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PubMed2005

Prevalence of eating disorders and psychiatric comorbidity in a clinical sample of type 2 diabetes mellitus patients.

BACKGROUND: A few studies have shown high rates of eating disorders and psychiatric morbidity in patients with type 2 diabetes mellitus. OBJECTIVE: Disturbed eating behavior and psychiatric comorbidity in a sample of T2DM patients. METHODS: Seventy type 2 diabetes mellitus patients between 40 and 65 years of age (mean, 52.9 +/- 6.8) from a diabetes outpatient clinic were sequentially evaluated. The Structured Clinical Interview for DSM-IV, Binge Eating Scale and Beck Depression Inventory were used to assess eating disorders and other psychiatric comorbidity. In addition to the descriptive analysis of the data, we compared groups divided based on the presence of obesity (evaluated by the body mass index) or an eating disorder. RESULTS: Twenty percent of the sample displayed an eating disorder. Binge eating disorder was the predominant eating disorder diagnosis (10%). Overall, the group of obese patients with type 2 diabetes mellitus presented rates of psychiatric comorbidity comparable to those seen in their nonobese counterparts. However, the presence of an eating disorder was associated with a significant increase in the frequency of anxiety disorders (57.1% x 28.6%; p = 0.044). CONCLUSIONS: In our study sample, the occurrence of eating disorders was increased compared to rates observed in the general population, with the predominance of binge eating disorder. The presence of an eating disorder in type 2 diabetes mellitus patients was associated with higher rates of anxiety disorders.

Adult↗

PubMed2006

Role of the ubiquitin-proteasome system in carotid plaque instability in diabetic patients.

In order to define the role of the ubiquitin-proteasome system in atherosclerotic plaque rupture in patients with type 2 diabetes mellitus (T2DM), we evaluated the amount of this system, of the main inflammatory cells, of the collagen content and some indexes indicative of oxidative stress in the carotid plaques of both diabetic and non-diabetic asymptomatic patients. Plaques were obtained from 31 type 2 diabetic and 27 non-diabetic patients undergoing endoterectomy. Both were examined for macrophages, T-lymphocytes, ubiquitin/proteasome 20S activity, NFkB, IkB-b, nitrotyrosine, matrix metalloproteinase-9 (MMP-9) and collagen. Diabetic plaques had more macrophages,T-lymphocytes, inflammatory cells (HLA-DR), ubiquitin/proteasome, NFkB, nitrotyrosine, MMP-9 and lower collagen content and IkB-b levels, in comparison with non-diabetic plaques. These findings indicate that in diabetic patients, ubiquitin/proteasome overactivity is associated with enhanced inflammatory activity induced by diabetic oxidative stress. This induces the NFkB release into the nucleus which, in turn, is responsible for the expression of inflammatory cytokines causing plaque rupture.

Aged↗

PubMed2000

Metabolic factors that affect beta-cell function and survival.

Several data suggest that, during the natural history of Type 2 diabetes (T2DM), whereas the degree of insulin resistance is quite stable in a single individual, insulin secretion is often progressively decreasing. The decline in beta-cell function seems, at least in part, acquired. This review focuses on data showing that chronically elevated levels of glucose and fatty acids may impair beta-cell function and, at a later stage, also affect beta-cell survival. Results obtained both in vitro and in vivo demonstrate that beta-cell function is impaired after chronic exposure to glucose and fatty acids, with many similarities between the two conditions. Basal insulin release is increased as a result of an increase of the low-Km component of glucose phosphorylation. Glucose-induced insulin release is blunted, probably due to an impairment of glucose oxidation. If the metabolic abnormality persists in vivo or the culture is prolonged in vitro, a significant increase in the rate of beta-cell death was observed, eventually leading to severe destruction of the islet architecture. An attractive hypothesis, currently under investigation, is that genetic susceptibility to diabetes may confer an increased sensitivity to the adverse effect of high glucose and non-esterified fatty acid levels on beta-cell survival.

Animals↗

PubMed2002

[Relationship between calpain-10 gene polymorphism, hypertension and plasma glucose].

OBJECTIVE: To detect the association among calpain-10(CAPN-10) gene polymorphism, hypentension and hyperglycemia. METHODS: 378 individuals in the present study were the second generation offsprings of 187 hypentensives and 19 1 nonhypertensives. Fasting plasma glucose (FPG), insulin, triglyceride and fibrinogen were determined. The polymorphism of UCSNP-43 and UCSNP-44 of CAPN 10 gene were analysed with PCR-SSCP method. RESULTS: (1)The frequency of G/G geno type of UCSNP-43 was higher in the second generation offsprings of the hypertensives than that in the nonhypertensive controls(86.6%, 75.4%, P < 0.05). (2) The frequenncy of G/G genotype of UCSNP-43 was higher in the hypertensive parents of the second generation offsprings in the hypertensive groups than that in the normotensive parent of the second generation offsprings of the nonhypertensive control groups (OR = 2.84, P = 0.01). After adjustment of age, sex and body mass index (BMI), the frequency of G/G genotype in the highest FPG-quartiles (FPG 5.42 +/- 0.1mmol/L) was much more than that in the lowest FPG quartiles (FPG 4.09 +/- 0.3 mmol/L) with OR of 3.32. CONCLUSIONS: Polymorphism of UCSNP-43 in CAPN-10 gene might be one of the genetic factors contributing to hypertension and diabetes mellitus in the population in Daqing city. It may be a predictor of type 2 diabetes mellitus (T2DM) in the decendents of hypertensives.

Adult↗

PubMed2003

[Prevalence of fibromyalgia in diabetes mellitus and obesity].

To determine the prevalence of fibromyalgia in diabetes mellitus and obesity, 121 consecutive patients have been observed: 27 with obesity (6 males and 21 females; mean age 57 years, range 20-57; mean body mass index [BMI] 34); 88 with type 2 diabetes mellitus (T2DM; 40 males and 48 females; mean age 63 years, range 44-78; mean BMI 28.8; mean glycated haemoglobin [HbA1c] in the last year 8.3%); 6 with type 1 diabetes mellitus (T1DM; 2 males and 4 females; mean age 52 years, range 26-76; mean BMI 24.5; mean HbA1c < 7%). An original questionnaire has been proposed (answer yes/not) as follows: 1) chronic (more than 3 months) and diffuse musculoskeletal pain; 2) sleep disturbances; 3) generalized fatigue; 4) paresthesias at the extremities; 5) swollen impression at hands and feet; 6) symptoms referred to irritable bowel syndrome; 7) headache; 8) symptoms change related with environmental climatic variations and/or exercise. A chronic and diffuse musculoskeletal pain has been reported by 62% of patients as well as in 9% of patients 11/18 positive tender points have been documented. In the patients with a BMI less that 26 the diagnosis of fibromyalgia was negative. Our data seem to reveal the presence of a significant clinical association between obesity, diabetes mellitus and fibromyalgia.

Adult↗

PubMed2003

Investigation on the accuracy of the blood glucose monitoring device Prestige IQ.

The aim of this study was to investigate the accuracy and reliability of the blood glucose self-monitoring system Prestige IQ (Home Diagnostics, Inc., Ft. Lauderdale, USA) in comparison to an established blood glucose reference method and four commercially available blood glucose self-monitoring devices. Over a 3-month period, 61 patients with Type 1 (T1DM) and Type 2 diabetes mellitus (T2DM) participated in this study. The patients entered the study clinic for two visits. Each visit consisted of 7 glucose determinations in samples of capillary whole blood drawn from the fingertip. The first and last measurements were determined using the laboratory reference and the mean of both readings was used as the reference value for statistical analysis. The 5 remaining glucose measurements were performed in randomized order using the 5 commercially available blood glucose devices. One hundred twenty-one data sets were generated and used to evaluate accuracy. Prestige IQ blood glucose results obtained from the fingertip agreed well with the laboratory reference (linear regression analysis: slope = 1.016; intercept = 0.4 mg/dl; SD = 13.555 mg/dl; correlation r = 0.972) and were comparable to the results generated using the other four blood glucose devices. Bland-Altman analysis for reliability confirmed that 119 out of 121 Prestige IQ results (98.3%) exhibited acceptable accuracy as defined in the new ISO/DIS guideline 15197.2 (85.1-99.2% in this area for the other devices). Error-grid-analysis shows all Prestige IQ glucose results in clinically acceptable zones A and B (95.9% in zone A and 4.1% in zone B). In conclusion, Prestige IQ showed excellent performance with clinically acceptable accuracy and reliability as compared to both the laboratory reference and the four commercially available self-monitoring blood glucose systems.

Aged↗

PubMed2004

Normal p21Ras/MAP kinase pathway expression and function in PBMC from patients with polycystic ovary disease.

Polycystic ovary disease (PCOD) is associated with insulin resistance and increased prevalence of type II diabetes mellitus (T2DM). The p21Ras/MAP kinase is a major intracellular signaling pathway mediating insulin signaling in insulin responsive tissues. The expression, regulation and function of the p21Ras/MAP kinase pathway in PCOD patients were examined. Peripheral blood mononuclear cells (PBMC) were isolated from ten patients with PCOD and ten controls. The expression of p21Ras and its regulatory proteins; hSOS1 and p120GAP were studied. The basal and phytohemaglutinin (PHA) or insulin stimulated phosphorylation of MAP kinase was determined. Expression of p21Ras, and its regulatory proteins hSOS1 and p120GAP were similar in PCOD patients and controls. Basal, PHA and insulin stimulated phosphorylation of MAP kinase, were also comparable in the two groups as well as their PBMC proliferative response. These data indicate that the expression and overall function of the p21Ras/MAP kinase pathway remain intact in non-diabetic patients with PCOD.

Adult↗

PubMed2004

Modification of beta-cell response to different postprandial blood glucose concentrations by prandial repaglinide and combined acarbose/repaglinide application.

This study was designed to compare the effects of repaglinide plus acarbose combination treatment to repaglinide alone on postprandial glucose, serum insulin, C-peptide and proinsulin concentrations. A total of 40 patients with Type 2 diabetes (T2DM) (fasting blood glucose: 120-180 mg/dl; postprandial blood glucose: 140-240 mg/dl) were included in this single-centre, controlled, randomised, single-dose, cross-over study. On two consecutive days, patients either received 2 mg repaglinide 15 min before breakfast followed by 100 mg acarbose with breakfast or repaglinide alone. Two fasting (7.30 h, 8.00 h) and five postprandial blood samples (from 8.30 h to 12.00 h) were taken for blood glucose, serum insulin, C-peptide and proinsulin determination. Repaglinide plus acarbose treatment significantly reduced the mean increase in postprandial blood glucose levels (24.2+/-18.2 mg/dl) compared to repaglinide alone (51.1+/-29.0 mg/dl; p<0.001). Serum insulin, C-peptide and proinsulin levels [mean area under the curve (AUC7.30-12.00h)] were significantly lower than those observed with repaglinide monotherapy (e.g. insulin: 1089.2+/-604.5 hr x pmol/l and 1596.8+/-1080.6 hr x pmol/l, resp., p<0.001), suggesting that acarbose modifies the rapid insulin release induced by repaglinide. Prandial treatment with a combination of acarbose and repaglinide results in an additive glucose lowering effect and modified insulin secretion compared to repaglinide alone. Postprandial hyperglycaemia is not abolished by rapid stimulation of insulin release induced by repaglinide. Additional reduction of postprandial blood glucose by acarbose modifies the stimulation of insulin release.

Acarbose↗

PubMed2004

[Molecular pathophysiology of late complications diabetes mellitus--hyperglycemia-induced changes].

Late diabetic complications due to vascular and extravascular impairments develop as a consequence of chronic diabetes mellitus. Extent of affection reflects disease duration and therapeutic compensation; however, other modulating factors are involved. Due to growing incidence and permanent shift to younger age diabetes represents serious health problem. T2DM develops in consequence of "dysadaptation" of human genome to rapidly changing environment and life style. Primary prevention of diabetes is rather limited at present, secondary prevention or minimalization of late consequences is practically achievable. Full understanding of pathogenesis and identification of high-risk diabetic subjects will help to upgrade therapeutical options and improve patient's prognosis. This review devoted to late diabetic complications will summarize recent findings about proximal hyperglycaemia-induced alterations leading to common pathogenic action - inhibition of glycolysis on the level of GAPDH due to increased ratio NADH/NAD+, generation of superoxide and intracellular accumulation of dicarbonyls. Activated expression of series of genes leads to tissue remodelation responsible for organ manifestation. Subsequent article will deal with putative genetic susceptibility to their development.

Diabetes Complications↗

PubMed2005

Insulin resistance syndrome. A review.

Insulin is a hormone and a growth factor that elicits a myriad variety of metabolic and mitogenic cellular actions. Insulin resistance (IR) could occur with any of the effects of insulin, even though it usually refers to its ability to stimulate glucose uptake in insulin-sensitive peripheral tissues such as fat and muscle. IR as it applies to the glucose-insulin relationship is distinctly different from the clinical concept of an IR syndrome, which applies to a cluster of metabolic disorders (type 2 diabetes mellitus [T2DM], central obesity, dyslipidemia, hypertension, increased prothrombotic and antifibrinolytic factors/ hypercoagulability and a predilection for heart disease). The rising obesity epidemic portends great significance, as it is associated with a high prevalence of IR. We review the etiopathogenesis of IR, the clinical spectrum, and review the clinical data on the management of IR.

Animals↗

PubMed2006

Psychological stress and new onset diabetes.

The precise role of psychological stress in mediating the development of various forms of diabetes is controversial. Recent data from animal studies and large epidemiological studies in humans provide strong linkage between psychological stress and diabetes. This review focuses on the current evidence linking T1DM and T2DM and psychological stress and illustrates the inherent difficulty in overcoming this controversial issue.

Adolescent↗

PubMed2005

Obese adolescent girls with polycystic ovary syndrome (PCOS) have more severe insulin resistance measured by HOMA-IR score than obese girls without PCOS.

UNLABELLED: The prevalence of obesity in Thai children is increasing. These individuals are at increased risks of metabolic syndrome that includes insulin resistance, type 2 diabetes mellitus (T2DM), polycystic ovary syndrome (PCOS), dyslipidemia and hypertension. PCOS has been known to be associated with insulin resistance. OBJECTIVES: To compare the insulin sensitivity between obese adolescent girls with PCOS and those without PCOS. MATERIAL AND METHOD: We reviewed demographic and hormonal data of 6 obese adolescent girls with PCOS and compared with 6 age, weight and BMI-matched non-PCOS controls. Each subject underwent an oral glucose tolerance test. RESULTS: Homeostasis model assessment of insulin resistance score (HOMA-IR score) in obese adolescent girls with PCOS was significantly higher than in girls without PCOS with median and range as follows (16.5 [3.8, 21.8] vs. 4.1 [3.3, 6.9], p = 0.04). Our study demonstrates that obese adolescent girls with PCOS have more severe insulin resistance measured by HOMA-IR score than girls without PCOS independent of the degree of obesity. Since insulin resistance is a metabolic precursor of future cardiovascular diseases, obese adolescent girls with PCOS might be at greater risk of developing cardiovascular disease in later adulthood than their non-PCOS counterparts.

Adolescent↗

PubMed2006

Low birth weight and endocrine dysfunction in postnatal life.

Small size at birth has long been recognized as a factor increasing neonatal morbidity and mortality. During the last decade, reduced growth in early life has also been strongly linked with a number of endocrine dysfunctions. Included among the most important alterations are insulin insensitivity, gonadal and somatotropic axis abnormalities and premature adrenarche. These have been associated with an escalating prevalence of T2DM and CHD abnormal gonads and genitalia, growth hormone resistance and decreased growth as well as early puberty. The usual hypothesis proposed to explain the development of these long term alterations relates to the thrifty phenotype as an adaptive response to in utero malnutrition and modifications thereof; called "Fetal Origins" and updated to "Developmental Origins" which include the additional contributions of the patterns of growth in infancy and childhood. In this paper the factors that participate in the programming of the fetus and infants that lead to endocrine dysfunction in postnatal life is reviewed.

Adrenal Glands↗

PubMedDate not supplied

[Nutritional genomics: toward a personalized diet].

Nutrigenomics is the application of high-throughput genomics tools to the study of diet-gene interactions in order to identify dietetic components having beneficial or detrimental health effects. Nutrition becomes indeed one of the environmental factors influencing gene expression. We can consider nutrigenomics as a multidisciplinary science that comes after the human genome characterization and that put the genomic techniques besides the biochemical and epidemiological aspects, with the aim to understand the etiologic aspects of chronic diseases such as cancer, type 2 diabetes mellitus (T2DM), obesity, cardiovascular diseases (CVD), metabolic syndrome, etc. Nutrigenomics is linked to nutrigenetics, which studies the genetic basis of the different individual response to the same nutritional stimulus. This phenomenon arises from gene polymorphism. As a consequence genes are important in determining a function, but nutrition is able to modify the degree of gene expression. These are however theories only at an early stage, but a perspective in the change of dietetic intervention is emerging. A really personalized diet will be a diet considering the nutritional status, the nutritional needs based on age, body composition, work and physical activities, but also considering the genotype. The integration of all these information and in particular the ones arising from genomic, proteomic and metabolomic analyses will be useful to define the "nutritional phenotype".

Diet↗

PubMed2006

[Clinical characteristics of early-onset type 2 diabetes and risk factors associated with its chronic complications].

OBJECTIVE: To investigate the clinical characteristics of early-onset type 2 diabetes (EOD) and the risk factors associated with its chronic complications. METHODS: A total of 2713 T2DM patients were recruited and divided into two groups: early- and late-onset groups EOD group (diagnosed at the age 40). The clinical characteristics were compared between two groups, and the risk factors were analyses within the early-onset group. RESULTS: (1) The EOD patients were characterized by significantly higher levels of triglycerides (2.5 +/- 2.4 mmol/L vs 1.9 +/- 1.5mmol/L, P < 0.01) and BMI (24.4 kg/m(2) +/- 4.6 kg/m(2) vs 23.6 kg/m(2) +/- 3.7 kg/m(2), P < 0.01), higher rates of smoking (29.2% vs 22.0%, P < 0.01), family history of diabetes (28.6% vs 13.1%, P < 0.01), and higher prevalence of metabolic syndrome (18.9% vs 10.7%, P < 0.01), higher proportion of patients with unacceptable HbA1c (>7.0%) (77.3% versus 72.7%, P < 0.05) and fasting blood glucose >or= 7.0 mmol/L, (80.8% versus 74.6%, P < 0.05). (2) The prevalence rates of microvascular complications were higher than those of macrovascular complications in the EOD group, and the prevalence rates of pain, anesthesia, diarrhea, and nephropathy were 10.6%, 6.20%, 6.00%, and 13.00% respectively, all significantly higher than those of the LOD group (7.10%, 2.80%, 3.70%, and 8.00% respectively, P < 0.05, < 0.01, < 0.05, and < 0.01). Linear regression analysis showed that certain subsets of chronic complications were associated with onset age, diabetes duration, hypertension, family history and high level of triglyceride. CONCLUSION: Early-onset DM patients present the clinical features of poorer metabolic profiles, which may contribute to the development of certain subsets of microvascular complications. Late-onset patients tend to be complicated with macrovascular diseases, such as cerebrovascular disease, angiocardiopathy, etc. Multiple factor comprehensive control is important for the prevention of the complications.

Adult↗

PubMed2026

Design, synthesis and biological evaluation of hydroxybenzothiazole-linked benzothiazole/benzoxazole conjugates as potent dual α-amylase and α-glucosidase inhibitors.

The current study focuses on the synthesis and evaluation of novel Hydroxybenzothiazole-Linked Benzothiazole/Benzoxazole Conjugates to target Diabetes Mellitus (DM) by inhibiting α-amylase and α-glucosidase. Spectroscopic methods, including 1H and 13C NMR spectroscopy, were employed to confirm the structures of newly synthesized conjugates. The findings of in-vitro analysis displayed that the synthesized derivatives inhibited α-amylase and α-glucosidase enzymes with IC50 values ranging from 3.65 ± 0.20 μM to 32.15 ± 3.20 μM on α-amylase and 5.92 ± 0.80 μM to 35.60 ± 3.40 μM on α-glucosidase, in contrast to the reference drug Acarbose (α-amylase IC50 = 8.25 ± 0.80 μM; α-glucosidase IC50 = 10.75 ± 1.10 μM). Among the series 9a-9f and 10a-10f, analogs 10 f, 10b, 9b, and 9e displayed superior anti-diabetic activity compared to the reference drug Acarbose. The inhibitory activity of these conjugates can be attributed to their favorable and stable interactions with critical amino acid residues of targeted enzymes, as revealed through molecular docking analysis. ADMET predictions and drug-likeness evaluations showed favorable pharmacokinetic features, while DFT investigations revealed electronic insights related to bioactivity. Experimental outcomes and in silico support display that these potent Hydroxybenzothiazole-Linked Benzothiazole/Benzoxazole Conjugates were comparable to an existing diabetic mellitus inhibitor while conserving an acceptable safety profile, specifying potential for further therapeutic development and optimization against diabetic Mellitus.

Benzothiazoles↗