Diabetology & Metabolic Syndrome - Most accessed articles

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.

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.

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.

Diabetic nephropathy

Themis Zelmanovitz — 2009-09-21T00:00:00Z

Diabetic nephropathy is the leading cause of chronic renal disease and a major cause of cardiovascular mortality. Diabetic nephropathy has been categorized into stages: microalbuminuria and macroalbuminuria. The cut-off values of micro- and macroalbuminuria are arbitrary and their values have been questioned. Subjects in the upper-normal range of albuminuria seem to be at high risk of progression to micro- or macroalbuminuria and they also had a higher blood pressure than normoalbuminuric subjects in the lower normoalbuminuria range. Diabetic nephropathy screening is made by measuring albumin in spot urine. If abnormal, it should be confirmed in two out three samples collected in a three to six-months interval. Additionally, it is recommended that glomerular filtration rate be routinely estimated for appropriate screening of nephropathy, because some patients present a decreased glomerular filtration rate when urine albumin values are in the normal range. The two main risk factors for diabetic nephropathy are hyperglycemia and arterial hypertension, but the genetic susceptibility in both type 1 and type 2 diabetes is of great importance. Other risk factors are smoking, dyslipidemia, proteinuria, glomerular hyperfiltration and dietary factors. Nephropathy is pathologically characterized in individuals with type 1 diabetes by thickening of glomerular and tubular basal membranes, with progressive mesangial expansion (diffuse or nodular) leading to progressive reduction of glomerular filtration surface. Concurrent interstitial morphological alterations and hyalinization of afferent and efferent glomerular arterioles also occur. Podocytes abnormalities also appear to be involved in the glomerulosclerosis process. In patients with type 2 diabetes, renal lesions are heterogeneous and more complex than in individuals with type 1 diabetes. Treatment of diabetic nephropathy is based on a multiple risk factor approach, and the goal is retarding the development or progression of the disease and to decrease the subject's increased risk of cardiovascular disease. Achieving the best metabolic control, treating hypertension (<130/80 mmHg) and dyslipidemia (LDL cholesterol <100 mg/dl), using drugs that block the renin-angiotensin-aldosterone system, are effective strategies for preventing the development of microalbuminuria, delaying the progression to more advanced stages of nephropathy and reducing cardiovascular mortality in patients with diabetes.

Combination therapy in hypertension: an update

Sanjay Kalra — 2010-06-24T00:00:00Z

Meticulous control of blood pressure is required in patients with hypertension to produce the maximum reduction in clinical cardiovascular end points, especially in patients with comorbidities like diabetes mellitus where more aggressive blood pressure lowering might be beneficial. Recent clinical trials suggest that the approach of using monotherapy for the control of hypertension is not likely to be successful in most patients. Combination therapy may be theoretically favored by the fact that multiple factors contribute to hypertension, and achieving control of blood pressure with single agent acting through one particular mechanism may not be possible. Regimens can either be fixed dose combinations or drugs added sequentially one after other. Combining the drugs makes them available in a convenient dosing format, lower the dose of individual component, thus, reducing the side effects and improving compliance. Classes of antihypertensive agents which have been commonly used are angiotensin receptor blockers, thiazide diuretics, beta and alpha blockers, calcium antagonists and angiotensin-converting enzyme inhibitors. Thiazide diuretics and calcium channel blockers are effective, as well as combinations that include renin-angiotensin-aldosterone system blockers, in reducing BP. The majority of currently available fixed-dose combinations are diuretic-based. Combinations may be individualized according to the presence of comorbidities like diabetes mellitus, chronic renal failure, heart failure, thyroid disorders and for special population groups like elderly and pregnant females.

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

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.

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.

Visceral adiposity, insulin resistance and cancer risk

Claire Donohoe — 2011-06-22T00:00:00Z

Background: There is a well established link between obesity and cancer. Emerging research is characterising this relationship further and delineating the specific role of excess visceral adiposity, as opposed to simple obesity, in promoting tumorigenesis. This review summarises the evidence from an epidemiological and pathophysiological perspective. Methods: Relevant medical literature was identified from searches of PubMed and references cited in appropriate articles identified. Selection of articles was based on peer review, journal and relevance. Results: Numerous epidemiological studies consistently identify increased risk of developing carcinoma in the obese. Adipose tissue, particularly viscerally located fat, is metabolically active and exerts systemic endocrine effects. Putative pathophysiological mechanisms linking obesity and carcinogenesis include the paracrine effects of adipose tissue and systemic alterations associated with obesity. Systemic changes in the obese state include chronic inflammation and alterations in adipokines and sex steroids. Insulin and the insulin-like growth factor axis influence tumorigenesis and also have a complex relationship with adiposity. There is evidence to suggest that insulin and the IGF axis play an important role in mediating obesity associated malignancy. Conclusions: There is much evidence to support a role for obesity in cancer progression, however further research is warranted to determine the specific effect of excess visceral adipose tissue on tumorigenesis. Investigation of the potential mechanisms underpinning the association, including the role of insulin and the IGF axis, will improve understanding of the obesity and cancer link and may uncover targets for intervention.

Effect of Carnitine and herbal mixture extract on obesity induced by high fat diet in rats

Kamal Amin — 2009-10-16T00:00:00Z

Background: Obesity-associated type 2 diabetes is rapidly increasing throughout the world. It is generally recognized that natural products with a long history of safety can modulate obesity.AimTo investigate the development of obesity in response to a high fat diet (HFD) and to estimate the effect of L-carnitine and an Egyptian Herbal mixture formulation (HMF) (consisting of T. chebula, Senae, rhubarb, black cumin, aniseed, fennel and licorice) on bodyweight, food intake, lipid profiles, renal, hepatic, cardiac function markers, lipid Peroxidation, and the glucose and insulin levels in blood and liver tissue in rats.MethodWhite male albino rats weighing 80-90 gm, 60 days old. 10 rats were fed a normal basal diet (Cr), 30 rats fed a high-fat diet (HFD) for 14 weeks during the entire study. Rats of the HFD group were equally divided into 3 subgroups each one include 10 rats. The first group received HFD with no supplement (HFD), the 2nd group HFD+L-carnitine and the third group received HFD+HMF. Carnitine and HMF were administered at 10th week (start time for treatments) for 4 weeks.Body weight, lipid profile & renal function (urea, uric acid creatinine) ALT & AST activities, cardiac markers, (LDH, C.K-NAC and MB) the oxidative stress marker reduced glutathione (GSH), and Malondialdehyde (MDA) catalase activity, in addition to glucose, insulin, and insulin resistance in serum & tissues were analyzed. Results: Data showed that feeding HFD diet significantly increased final body weight, triglycerides (TG), total cholesterol, & LDL concentration compared with controls, while significantly decreasing HDL; meanwhile treatment with L-carnitine, or HMF significantly normalized the lipid profile.Serum ALT, urea, uric acid, creatinine, LDH, CK-NAC, CK-MB were significantly higher in the high fat group compared with normal controls; and administration of L-carnitine or herbal extract significantly lessened the effect of the HFD. Hyperglycemia, hyperinsulinemia, and high insulin resistance (IR) significantly increased in HFD in comparison with the control group. The treatment with L-carnitine or HMF improved the condition. HFD elevated hepatic MDA and lipid peroxidation associated with reduction in hepatic GSH and catalase activity; whereas administration of L-carnitine or herbal extract significantly ameliorated these hepatic alterations. Conclusion: HFD induced obesity associated with a disturbed lipid profile, defective antioxidant stability, and high values of IR parameters; this may have implications for the progress of obesity related problems. Treatment with L-carnitine, or HMF extract improved obesity and its associated metabolic problems in different degrees. Also HMF has antioxidant, hypolipidaemic insulin sensitizing effects. Moreover HMF might be a safe combination on the organs whose functions were examined, as a way to surmount the obesity state; and it has a distinct anti-obesity effect.