High prevalence of metabolic syndrome among Kuwaiti adults--a wake-up call for public health intervention

The socio-economic development which followed the discovery of oil resources brought about considerable changes in the food habits and lifestyle of the Kuwaiti population. Excessive caloric intake and decreased energy expenditure due to a sedentary lifestyle have led to a rapid increase in obesity, diabetes and other non-communicable chronic diseases in the population. In this paper, we examine the prevalence of the Metabolic Syndrome (MetS) among Kuwaiti adults (≥20 years) using data from the first national nutrition survey conducted between July 2008 and November 2009. The prevalence of MetS was 37.7% in females and 34.2% in males by NCEP criteria, whereas the values were 40.1% in females and 41.7% in males according to IDF criteria. Prevalence of MetS increased with age and was higher in females than males. The high prevalence of the MetS in Kuwaiti adults warrants urgent public health measures to prevent morbidity and mortality due to cardiovascular complications in the future.     

Explanations of socioeconomic differences in excess risk of type 2 diabetes in Swedish men and women

OBJECTIVE: We investigated to what extent socioeconomic differences in type 2 diabetes risk could be explained by established risk factors (obesity, physical inactivity, smoking, and heredity) and psychosocial factors (low decision latitude at work and low sense of coherence). RESEARCH DESIGN AND METHODS: This cross-sectional study comprised 3,128 healthy Swedish men and 4,821 women, aged 35-56 years, living in the Stockholm area. An oral glucose tolerance test identified 55 men and 52 women with type 2 diabetes. The relative contribution of established and psychosocial factors to socioeconomic differences in diabetes risk was assessed by comparing analyses with adjustment for different sets of these factors. RESULTS: The relative risks (RRs) for type 2 diabetes in middle and low socioeconomic groups in men were 2.4 (95% CI 1.0-5.3) and 2.9 (1.5-5.7), respectively, and in women 3.2 (1.5-6.6) and 2.7 (1.3-5.9), respectively. In men, the RRs decreased to 1.9 (0.8-4.4) and 2.1 (1.0-4.2) after adjustment for established risk factors; no further change was found when psychosocial factors were included. In women, the RRs changed to 2.4 (1.1-5.2) and 1.6 (0.7-3.8) by including established risk factors and to 2.3 (1.0-5.1) and 1.9 (0.8-4.3) by inclusion of psychosocial factors. After adjustment for both established and psychosocial factors, the RRs were 1.4 (0.6-3.6) and 1.0 (0.4-2.5), respectively. CONCLUSIONS: In men, the excess risk of type 2 diabetes was partly explained by established risk factors (36-42%), whereas psychosocial factors had no effect. In women, most of the socioeconomic differences in type 2 diabetes were explained by simultaneous adjustment for established risk factors and psychosocial factors (81-100%).     

Variables associated with subclinical atherosclerosis among rheumatoid arthritis patients of Gulf Cooperative Council countries

Objectives:To evaluate the cardiovascular disease (CVD) as demonstrated by carotid intima-media thickness (cIMT) and the cluster risk factors of CVD including traditional and non-traditional, urinary functions, iron buildup, and hemorheology in rheumatoid arthritis (RA) patients of Gulf Cooperative Council (GCC) countries.Methods:Carotid intima-media thickness was obtained from 216 RA patients, free of atherosclerotic diseases. The correlation between cIMT and the possible CVD risk factors was carried out using regression analysis.Results:The mean cIMT was observed as 0.58±0.11 mm. Mean age was 48±13 years. Univariate analysis revealed a positive association (p<0.05) between cIMT and age, body mass index, systolic blood pressure (SBp), and diastolic blood pressure, c-reactive protein (CRP), triglycerides (TG), low-density lipoprotein (LDL), erythrocyte sedimentation rate (ESR), hemoglobin (Hb), hematocrit (Hct), mean cell volume, platelet, monocytes, eosinophils, ferritin, creatinine, and uric acid. Negative relationship was observed between cIMT and glomerular filtration rate (GFR), transferrin, and high-density lipoprotein. Multiple linear regression analysis exhibited a positive association between cIMT and the age, LDL, eosinophil, SBp, and the ESR, whereas, negative connection with the GFR and transferrin.Conclusion:In this study, we found that the eosinophils, and low transferrin, are the potential candidates for the CVD risk factors in RA patients. Fasting blood glucose level was also observed to be a significant risk factor in diabetic as well as non-diabetic RA. The remaining CVD risk factors in RA patients of GCC countries including older age, high SBp, ESR, LDL, and low GFR were similar to the international population.     

Acute ischemic stroke: Relationship of brain lesion location & functional outcome

Purpose. To establish, using brain spiral computerised tomography (SCT) and modified Barthel index (MBI), whether the location of cerebral infarction could be correlated with functional outcome in acute ischemic stroke patients who undergo early intensive rehabilitation.

Methods. Observational cohort, assessor blinded and correlational prospective 12-weeks study that included 111 acute ischemic stroke patients, admitted consecutively to an early intensive inpatient rehabilitation programme (5 days a week, 3–5 h a day) during 2003. Confirmation of diagnosis and stratification was done by brain SCT. Brain lesion locations were correlated to motor performance and functional outcome, on admission and discharge, using MBI.

Results. Statistical analysis demonstrated a significant correlation between motor performance, functional outcome and brain lesion locations. The groups with deep, combined deep and large superficial, small superficial and large superficial infarcts showed the most consistent improvement in that order of frequency. Normal brain SCT group did not reach statistical significance (p = 0.051) while the bi-hemispheric infarcts group did not show any change. The inter and intra group differences were highly significant (p < 0.05).

Conclusions. Immediate non-contrasted brain SCT may act as an independent predictor of final functional outcome in acute ischemic stroke. It may provide clinicians with an opportunity to offer realistic expectations to stroke patients and their relatives.     

Insulin resistance in type 2 diabetes: association with truncal obesity,impaired fitness,and atypical malonyl coenzyme A regulation

Abdominal obesity and physical inactivity are associated with insulin resistance in humans and contribute to the development of type 2 diabetes. Likewise, sustained increases in the concentration of malonyl coenzyme A (CoA), an inhibitor of fatty-acid oxidation, have been observed in muscle in association with insulin resistance and type 2 diabetes in various rodents. In the present study, we assessed whether these factors are present in a defined population of slightly overweight (body mass index, 26.2 kg/m2), insulin-resistant patients with type 2 diabetes. Thirteen type 2 diabetic men and 17 sex-, age-, and body mass index-matched control subjects were evaluated. Insulin sensitivity was assessed during a two-step euglycemic insulin clamp (infusion of 0.25 and 1.0 mU/kg x min). The rates of glucose administered during the low-dose insulin clamp were 2.0 +/- 0.2 vs. 0.7 +/- 0.2 mg/kg body weight x min (P < 0.001) in the control and diabetic subjects, respectively; rates during the high-dose insulin clamp were 8.3 +/- 0.7 vs. 4.6 +/- 0.4 mg/kg body weight x min (P < 0.001) for controls and diabetic subjects. The diabetic patients had a significantly lower maximal oxygen uptake than control subjects (29.4 +/- 1.0 vs. 33.4 +/- 1.4 ml/kg x min; P = 0.03) and a greater total body fat mass (3.7 kg), mainly due to an increase in truncal fat (16.5 +/- 0.9 vs. 13.1 +/- 0.9 kg; P = 0.02). The plasma concentration of free fatty acid and the rate of fatty acid oxidation during the clamps were both higher in the diabetic subjects than the control subjects (P = 0.002-0.007). In addition, during the high-dose insulin clamp, the increase in cytosolic citrate and malate in muscle, which parallels and regulates malonyl CoA levels, was significantly less in the diabetic patients (P < 0.05 vs. P < 0.001). Despite this, a similar increase in the concentration of malonyl CoA was observed in the two groups, suggesting an abnormality in malonyl CoA regulation in the diabetic subjects. In conclusion, the results confirm that insulin sensitivity is decreased in slightly overweight men with mild type 2 diabetes and that this correlates closely with an increase in truncal fat mass and a decrease in physical fitness. Whether the unexpectedly high levels of malonyl CoA in muscle, together with the diminished suppression of plasma free fatty acid, explains the insulin resistance of the diabetic patients during the clamp remains to be determined.     

Defective glucose-stimulated insulin release in the diabetic Goto-Kakizaki (GK) rat coincides with reduced activity of the islet carbon monoxide signaling pathway

The Goto-Kakizaki (GK) rat displays a markedly reduced insulin response to glucose, a defect that is thought to be coupled to an impaired glucose signaling in the beta-cell. We have examined whether carbon monoxide (CO), derived from beta-cell heme oxygenase (HO), might be involved in the secretory dysfunction. Immunocytochemical labeling of constitutive HO (HO-2) showed no overt difference in fluorescence pattern in islets from GK vs. Wistar controls. However, isolated islets from GK rats displayed a markedly impaired HO activity measured as CO production (-50%), and immunoblotting revealed an approximately 50% reduction of HO-2 protein expression compared with Wistar controls. Furthermore, there was a prominent expression of inducible HO (HO-1) in GK islets. Incubation of isolated islets showed that the glucose-stimulated CO production and the glucose-stimulated insulin response were considerably reduced in GK islets compared with Wistar islets. Addition of the HO activator hemin or gaseous CO to the incubation media brought about a similar amplification of glucose-stimulated insulin release in GK and Wistar islets, suggesting that distal steps in the HO-CO signaling pathway were not appreciably affected. We conclude that the defective insulin response to glucose in the GK rat can be explained, at least in part, by a marked impairment of the glucose-HO-CO signaling pathway as manifested by a prominent decrease in glucose stimulation of islet CO production and a reduced expression of HO-2. A possible role of HO-1 expression as a compensatory mechanism in the GK islets is presently unclear.     

On the pathogenesis of maturity-onset diabetes mellitus

Conclusions At the 6th IDF Congress in Stockholm in 1967, a hypothesis for the pathogenesis of maturity-onset diabetes under the title ‘What is inherited — what is added?’ was put forward. Investigations over the past 10 years, on the whole, tend to confirm our concept that the capacity of the pancreatic beta-cell to respond to a standardized glucose infusion with insulin production, to a major degree, is genetically controlled. Therefore, our original idea that impaired insulin response to glucose is a marker of genetic diabetes in all its stages (prediabetes, chemical diabetes, manifest diabetes) seems plausible. Accordingly, a malfunction in the transmission of information about the blood glucose level in the extracellular fluid to those sites in the cells which regulate insulin release, would be the primary defect in genetic diabetes. Our studies suggest that, due to increased sensitivity of the liver to insulin in the portal vein, most prediabetics retain a relatively normal — although somewhat low — glucose tolerance. This compensatory mechanism becomes insufficient and glucose intolerance is precipitated, e.g., when the demand for insulin release is increased. This occurs when the sensitivity of the body for insulin diminishes as in the case of obesity, acromegaly and pregnancy and, maybe, also during the process of aging.     

Molecular characterization of glucose-6-phosphate dehydrogenase deficiency in the Eastern Province of Saudi Arabia.

The level of activity of the enzyme glucose-6-phosphate dehydrogenase (G6PD) was determined in 154 unrelated Saudi males and females with G6PD deficiency who were residing in the Eastern Province of Saudi Arabia. DNA was extracted from blood samples and analyzed for known G6PD mutations by polymerase chain reaction (PCR) and restriction fragment length polymorphism techniques. Two different polymorphic mutations were identified which accounted for 90% of the samples analyzed. Of 114 G6PD-deficient males, 96 had G6PD Mediterranean, nine had African deficient variant G6PD A- and in nine the mutation has not been identified. Of the 40 G6PD-deficient females, 34 were homozygous for the G6PD Mediterranean mutation and six were genetic compound, G6PD Mediterranean/G6PD A-. The data indicate that the G6PD Mediterranean mutation is the most common (84%) in the Eastern Province, followed by G6PD A- (5.8%). Seventy one subjects who suffered from favism were found to carry the Mediterranean mutation.