay be an important public policy goal to improve health outcomes, especially amongwomen.

Fibronectin glycation increases IGF-I induced proliferation of human aortic smooth muscle cells

Maria Lúcia Corrêa-Giannella — 2012-05-03T00:00:00Z

The advanced glycation end products, namely AGEs, contribute to long-termedcomplications of diabetes mellitus, including macroangiopathy, where smooth muscle cells(SMC) proliferation stimulated by platelet-derived growth factor (PDGF) isoforms andinsulin-like growth factor-I (IGF-I) plays an important role. The objective of the presentstudy was to investigate the effect of an AGE-modified extracellular matrix protein on IGF-Iinduced SMC proliferation and on the IGF-I-IGF binding protein 4 (IGFBP-4) axis underbasal conditions and after stimulation with PDGF-BB. IGF-I resulted in significantly higherthymidine incorporation in SMC seeded on AGE-modified fibronectin (AGE-FN) incomparison to cells seeded on fibronectin (FN). This augmented proliferation could not beaccounted for by increased expression of IGF-IR, by decreased secretion of IGFBP-4, abinding protein that inhibits IGF-I mitogenic effects or by increased IGF-IRautophosphorylation. PDGF-BB did not modulate IGF-IR and IGFBP-4 mRNA expression inany of the substrata, however, this growth factor elicited opposite effects on the IGFBP-4content in the conditioned media, increasing it in cells plated on FN and diminishing it incells plated on AGE-FN. These findings suggest that one mechanism by which AGEmodifiedproteins is involved in the pathogenesis of diabetes-associated atherosclerosis mightbe by increasing SMC susceptibility to IGF-I mitogenic effects.

Sleep-wake cycle irregularities in type 2 diabetics

Tomoko Nakanishi-Minami — 2012-05-02T00:00:00Z

Background: The incidence of type 2 diabetes mellitus (T2DM) has been increasing in recent years. Sleep loss and circadian rhythm abnormalities are thought to be one of the underlying causes of adverse metabolic health. However, little is known about sleep-wake cycle irregularities in T2DM. The present study compared the bedtime, waking time, and estimated sleep duration between T2DM and non-T2DM subjects. Methods: The study subjects were 106 consecutive outpatients with lifestyle-related diseases (males/females = 56/50), who answered a questionnaire on sleep status. Subjects were divided into two groups; non-T2DM (n = 32) and T2DM (n = 74) subjects. Results: T2DM subjects retired to bed on weekdays and holidays significantly later than non-T2DM subjects (23:43 versus 22:52, p = 0.0032; 23:45 versus 22:53, p = 0.0038, respectively), and woke up significantly later on weekdays and holidays, compared with non-T2DM subjects (06:39 versus 06:08, p = 0.0325; 06:58 versus 06:24, p = 0.0450, respectively). There was no significant difference in the estimated sleep duration between the two groups. Daytime sleepiness was reported significantly more commonly by T2DM subjects than non-T2DM subjects (p = 0.0195). Conclusions: Sleep-wake cycle irregularities are more common in T2DM subjects than non-T2DM. Confirmation that such irregularity plays a role in the metabolic abnormalities of T2DM requires further investigation in the future.Trial registrationUMIN 000002998https://upload.umin.ac.jp/cgi-open-bin/ctr/ctr.cgi?function=brows&action=brows&type=summary&recptno=R000003635&language=E

Activities of asymmetric dimethylarginine-related enzymes in white adipose tissue are associated with circulating lipid biomarkers

Hiroaki Iwasaki — 2012-04-30T00:00:00Z

Background: Asymmetric NG,NG-dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, is regulated by the enzymatic participants of synthetic and metabolic processes, i.e., type I protein N-arginine methyltransferase (PRMT) and dimethylarginine dimethylaminohydrolase (DDAH). Previous reports have demonstrated that circulating ADMA levels can vary in patients with type 1 and type 2 diabetes mellitus (T2DM). White adipose tissue expresses the full enzymatic machinery necessary for ADMA production and metabolism; however, modulation of the activities of adipose ADMA-related enzymes in T2DM remains to be determined. Methods: A rodent model of T2DM using 11- and 20-week old Goto-Kakizaki (GK) rats was used. The expression and catalytic activity of PRMT1 and DDAH1 and 2 in the white adipose tissues (periepididymal, visceral and subcutaneous fats) and femur skeletal muscle tissue were determined by immunoblotting, in vitro methyltransferase and in vitro citrulline assays. Results: Non-obese diabetic GK rats showed low expression and activity of adipose PRMT1 compared to age-matched Wistar controls. Adipose tissues from the periepididymal, visceral and subcutaneous fats of GK rats had high DDAH1 expression and total DDAH activity, whereas the DDAH2 expression was lowered below the control value. This dynamic of ADMA-related enzymes in white adipose tissues was distinct from that of skeletal muscle tissue. GK rats had lower levels of serum non-esterified fatty acids (NEFA) and triglycerides (TG) than the control rats. In all subjects the adipose PRMT1 and DDAH activities were statistically correlated with the levels of serum NEFA and TG. Conclusion: Activities of PRMT1 and DDAH in white adipose tissues were altered in diabetic GK rats in an organ-specific manner, which was reflected in the serum levels of NEFA and TG. Changes in adipose ADMA-related enzymes might play a part in the function of white adipose tissue.

Metabolic syndrome markers in wistar rats of different ages

Ana Carolina Ghezzi — 2012-04-27T00:00:00Z

In recent decades, metabolic syndrome has become a public health problem throughout theworld. Longitudinal studies in humans have several limitations due to the invasive nature ofcertain analyses and the size and randomness of the study populations. Thus, animal modelsthat are able to mimic human physiological responses could aid in investigating metabolicdisease. Thus, the present study was designed to analyze metabolic syndrome markers inalbino Wistar rats (Rattus norvegicus) of different ages. The following parameters wereassessed at two (young), four (adult), six (adult), and twelve (mature) months of age: glucosetolerance (glucose tolerance test); insulin sensitivity (insulin tolerance test); fasting serumglucose, triglycerides, total cholesterol, HDL cholestero, and LDL cholesterol concentrations;glucose uptake in isolated soleus muscle; and total lipid concentration in subcutaneous,mesenteric, and retroperitoneal adipose tissue. We found that aging triggered signs ofmetabolic syndrome in Wistar rats. For example, mature rats showed a significant increase inbody weight that was associated. In addition, mature rats showed an increase in the serumconcentration of triglycerides, total cholesterol, and LDL cholesterol, which is characteristicof dyslipidemia. There was also an increase in serum glucose compared with the youngergroups of animals. Therefore, aging Wistar rats appear to be an interesting model to study thechanges related to metabolic syndrome.

The skin function: a factor of anti-metabolic syndrome

Shi-Sheng Zhou — 2012-04-26T00:00:00Z

The body's total antioxidant capacity represents a sum of the antioxidant capacity of varioustissues/organs. A decrease in the body's antioxidant capacity may induce oxidative stress andsubsequent metabolic syndrome, a clustering of risk factors for type 2 diabetes andcardiovascular disease. The skin, the largest organ of the body, is one of the majorcomponents of the body's total antioxidant defense system, primarily through itsxenobiotic/drug biotransformation system, reactive oxygen species-scavenging system, andsweat glands- and sebaceous glands-mediated excretion system. Notably, unlike othercontributors, the skin contribution is variable, depending on lifestyles and ambienttemperature or seasonal variations. Emerging evidence suggests that decreased skin'santioxidant and excretory functions (e.g., due to sedentary lifestyles and low ambienttemperature) may increase the risk for metabolic syndrome. This review focuses on therelationship between the variability of skin-mediated detoxification and elimination ofexogenous and endogenous toxic substances and the development of metabolic syndrome.The potential role of sebum secretion in lipid and cholesterol homeostasis and its impact onmetabolic syndrome, and the association between skin disorders (acanthosis nigricans, acne,and burn) and metabolic syndrome are also discussed.

Salivary uric acid as a noninvasive biomarker of metabolic syndrome

Maria Soukup — 2012-04-19T00:00:00Z

Background: Elevated serum uric acid is associated with obesity, hypertension and metabolic syndrome.Because a linear relationship exists between serum and salivary uric acid (SUA)concentration, saliva testing may be a useful noninvasive approach for monitoringcardiometabolic risk. The goal of this pilot study was to determine if SUA is increased inpatients with metabolic syndrome and to investigate correlations between SUA andindividual cardiometabolic risk factors.FindingsVolunteers between the ages of 18 and 65 without conditions known to affect serum uric acidlevels were recruited. Height, weight, blood pressure and waist circumference were measuredand a full lipid panel along with fasting blood glucose was obtained. Saliva samples werecollected and uric acid levels were determined. 78 volunteers, 35 % of whom had metabolicsyndrome, completed the study. SUA was significantly elevated in patients with metabolicsyndrome (p = .002). The incidence of metabolic syndrome in the 4th quartile for SUA was 67% compared to 25 % in quartiles1-3 combined. Significant correlations were seen betweenSUA and systolic blood pressure (r = .440, p = .000), diastolic blood pressure ( r = .304,p = .007), waist circumference (r = .332, p = .003), BMI ( r = .269, p = .018), fasting bloodglucose ( r = .341, p = .002), triglycerides (r = .431, p = .000), HDL ( r = .237, p = .036) andthe number of cardiometabolic risk factors present (r = 0.257, p = .023). Conclusions: These results suggest that SUA may be a useful biomarker for noninvasive monitoring ofcardiometabolic risk. Larger studies are needed to validate this approach.

Effects of zinc supplementation on diabetes mellitus: a systematic review and meta-analysis

R Jayawardena — 2012-04-19T00:00:00Z

The number of people with diabetes and pre-diabetes are exponentially increasing. Studies onhumans have also shown the beneficial effects of Zinc supplementation in patients withdiabetes. The present study aims to systematically evaluate the literature and meta-analyzethe effects of Zinc supplementation on diabetes. A systematic review of published studiesreporting the effects of Zinc supplementations on diabetes mellitus was undertaken. Theliterature search was conducted in the following databases; PubMed, Web of Science andSciVerse Scopus. A meta-analysis of studies examining the effects of Zinc supplementationon clinical and biochemical parameters in patients with diabetes was performed. The totalnumber of articles included in the present review is 25, which included 3 studies on type-1diabetes and 22 studies on type-2 diabetes. There were 12 studies comparing the effects ofZinc supplementation on fasting blood glucose in patients with type-2 diabetes. The pooledmean difference in fasting blood glucose between Zinc supplemented and placebo groups was18.13 mg/dl (95%CI:-33.85,-2.41; p < 0.05). 2-h post-prandial blood sugar also shows asimilar distinct reduction in (34.87 mg/dl [95%CI:-75.44; 5.69]) the Zinc treated group. Thereduction in HbA1c was 0.54 % (95%CI:-0.86;-0.21) in the Zinc treated group. There were8 studies comparing the effects of Zinc supplementation on lipid parameters in patients withtype-2 diabetes. The pooled mean difference for total cholesterol between Zinc supplementedand placebo groups was 32.37 mg/dl (95%CI:-57.39,-7.35; p < 0.05). Low-densitylipoprotein cholesterol also showed a similar distinct reduction in the Zinc treated group, thepooled mean difference from random effects analysis was 11.19 mg/dl (95%CI:-21.14,-1.25; p < 0.05). Studies have also shown a significant reduction in systolic and diastolic bloodpressures after Zinc supplementation. This first comprehensive systematic review and metaanalysison the effects of Zinc supplementation in patients with diabetes demonstrates thatZinc supplementation has beneficial effects on glycaemic control and promotes healthy lipidparameters. Further studies are required to identify the exact biological mechanismsresponsible for these results.

High plasma uric acid concentration: causes and consequences

Erick Prado de Oliveira — 2012-04-04T00:00:00Z

High plasma uric acid (UA) is a precipitating factor for gout and renal calculi as well as a strong risk factor for Metabolic Syndrome and cardiovascular disease. The main causes for higher plasma UA are either lower excretion, higher synthesis or both. Higher waist circumference and the BMI are associated with higher insulin resistance and leptin production, and both reduce uric acid excretion. The synthesis of fatty acids (tryglicerides) in the liver is associated with the de novo synthesis of purine, accelerating UA production. The role played by diet on hyperuricemia has not yet been fully clarified, but high intake of fructose-rich industrialized food and high alcohol intake (particularly beer) seem to influence uricemia. It is not known whether UA would be a causal factor or an antioxidant protective response. Most authors do not consider the UA as a risk factor, but presenting antioxidant function. UA contributes to > 50% of the antioxidant capacity of the blood. There is still no consensus if UA is a protective or a risk factor, however, it seems that acute elevation is a protective factor, whereas chronic elevation a risk for disease.

Evaluating the mitochondrial function

Emin Akgul — 2012-04-04T00:00:00Z

We have read the article by Xia et.al. entitled as "L-carnitine ameliorated fatty liver in high-calorie diet/STZ induced type 2 diabetic mice by improving mitochondrial function" with great interest. In this article, the authors concluded that L-carnitine might be an effective liver cell protector for delaying the progression of type 2 diabetes mellitus complications. They supported this conclusion by using biochemical and morphological differences between control and L-carnitine-treated groups. However, we have some reservations the terms they used throughout the article: Firstly, the term of "mitochondrial function" has a very broad meaning and might be a little bit confusing as well. As known, mitochondria basically have three biochemical systems: i) beta-oxidation, ii) tricarboxylic acid cycle (TCA cycle) and iii) electron transport chain. Although all these systems are interconnected and coexist in mitochondria at the same time, only dysfunctions of electron transport chain are enumerated among the mitochondrial diseases. In this article, we understand that the mitochondrial complex activities were not measured at all. Therefore, we think that the conclusion saying "L-carnitine stimulates fat metabolism" is acceptable. But, using the term of "improvement of mitochondrial function" in this context is not scientifically very appropriate. Secondly, the authors did not describe the method(s) they used in "morphological assessment of hepatic tissue" in detail. They said that tissue samples have been fixed in 4% paraformaldehyde in the third page of the paper. But, as far as we know, oil red O staining works only with fresh frozen tissues. Besides, the red dots in figure 2 were presented as lipid droplets. If these are lipid droplets, then the other unstained vacuoles in the same figure were remained to be identified. We think that the tissues stained with oil red O must be fresh-frozen samples, and at least some of that unstained vacuoles were actually freezing artifacts. Discrimination between freezing artifacts and lipid vacuoles are important because the authors assumed that L-carnitine was decreasing "lipid area percentage" in hepatic tissue.