Prevalence Of Non-insulin-dependent Diabetes Mellitus Research Articles

Clinical and genetic features of maturity-onset diabetes of the young in pediatric patients: a 12-year monocentric experience

BackgroundA retrospective observational study was conducted to assess the prevalence of maturity onset diabetes of the young (MODY) in a large paediatric population of Southern Italy newly diagnosed with diabetes. Clinical and genetic features of the identified MODY patients were also described.MethodsGenetic testing was performed in children and adolescents newly diagnosed with diabetes who presented autoantibody negativity and fasting C-peptide levels ≥ 0.8 ng/mL. Patients with a low insulin daily dose and optimal glycaemic control after two years from diabetes onset were also investigated for monogenic diabetes, regardless of their autoimmunity status and/or C-peptide levels.ResultsA prevalence of 6.5% of MODY was found. In particular, glucokinase-MODY was the most common type of MODY. The mean age at diagnosis was 9.1 years. Clinical presentation and biochemical data were heterogeneous also among patients belonging to the same MODY group.ConclusionsWe found a relatively high prevalence of MODY among paediatric patients with a new diagnosis of diabetes in comparison to literature data. Our findings highlight that a more detailed clinical evaluation along with easier and less expensive approachability to genetic testing may allow diagnosing an increasing number of MODY cases. A correct, prompt diagnosis is crucial to choose the most appropriate treatment and offer adequate genetic counselling.

Epidemiology, genetic landscape and classification of childhood diabetes mellitus in the State of Qatar.

Aims/IntroductionTo study the epidemiology, genetic landscape and causes of childhood diabetes mellitus in the State of Qatar.Materials and methodsAll patients (aged 0–18 years) with diabetes mellitus underwent biochemical, immunological and genetic testing. American Diabetes Association guidelines were used to classify types of diabetes mellitus. The incidence and prevalence of all the different types of diabetes mellitus were calculated.ResultsTotal number of children with diabetes mellitus was 1,325 (type 1 n = 1,096, ≥1 antibody; type 2 n = 104, type 1B n = 53; maturity onset diabetes of the young n = 20; monogenic autoimmune n = 4; neonatal diabetes mellitus n = 10;, syndromic diabetes mellitus n = 23; and double diabetes mellitus n = 15). The incidence and prevalence of type 1 diabetes were 38.05 and 249.73 per 100,000, respectively, and for type 2 were 2.51 and 23.7 per 100,000, respectively. The incidence of neonatal diabetes mellitus was 34.4 per 1,000,000 live births, and in indigenous Qataris the incidence was 43.6 per 1,000,000 live births. The prevalence of type 1 diabetes and type 2 diabetes in Qatari children was double compared with other nationalities. The prevalence of maturity onset diabetes of the young in Qatar was 4.56 per 100,000.ConclusionsThis is the first prospective and comprehensive study to document the epidemiology and genetic landscape of childhood diabetes mellitus in this region. Qatar has the fourth highest incidence of type 1 diabetes mellitus, with the incidence and prevalence being higher in Qatari compared with non‐Qatari. The prevalence of type 2 diabetes mellitus is also higher in Qatar than in Western countries. The incidence of neonatal diabetes mellitus is the second highest in the world. GCK is the most common form of maturity onset diabetes of the young, and a large number of patients have type 1B diabetes mellitus.

Genetic causes of maturity onset diabetes of the young may be less prevalent in American pregnant women recently diagnosed with diabetes mellitus than in previously studied European populations

Context: There are many causes of impaired glucose tolerance in pregnant women. It is unclear whether genetic etiologies are a source of impaired glucose tolerance in pregnant women.Objective: To prospectively determine the prevalence of maturity onset diabetes of the young (MODY) due to glucokinase (GCK) mutations in an American population of women with recent onset diabetes mellitus and gestational diabetes. We hypothesized that based on America’s higher prevalence of gestational diabetes mellitus (GDM) and Type 2 diabetes, there may be an increased prevalence of GK mutations in our population than in previously reported studies from European studies.Design: Over a three-year period, 72 pregnant women with recently diagnosed diabetes mellitus were prospectively assessed for presence of the most common pathogenic GCK mutations.Setting: This study was performed in a gestational diabetes clinic in Urban America and a high-risk pregnancy clinic that served the military and their families on an American military base in Germany.Patients: Seventy-two women; 65 with diagnosis of diabetes mellitus in this pregnancy (GDM/overt diabetes) and 7 with diagnosis in the last nine years prior to pregnancy were recruited during pregnancy and blood samples were obtained.Interventions: None.Main outcome measures: Each study participant’s blood sample was analyzed with restriction fragment length polymorphism to assess for mutations in the GCK gene.Results: There were 38 female and 34 male neonates born at 38 weeks gestation ±1.2 weeks. Mean birth weight was 3351 g ± 450 g. There were no patients with GCK mutations found in our population 0/72. This prevalence is not greater than that seen in previous a similar study in European women with gestational diabetes, but in fact significantly less (p = 0.03).Conclusion: American women with recently diagnosed diabetes mellitus likely have no higher prevalence of MODY than in previously studied European women with diabetes mellitus and may have a lower prevalence.

Prevalence of Microalbuminuria in NIDDM Hypertensives and Non-Diabetic Hypertensives A Comparative Study

Urinary albumin excretion is indicative of glomerular permeability with increasing levels of albumin in the urine indicates renal damage. An excretion rate of 300mg/day is macroalbuminuria. Microalbuminuria of 20-200µg/min (30-300 mg/day) is an early indicator of renal injury and predicts the development of proteinuria and progressive renal failure. Microalbuminuria is also an important predictor of cardiovascular events in patients with both insulin dependent diabetes mellitus (IDDM) and non insulin dependent diabetes mellitus (NIDDM). Urinary albumin excretion depends on permselectivity of the glomerular basement membrane (GBM). Majority of patients with nephropathy have NIDDM due to higher prevalence of NIDDM ( 90% ) in general population. Hypertension accelerates rate of decline of renal function and more closely related to higher blood pressure and longer duration. Increased glomerular hydrostatic pressure and increased permeability of GBM are two proposed mechanisms for increased Urinary Albumin Excretion ( UAE ). The aim of study is to compare the prevalence of microalbuminuria in non insulin dependent diabetic (NIDDM) hypertensives with non-diabetic hypertensives and to correlate with sex, age, family history, body mass index(BMI), mean arterial pressure(MAP) risk factors. Only type2 diabetic hypertensives and non diabetic hypertensives were included. IDDM patients and hypertensives on angiotensin converting enzyme inhibitors (ACEI), angiotensin II receptor blockers (ARBS) were excluded from the study. 150 persons were enrolled into the study. 50 non insulin dependent diabetic hypertensives, 50 non-diabetic hypertensives and 50 healthy individuals were included as controls. Urinary Albumin Excretion(UAE) was estimated by particle enhanced Immunoturbidimetric test in 24 hr urinary sample. The study showed higher prevalence of microalbuminuria in NIDDM with HTN group (74%) than non-diabetic hypertensive group (38%). Males showed higher prevalence of microalbuminuria 56.75% in NIDDM with HTN and 68.42% in hypertensives than females in both groups. The study showed patients in higher age group 50-60yrs had higher prevalence of microalbuminuria 78.37% in NIDDM with HTN and 63.15% in non diabetic hypertensives. It has been observed that increasing of age associated with increased prevalence of microalbuminuria. 74% of patients in NIDDM with HTN and 54% of patients in non diabetic hypertensives showed positive family history. Higher BMI 25-35 showed higher prevalence of microalbuminuria 67.56% in NIDDM with HTN and 42% in HTN group. Higher prevalence of microalbuminuria 74% in diabetic hypertensives and 38% in non diabetic hypertensives with MAP ranging between 111-150 mmHg. The results were analysed by applying Chi-square test. p-value calculated and compared among three groups. P- value < 0.005 which is highly significant..

Patients With Celiac Disease Have a Lower Prevalence of Non–Insulin-Dependent Diabetes Mellitus and Metabolic Syndrome

We investigated whether risk for non-insulin-dependent diabetes mellitus (NIDDM) and metabolic syndrome are affected by celiac disease. We examined the prevalence of NIDDM and metabolic syndrome among adults with celiac disease, compared with matched controls. We assessed medical records of 840 patients with biopsy-proven celiac disease for diagnoses of NIDDM, hypertension, or hyperlipidemia; body mass index (BMI); lipid profile; and levels of glucose or glycosylated hemoglobin, to identify those with metabolic syndrome. Patients without celiac disease were matched for age, sex, and ethnicity (n = 840 controls). The prevalence of NIDDM and metabolic syndrome in the celiac disease cohort was compared with that of the controls and subjects included in the National Health and Nutrition Examination Survey. Twenty-six patients with celiac disease (3.1%) had NIDDM compared with 81 controls (9.6%) (P < .0001). Similarly, the prevalence of metabolic syndrome was significantly lower among patients with celiac disease than controls (3.5% vs 12.7%; P < .0001). The mean BMI of patients with celiac disease was significantly lower than that of controls (24.7 vs 27.5; P < .0001). However, celiac disease was still associated with a lower risk of NIDDM, after controlling for BMI. The prevalence of NIDDM and metabolic syndrome are lower among patients with celiac disease than in matched controls and the general population. These differences are not explained by differences in BMI. Studies are needed to determine the mechanisms by which celiac disease affects the risk for NIDDM and metabolic syndrome.

Lipoprotein (a) and comprehensive lipid tetrad index as a marker for coronary artery disease in NIDDM patients in South India

Background Coronary artery disease (CAD) is reaching epidemic proportions in India, in the absence of traditional risk factors. Lipoprotein (a) (Lp(a)) concentrations are related to both atherogenesis and thrombogenesis and may be a key link between lipid and CAD. We studied the role of Lp(a) and comprehensive lipid tetrad index as markers for CAD in South Indian patients with non-insulin-dependent diabetes mellitus (NIDDM). Methods Lp(a) concentrations and lipid profile were estimated in 53 NIDDM patients with CAD (Group 1), 53 NIDDM patients without CAD (Group 2), and 52 control subjects (Group 3). Comprehensive lipid tetrad index was calculated in all patients and controls. Results Lp(a) concentrations were significantly higher in Group 1 patients, when compared with Groups 2 and 3. In NIDDM patients with CAD, only total cholesterol and low-density cholesterol concentrations correlated significantly positively with lipoprotein (a) concentrations ( r = 0.184, p = 0.03 and r = 0.168, p = 0.02). Mean comprehensive lipid tetrad index was 45,487 ± 2747 in Group 1, 10,866 ± 1163 in Group 2 and 4582 ± 348 in Group 3 subjects. Conclusion Based on the foregoing data, high Lp(a) concentrations show strong correlation with CAD in NIDDM patients of South India. High concentrations of Lp(a) and comprehensive lipid tetrad index, along with high prevalence of NIDDM, may render Indians particularly vulnerable to malignant atherosclerosis at a young age. As NIDDM is increasing in prevalence in India, the above observations have ominous dimensions in terms of total burden of CAD in India.

Clinical, haemodynamic, anthropometric, metabolic and insulin profile of men with high‐stage and high‐grade clinical prostate cancer

Aims: Previous studies have shown that non‐insulin‐dependent diabetes mellitus (NIDDM), hypertension, atherosclerotic disease manifestations, tallness, obesity, dyslipidaemia, hyperuricaemia, hyperinsulinaemia and high alanine aminotransferase (ALAT) levels are risk factors for development of benign prostatic hyperplasia (BPH). This indicates that BPH is a component of the metabolic syndrome. In a subsequent study, we found that there was an association between the BPH growth rate and the development of clinical prostate cancer. These findings generated a hypothesis that clinical prostate cancer also was a component of the metabolic syndrome. In the present study, this hypothesis was tested on 299 patients with recently diagnosed clinical prostate cancer. If this hypothesis is true, patients with clinical prostate cancer of high stage and grade would have a larger prostate gland volume, a faster BPH growth rate and a more pronounced clinical, haemodynamic, anthropometric, metabolic and insulin profile than patients with clinical prostate cancer of low stage and grade have. Methods: Two hundred and ninety‐nine patients in whom clinical prostate cancer was diagnosed were consecutively included. The prevalence of NIDDM, treated hypertension and atherosclerotic manifestations was provided by the respective patient's medical history. Body length, body weight, waist measurement, hip measurement and blood pressure were determined. Body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn to determine triglycerides, total cholesterol, high‐density lipoprotein (HDL)‐cholesterol, low‐density lipoprotein (LDL)‐cholesterol, uric acid, ALAT and the fasting plasma insulin level. The prostate gland volume was measured using transrectal ultrasound. The annual BPH growth rate was calculated. The prostate cancer diagnosis was established. Results: Patients with clinical prostate cancer, prostate‐specific antigen (PSA) < 50 ng/ml, stage T3, had a bigger prostate gland volume (p < 0.001), a faster BPH growth rate (p < 0.001), were more obese, as measured by body weight (p = 0.062), BMI (p = 0.003), waist measurement (p = 0.011) and hip measurement (p = 0.051) and showed a higher systolic blood pressure (p < 0.070) than patients with T2 clinical prostate cancer. When patients with clinical prostate cancer, PSA >50 ng/ml, were included at the comparison, T3 tumour patients showed a higher prevalence of treated hypertension (p = 0.026) than patients with T2 tumours. Patients with clinical prostate cancer, PSA <50 ng/ml, G3, had a greater prostate gland volume (p = 0.004), a faster BPH growth rate (p = 0.005) and were more obese as determined by waist measurement (p = 0.044) and WHR (p = 0.073). Moreover, subjects with a G3 tumour were more dyslipidaemic, as shown by a higher triglyceride level (p = 0.019) and a lower HDL‐cholesterol level (p = 0.005), and were more hyperuricaemic (p = 0.023), showed a higher plasma insulin level (p = 0.019) and a higher ALAT level (p = 0.061) than those with a G1 tumour. When patients with clinical prostate cancer, PSA >50 ng/ml, were included at the comparison, G3 patients had a greater prostate gland volume (p = 0.002) and a faster BPH growth rate (p = 0.003) than patients with G1 tumours. Conclusions: The results of the present study suggest that the prostate gland volume, the BPH growth rate, hypertension, obesity, dyslipidaemia, hyperuricaemia, hyperinsulinaemia and high ALAT levels are risk factors for the development of clinical prostate cancer. Thus, our results support the hypothesis that clinical prostate cancer is a component of the metabolic syndrome. Patients with clinical prostate cancer may have the same metabolic abnormality of a defective insulin‐stimulated glucose uptake and secondary hyperinsulinaemia as patients with the metabolic syndrome. Our data also support the hypothesis that hyperinsulinaemia is a promoter of clinical prostate cancer.

Cardiovascular implications of insulin resistance and non–insulin-dependent diabetes mellitus

PATIENTS WITH TYPE 2 diabetes mellitus, or non–insulin-dependent diabetes mellitus (NIDDM), represent 10% to 15% of the population seen by physicians who regularly treat coronary artery disease (CAD). Given an increasing prevalence of NIDDM in developed countries and its association with obesity, high caloric intake, and sedentary lifestyle, 1 O'Rahilly S Science, medicine and the future: Non-insulin-dependent diabetes mellitus: The gathering storm. BMJ. 1997; 314: 955-959 Crossref PubMed Google Scholar , 2 Harris MI Hadden WC Knowler WC et al. Prevalence of diabetes and impaired glucose tolerance and plasma glucose levels in U.S. population aged 20-74 yr. Diabetes. 1987; 36: 523-534 Crossref PubMed Google Scholar , 3 Matthaei S Stumvall M Kellerer M et al. Pathophysiology and pharmacologic treatment of insulin resistance. Endocr Rev. 2000; 21: 585-618 Crossref PubMed Scopus (212) Google Scholar this percentage is almost certain to rise. In the 1980s, the Framingham study showed that the presence of NIDDM increased cardiovascular mortality 2-fold in men and almost 4-fold in premenopausal women. 4 Kannel WB McGee DL Diabetes and glucose tolerance as risk factors for cardiovascular disease: The Framingham Study. Diabetes Care. 1979; 2: 120-126 Crossref PubMed Google Scholar NIDDM adversely affects the natural history of CAD and the therapeutic benefits from percutaneous and surgical coronary revascularization procedures. 5 Brooks MM Jones RJ Bach RG et al. Predictors of morbidity and mortality from cardiac causes in the Bypass Angioplasty Revascularization Investigation (BARI) randomized trial and registry. Circulation. 2000; 101: 2682-2689 Crossref PubMed Google Scholar , 6 Kornowski R Mintz GS Kent KM et al. Increased restenosis in diabetes mellitus after coronary interventions is due to exaggerated intimal hyperplasia. Circulation. 1997; 95: 1366-1369 Crossref PubMed Google Scholar This adverse impact has been documented in all contemporary cardiovascular databases, 7 Stamler J Vaccaro O Neaton JD et al. Diabetes, other risk factors, and 12-year cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial. Diabetes Care. 1993; 16: 434-444 Crossref PubMed Google Scholar and the association between macrovascular disease (eg, myocardial infarction and stroke) and NIDDM has become stronger over time. 8 Zimmet PZ The changing face of macrovascular disease in non-insulin-dependent diabetes mellitus: An epidemic in progress. Lancet. 1997; 350: 1-4 Abstract Full Text Full Text PDF PubMed Google Scholar , 9 Nathan DM Meigs J Singer DE The epidemiology of cardiovascular disease in type 2 diabetes mellitus: How sweet it isor is it?. Lancet. 1997; 350: 4-9 Abstract Full Text Full Text PDF PubMed Google Scholar The pathophysiologic mechanisms responsible for this adverse impact are incompletely understood, however. Despite considerable improvements in pharmacologic and operative treatment of CAD, little improvement in outcome has occurred in these patients.

Increased risk of non-insulin dependent diabetes mellitus, arterial hypertension and coronary artery disease in perimenopausal women with a history of the polycystic ovary syndrome.

The aim of the study was to determine the prevalence of non-insulin dependent diabetes mellitus (NIDDM), arterial hypertension, coronary artery disease and the risk factors for these diseases in perimenopausal women with a history of polycystic ovary syndrome (PCOS) treatment. A group of 28 women was selected from a large group of patients who had undergone wedge ovarian resection. A total of 752 controls was selected by age (45-59 years) from a random female population sample. There was no difference between the two groups in body mass index, waist circumference or waist-hip ratio. Both groups were found to have identical family histories of NIDDM, hypertension, and coronary artery disease and identical smoking habits. We did not find a difference between the mean concentrations of lipids and fasting glucose. The two groups did not differ in the proportions of women with elevated lipid concentrations. The prevalence of NIDDM and coronary artery disease was significantly higher in PCOS women. In conclusion, women in the general population have the same level of risk factors at perimenopausal age as PCOS women. Patients with markedly expressed clinical symptoms of PCOS made up a subgroup in the general population at high risk for developing NIDDM and coronary artery disease.

Prevalence of NIDDM in Mexicans with paraphyletic and polyphyletic surnames.

It has been hypothesized that the greater prevalence of non-insulin-dependent diabetes mellitus (NIDDM) in Mexicans may be related to their greater degree of Amerindian genetic admixture (AGA). The aim of this unmatched case-control study was to correlate the prevalence of NIDDM with AGA in 10 Mexican Mestizo populations non-randomly selected by surname. A sample of 1,699 unrelated persons, >44 years and residing in the state of Nuevo León, was selected on the basis of paraphyletic or polyphyletic surnames and interviewed in the Instituto Mexicano del Seguro Social (IMSS). All subjects received a medical examination, and diabetes was diagnosed on the basis of World Health Organization criteria. Three genetic marker systems were analyzed, and the percentage of AGA was calculated. Logistic regression analysis was performed with the prevalence as the dependent variable and sex and surname as the independent variables. The Spearman rank-order correlation analysis was calculated between the age-adjusted prevalence (45-75+ years) and AGA. The correlation revealed a pattern of increasing prevalence of NIDDM with increasing Amerindian ancestry by surname. Am. J. Hum. Biol. 12:721-728, 2000. Copyright 2000 Wiley-Liss, Inc.

Clinical, Anthropometric, Metabolic and Insulin Profile of Men with Fast Annual Growth Rates of Benign Prostatic Hyperplasia

The purpose of this study was to test the hypothesis of a causal relationship between high insulin levels and the development of benign prostatic hyperplasia (BPH) and to determine the clinical, anthropometric, metabolic and insulin profile in men with fast-growing BPH compared with men with slow-growing BPH. The present study was designed as a risk factor analysis of BPH in which the estimated annual BPH growth rate was related to components of the metabolic syndrome. Two hundred and fifty patients referred to the Urological Section, Department of Surgery, Central Hospital, Varberg, Sweden, with lower urinary tract symptoms with or without manifestations of the metabolic syndrome were consecutively included. The prevalences of atherosclerotic disease manifestations, non-insulin-dependent diabetes mellitus (NIDDM) and treated hypertension were obtained. Data on blood pressure, waist and hip measurement, body height and weight were collected and body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn from fasting patients to determine insulin, total cholesterol, triglycerides, HDL and LDL cholesterol, uric acid, alanine aminotransferase (ALAT) and prostate-specific antigen (PSA). The prostate gland volume was determined using ultrasound. The median annual BPH growth rate was 1.04 ml/year. Men with fast-growing BPH had a higher prevalence of NIDDM (p = 0.023) and treated hypertension (p = 0.049). These patients were also taller (p=0.004) and more obese as measured by body weight (p<0.001), BMI (p=0.026), waist measurement (p <0.001), hip measurement (p = 0.006) and WHR (p=0.029). Moreover, they had elevated fasting plasma insulin levels (p = 0.018) and lower HDL cholesterol levels (p = 0.021) than men with slow-growing BPH. The annual BPH growth rate correlated positively with diastolic blood pressure (rs = 0.14; p = 0.009), BMI (rs = 0.24; p < 0.001) and four other expressions of obesity and fasting plasma insulin level (rs = 0.18; p = 0.008), and negatively with the HDL cholesterol level (rs = -0.22; p = 0.001). In conclusion, the data suggest that NIDDM, hypertension, tallness, obesity, high insulin and low HDL cholesterol levels constitute risk factors for the development of BPH. The results also suggest that BPH is a component of the metabolic syndrome and that BPH patients may share the same metabolic abnormality of a defective insulin-mediated glucose uptake and secondary hyperinsulinaemia, as patients with the metabolic syndrome. The findings support the hypothesis of a causal relationship between high insulin levels and the development of BPH, and give rise to a hypothesis of increased sympathetic nerve activity in men with BPH.

Hyperinsulinism and sex hormones in young adult African Americans

Hyperinsulinemia is a risk factor for cardiovascular disease, and is linked with non—insulin-dependent diabetes mellitus (NIDDM), hyperlipidemia, obesity, and hypertension. Sex hormones also play a role in the metabolic alterations associated with the risk for cardiovascular disease. A reduction in sex hormone—binding globulin (SHBG) may be predictive of future NIDDM particularly in women. The postmenopausal decline in estrogen is also associated with an increase in risk factor expression in women. Since African Americans experience a greater prevalence of NIDDM, obesity, and hypertension, conditions associated with hyperinsulinemia, the purpose of this study was to determine if alterations in sex hormone levels are associated with the plasma insulin concentration in young adult African Americans, and to determine if there are sex differences in the effect of insulin on lipids and sex hormones. In a sample of 221 nondiabetic African American men (n = 105) and women (n = 116) with a mean age of 31 years, we examined the relationship of the plasma insulin concentration with the body mass index (BMI), blood pressure, plasma lipids, and sex hormones, including free testosterone, estradiol, and SHBG. Plasma insulin increased with the BMI and other measures of adiposity ( P < .001) in men and women. Significant correlations of insulin with plasma lipids were also present in both sexes. There was a significant inverse correlation of insulin with SHBG in both men ( r = .28, P = .007) and women ( r = .27, P = .02). There was a significant direct correlation of insulin with free testosterone in women ( r = .032, P < .001). Stepwise multiple regression analyses with insulin as the dependent variable detected the BMI, triglyceride, and apolipoprotein A1 as significant contributors to the plasma insulin concentration in men. In women, the multiple regression model detected percent body fat, low-density lipoprotein (LDL) cholesterol, and the testosterone as significant contributors to plasma insulin. These data on young African Americans demonstrate a significant relationship between hyperinsulinemia and obesity, atherogenic lipid status, and lower SHBG. In the premenopausal women, the lower SHBG is linked with higher free testosterone, favoring a condition of relative androgen excess.

Non-insulin-dependent diabetes in Kuwait: prevalence rates and associated risk factors

Non-insulin-dependent diabetes mellitus (NIDDM) is a major clinical and public health problem in Kuwait. The objective of the study was to determine prevalence rates of NIDDM among a representative sample of the Kuwaiti adult population aged 20 and older in two out of five governorates and identify the associated risk factors for the disease. A total of 3003 subjects (1105 men and 1898 women) were interviewed and examined by the research team during the period September 1995 to June 1996. A specially designed questionnaire was completed and the physical examination included height, weight and blood pressure measurements. Fasting blood samples were withdrawn, centrifuged immediately and refrigerated. Interpretation of oral glucose tolerance tests were based on the World Health Organisation diagnostic criteria for diabetes mellitus (1985). The denominator used for computing the prevalence was obtained from the 1995 Kuwait census. The overall prevalence of NIDDM in this study was found to be 14.8% (14.7% in men, 14.8% in women). Diabetic subjects presented at a relatively young age, prevalence rate in the age group 20–39 was 5.7% (95% confidence interval, 4.4–7.0) and in the age group 40–59 was 18.3% (95% confidence interval, 16.1–20.6). Obesity was found to be a significant risk factor, P<0.001. The strong association of family history of NIDDM (adjusted odds ratio=1.80, P<0.001) suggests a genetic component. Hypertension was markedly associated with NIDDM and IGT ( P<0.001). With the demographic transition which already started among the Kuwaiti population and if the prevalence of NIDDM remains the same, aging of the population will contribute to even more upward trends in prevalence of abnormal glucose tolerance with its serious impact on morbidity and mortality among the Kuwaiti population. The strong association between hypertension and NIDDM may suggest a common approach to the prevention and control of these two conditions.

Fetal origin of maturity-onset diabetes mellitus: genetic or environmental cause?

Low birthweight is a risk factor for a number of diseases of adult life including non-insulin-dependent diabetes mellitus (NIDDM). This implies that either genetic constitution or factors operating during intrauterine development have a causal role in NIDDM. One reason for rejecting a genetic cause, however, is that there is a rapidly changing prevalence of NIDDM with the onset and establishment of affluence, which does not fit with conventional models of multifactorial genetic disease. But in this article a new model of genetic disease based on the concept of redundancy is explored. The idea is that mutant genes interact synergistically in highly redundant systems to degrade performance and increase the risk of disease. The mutational load is in turn determined by the pre-conceptual environment. This model can explain a rapidly changing prevalence of NIDDM.

Insulin Downregulates Pyruvate Dehydrogenase Kinase (PDK) mRNA: Potential Mechanism Contributing to Increased Lipid Oxidation in Insulin-Resistant Subjects

Oxidative metabolism of glucose is regulated by pyruvate dehydrogenase (PDH) that can be inhibited by isoforms of PDH kinase (PDK). Recently, increased PDK activity has been implicated in the pathogenesis of insulin resistance and non-insulin-dependent diabetes mellitus (NIDDM) in obese subjects. Using quantitative RT-PCR, we measured mRNA of PDK2 and PDK4 isoforms in skeletal muscle biopsies from nondiabetic Pima Indians, a population with a high prevalence of NIDDM associated with obesity. PDK2 and PDK4 mRNAs were positively correlated with fasting plasma insulin concentration, 2-h plasma insulin concentration in response to oral glucose, and percentage body fat, whereas both isoforms were negatively correlated with insulin-mediated glucose uptake rates. Measurements of PDK2 and PDK4 mRNA during the hyperinsulinemic-euglycemic clamp and of PDK2 in cell culture indicated that both transcripts decrease in response to insulin. Increased fatty acid (FA) oxidation has been traditionally viewed as the cause for increased PDK activity contributing to insulin resistance in obese subjects. In contrast, our data indicate that insufficient downregulation of PDK mRNA in insulin-resistant individuals could be a cause of increased PDK expression leading to impaired glucose oxidation followed by increased FA oxidation.

Эпидемиология инсулиннезависимого сахарного диабета

The relevance of epidemiological studies of non-insulin-dependent diabetes mellitus (NIDDM) is due primarily to the fact that its share among other forms of diabetes reaches 85–90% [57]. The second important circumstance is that the actual prevalence of NIDDM is 2-3 times higher than its registered prevalence in terms of circulation [30]. These two factors determine its medical and social significance not only among other forms of diabetes, but also among chronic non-communicable diseases.

Primary prevention of coronary heart disease: guidance from Framingham: a statement for healthcare professionals from the AHA Task Force on Risk Reduction. American Heart Association.

The Framingham Heart Study has contributed importantly to understanding of the causes of coronary heart disease (CHD), stroke, and other cardiovascular diseases. Framingham research has helped define the quantitative and additive nature of these causes or, as they are now called, “cardiovascular risk factors.”1 The National Cholesterol Education Program (NCEP)2 3 has made extensive use of Framingham data in developing its strategy for preventing CHD by controlling high cholesterol levels. The NCEP guidelines2 3 adjust the intensity of cholesterol-lowering therapy with absolute risk as determined by summation of risk factors. The National High Blood Pressure Education Program (NHBPEP) has set forth a parallel approach for blood pressure control. In contrast to the NCEP,2 however, earlier NHBPEP reports issued through the Joint National Committee4 did not match the intensity of therapy to absolute risk for CHD. “Normalization” of blood pressure is the essential goal of therapy regardless of risk status. Blood pressure–lowering therapy is carried out as much for prevention of stroke and other cardiovascular complications as for reduction of CHD risk. Nonetheless, risk assessment could be important for making decisions about type and intensity of therapy for hypertension. Thus, the most recent Joint National Committee report5 gives more attention to risk stratification for adjustment of therapy for hypertension. Although Framingham data have already been influential in the development of national guidelines for risk factor management, the opportunity may exist for both cholesterol and blood pressure programs to draw more extensively from Framingham results when formulating improved risk assessment guidelines and recommending more specific strategies for risk factor modification. The American Heart Association has previously used Framingham risk factor data to prepare charts for estimating CHD risk. Framingham investigators of the National Heart, Lung, and Blood Institute prepared the original charts and have now revised …

Prevalencia de diabetes mellitus no insulinodependiente en la población rural de Durango, México

This study was carried out to determine the prevalence of non-insulin-dependent diabetes mellitus (NIDDM) in rural inhabitants of Durango, Mexico, and some of the risk factors for the disease. A random samples of 30,996 individuals aged 30 years and over was selected from 627 rural communities in Durango. These persons were interviewed between November 1993 and December 1994 to obtain information on several sociodemographic variables. A capillary blood sample was collected from each individual to determine his or her glucose level after 10-12 hours of fasting. Measures of central tendency and dispersion were calculated, and percentage distributions for the study variables were determined. Comparisons among proportions were made utilizing the chi-square test, and means were compared using Student's t test. The strength of associations was estimated with odds ratios, and 95% confidence intervals (CI 95%) were calculated for proportions. The final sample consisted of 31,028 persons, of whom 22,890 (73.8%) were women and 8,138 (26.2%) were men. A total of 1,004 cases of NIDDM were detected (3.2%; CI 95%:3.0 to 3.4), 767 in women and 237 in men. Only 9.2% of the study population was obese. The highest frequency of NIDDM was documented in persons 60 to 69 years of age. Family history of NIDDM was identified in 59.5% of the persons with the disease (CI 95%: 58.9 to 60.0) and in 26.3% of the healthy persons (CI 95%: 25.8 to 26.8). The low prevalence of NIDDM found in this study may be related to the low level of obesity in the population surveyed.

Comparison of the prevalence in two diabetes surveys in Pu-Li, Taiwan, 1987–1988 and 1991–1992

The objective of this study was to investigate the prevalence of non-insulin-dependent diabetes mellitus (NIDDM) in Pu-Li, Taiwan from 1991–1992, and to compare the results with a similar study conducted in 1987–1988. We also wished to compare different approaches in asking about patient history and to determine how this effects data authenticity. Both were community-based cross-sectional studies with stratified cluster sampling of residents age≥30. Blood samples were taken for screening and 75 g oral glucose tolerance tests were performed for diagnosis. The total number of eligible subjects in the second study was 2719 (1424 men, 1295 women). Complete data and samples were collected for 1118 (536 men, 582 women). The response rate was 41.1% (37.6% for men, 44.9% for women). The crude prevalence was 10.3% (5.6% known, 4.7% new). Using standard world population (Segi), the age-adjusted prevalence rate was 8.3% (4.0% known, 4.3% new). The 1991–1992 study had a response rate (crude 41.1%, adjusted 51.3%) which was slightly lower than the 1987–1988 study (crude 44.8%, adjusted 55.9%). The age-adjusted prevalence rates for new NIDDM were similar (4.4 vs. 4.3%) while the age-adjusted prevalence of known NIDDM in the second survey (4.0%) was lower than the first survey (6.9%), which apparently was overestimated due to the simplicity of questions regarding history. In conclusion, prevalence of new DM in this area appears to be stable, and when doing a survey regarding previous DM, it is better to include treatment history rather than depending on self-reporting of NIDDM alone.

Recessive Inheritance of Obesity in Familial Non—Insulin-Dependent Diabetes Mellitus, and Lack of Linkage to Nine Candidate Genes

Segregation analysis of body-mass index (BMI) supported recessive inheritance of obesity, in pedigrees ascertained through siblings with non-insulin dependent diabetes mellitus (NIDDM). BMI was estimated as 39 kg/m2 for those subjects homozygous at the inferred locus. Two-locus segregation analysis provided weak support for a second recessive locus, with BMI estimated as 32 kg/m2 for homozygotes. NIDDM prevalence was increased among those subjects presumed to be homozygous at either locus. Using both parametric and nonparametric methods, we found no evidence of linkage of obesity to any of nine candidate genes/regions, including the Prader-Willi chromosomal region (PWS), the human homologue of the mouse agouti gene (ASP), and the genes for leptin (OB), the leptin receptor (OBR/DB), the beta3-adrenergic receptor (ADRB3), lipoprotein lipase (LPL), hepatic lipase (LIPC), glycogen synthase (GYS), and tumor necrosis factor alpha (TNFA).