Non-obese Diabetics Research Articles

SHORT TERM EFFECT OF LAPAROSCOPIC SLEEVE GASTRECTOMY ON CLINICAL, RENAL PARAMETERS AND URINARY NGAL LEVELS IN DIABETIC AND NON DIABETIC OBESITY.

Although diseases such as diabetes, hypertension, obstructive sleep apnea and hyperlipidemia are clearly documented as obesity associated diseases, it is not well-known whether obesity causes renal pathologies. The aim of the present study was to evaluate the effect of weight loss following laparoscopic sleeve gastrectomy on clinical, renal parameters and urinary Neutrophil gelatinase-associated lipocalin (NGAL) levels in diabetic and non-diabetic obese patients. Nineteen morbidly obese patients (10 diabetic and 9 non diabetic) who underwent laparoscopic sleeve gastrectomy were evaluated clinically (anthropometric measurements) and biochemically before surgery and at 6 months from surgery. Significant decreases in weight, BMI, FPG, PPG and HbA1c levels were observed in the diabetic group when the baseline and 6th month parameters of the patients were compared. There was also a significant decrease in SBP and DBP. At 6th month following laparoscopic sleeve gastrectomy, renal parameters such as creatinine, mAlb/creatinine, NGAL/creatinine did not differ in the diabetic group. In the nondiabetic group, serum creatinine levels were significantly decreased, but other renal parameters such as mAlb/creatinine and NGAL/creatinine were not significantly different. Our findings revealed significant decreases in weight, body mass index and glycemic parameters after sleeve gastrectomy in diabetic and non-diabetic patients, while no significant alteration was noted in renal functions, urinary NGAL and microalbumin levels.

Metabolomic analysis of obesity, metabolic syndrome, and type 2 diabetes: amino acid and acylcarnitine levels change along a spectrum of metabolic wellness.

BackgroundMetabolic syndrome (MS) is a construct used to separate “healthy” from “unhealthy” obese patients, and is a major risk factor for type 2 diabetes (T2D) and cardiovascular disease. There is controversy over whether obese “metabolically well” persons have a higher morbidity and mortality than lean counterparts, suggesting that MS criteria do not completely describe physiologic risk factors or consequences of obesity. We hypothesized that metabolomic analysis of plasma would distinguish obese individuals with and without MS and T2D along a spectrum of obesity-associated metabolic derangements, supporting metabolomic analysis as a tool for a more detailed assessment of metabolic wellness than currently used MS criteria.MethodsFasting plasma samples from 90 adults were assigned to groups based on BMI and ATP III criteria for MS: (1) lean metabolically well (LMW; n = 24); (2) obese metabolically well (OBMW; n = 26); (3) obese metabolically unwell (OBMUW; n = 20); and (4) obese metabolically unwell with T2D (OBDM; n = 20). Forty-one amino acids/dipeptides, 33 acylcarnitines and 21 ratios were measured. Obesity and T2D effects were analyzed by Wilcoxon rank-sum tests comparing obese nondiabetics vs LMW, and OBDM vs nondiabetics, respectively. Metabolic unwellness was analyzed by Jonckheere-Terpstra trend tests, assuming worsening health from LMW → OBMW → OBMUW. To adjust for multiple comparisons, statistical significance was set at p < 0.005. K-means cluster analysis of aggregated amino acid and acylcarnitine data was also performed.ResultsAnalytes and ratios significantly increasing in obesity, T2D, and with worsening health include: branched-chain amino acids (BCAAs), cystine, alpha-aminoadipic acid, phenylalanine, leucine + lysine, and short-chain acylcarnitines/total carnitines. Tyrosine, alanine and propionylcarnitine increase with obesity and metabolic unwellness. Asparagine and the tryptophan/large neutral amino acid ratio decrease with T2D and metabolic unwellness. Malonylcarnitine decreases in obesity and 3-OHbutyrylcarnitine increases in T2D; neither correlates with unwellness. Cluster analysis did not separate subjects into discreet groups based on metabolic wellness.DiscussionLevels of 15 species and metabolite ratios trend significantly with worsening metabolic health; some are newly recognized. BCAAs, aromatic amino acids, lysine, and its metabolite, alpha-aminoadipate, increase with worsening health. The lysine pathway is distinct from BCAA metabolism, indicating that biochemical derangements associated with MS involve pathways besides those affected by BCAAs. Even those considered “obese, metabolically well” had metabolite levels which significantly trended towards those found in obese diabetics. Overall, this analysis yields a more granular view of metabolic wellness than the sole use of cardiometabolic MS parameters. This, in turn, suggests the possible utility of plasma metabolomic analysis for research and public health applications.

Irisin levels in LMNA-associated partial lipodystrophies

AimThe adipo-myokine irisin regulates energy expenditure and fat metabolism. LMNA-associated familial partial lipodystrophy (FPLD2) comprises insulin resistance, muscle hypertrophy and lipoatrophy. The aim of this study was to investigate whether irisin could be a biomarker of FPLD2. Patients and methodsThis case control study included 19 FPLD2 subjects, 13 obese non-diabetic (OND) patients and 19 healthy controls (HC) of normal weight (median BMI: 26, 39 and 22 kg/m2, respectively). Serum irisin and leptin levels, body composition (DXA/MRI) and metabolic/inflammatory parameters were compared in these three groups. ResultsBMI and MRI intra-abdominal fat significantly differed among these three groups, whereas DXA total fat mass and leptin levels were higher in the OND group, but did not differ between HC and FPLD2. Lipodystrophy patients had higher intra-abdominal/total abdominal fat ratios than the other two groups. Irisin levels were higher in FPLD2 and OND patients than in HC (medians: 944, 934 and 804 ng/mL, respectively). However, irisin/leptin ratios and lean body mass percentages were strikingly higher, and lean mass indices lower, in FPLD2 and HC than in the OND (median irisin/leptin ratios: 137, 166 and 21, respectively). In the entire study group, irisin levels positively correlated with BMI, lean body mass and index, intra-abdominal/total abdominal fat ratio, triglyceride, cholesterol, insulin, glucose and HbA1c levels. Also, intra-abdominal/total abdominal fat ratio and lean body mass better differentiated the three groups only in female patients. ConclusionCirculating irisin is similarly increased in FPLD2 and OND patients, who are characterized by higher lean body mass regardless of their clearly different fat mass. However, irisin/leptin ratios, strikingly higher in FPLD2 than in OND patients, could help to make the diagnosis and prompt genetic testing in clinically atypical cases.

Elevated ANGPTL5 Level in the Circulation of Obese and Type 2 Diabetic People

Angiopoetin like protein family is composed of eight members that are involved in regulating various metabolic processes. ANGPTL5 is one of the members of this family that is mainly expressed in the heart and was showed to stimulate the expansion of human cord blood hematopoietic stem cell ex-vivo. This study was designed to investigate the expression level of this protein in the plasma of obese and diabetic people. Methods: A total of 204 people were enrolled in this study including 109 nondiabetic and 95 type 2 diabetics. The nondiabetic people included 70 non-obese (BMI&amp;lt;30 Kg/m2) and 39 obese people (BMI&amp;lt;30 Kg/m2), while the diabetic people included 34 non-obese and 61 obese people. ANGPTL5 plasma level was measured by ELISA. Results: In this study we showed that ANGPTL5 level was increased in the plasma of diabetic people (5.78±2.59 ng/mL) compared to nondiabetics (4.42 ± 2.32 ng/mL) (p-Value&amp;lt;0.0001). Obese nondiabetics had a significantly higher level of ANGPTL5 (5.12±2.23 ng/mL) compared to non-obese people (4.02 ± 2.27 ng/mL) (p-Value=0.029). Obese diabetic had higher level of ANGPTL5 compared non-obese yet did not reach significance (p-Value=0.064). ANGPTL5 was significantly associated with glycated haemoglobin 1C and insulin resistance as measured by HOMA-IR. Conclusion: Our data shows for the first time that ANGPTL5 was increased in diabetic and obese people. Given its unique tissue expression in the heart, ANGPTL5 might modulate its response to insulin resistance through its interaction with other proteins including other ANGPTL proteins. Further analysis will be required to better understand the interaction between ANGPTL5 and other metabolic related biomarkers to shed more light on its role in diabetes and obesity. Disclosure N. Alhasawi: None. M. Qaddoumi: None. F. Almulla: None. J. Tuomilehto: None. M. Alanbaei: None. J. Abubaker: None.

From diabetes remedy to diabetes remission; could single-anastomosis gastric bypass be a safe bridge to reach target in non-obese patients?

Type 2 diabetes mellitus (T2DM) is considered a chronic progressive incurable metabolic disease. Single-anastomosis gastric bypass (SAGB) has proved to be effective in obese patients, yet its impact on non-obese diabetics is not extensively studied. The aim is to determine the anthropometric and glycemic outcomes of SAGB as a proposed line of treatment for T2DM patients with body mass index (BMI) 25-30 kg/m2. From November 2013 to March 2016, a prospective study has been conducted at Ain-Shams University Hospitals on 17 consecutive patients who have undergone SAGB. The demographic and anthropometric data, as well as the relevant laboratory results, were reported. Complete T2DM remission is considered if glycosylated hemoglobin (HbA1c) <6 % for at least 1 year without medication, whereas partial remission is considered if HbA1c<6.5%. The mean age was 42.6 ±13.8 years, mean BMI was 26.7 ± 2.3 kg/m2 and mean duration of DM was 6.3 ± 2.7 years. The mean baseline values of HbA1c, FPG (fasting plasma glucose), and 2-hours postprandial glucose (2-H PPG) were 9.9%, 176.3 mg/dl, and 310.3 mg/dl respectively. These values significantly dropped at the 18th month to reach 5.8%, 93.4 mg/dl, and 156.2 mg/dl, with 13/17 patients became off-treatment (complete remission rate 76.4%). T2DM patients with BMI 25-30 kg/m2 are considered the most controversial group. SAGB is an efficient metabolic procedure and could be integrated into the treatment algorithm of T2DM. Such line of treatment opens new horizons to change the concept of treatment from diabetes remedy to diabetes remission.

Elevated glycohemoglobin HbA1c is associated with low back pain in nonoverweight diabetics

Background ContextLow back pain (LBP) is a common complaint in clinical practice of multifactorial origin. Although obesity has been thought to contribute to LBP primarily by altering the distribution of mechanical loads on the spine, the additional contribution of obesity-related conditions such as diabetes mellitus (DM) to LBP has not been thoroughly examined. PurposeTo determine if there is a relationship between DM and LBP that is independent of body mass index (BMI) in a large cohort of adult survey participants. Study DesignRetrospective analysis of prospectively collected National Health and Nutrition Examination Survey (NHANES) data to characterize associations between LBP, DM, and BMI in adults subdivided into 6 subpopulations: normal weight (BMI 18.5–25), overweight (BMI 25–30), and obese (BMI >30) diabetics and nondiabetics. Diabetes was defined with glycohemoglobin A1c (HbA1c) ≥6.5%. Patient Sample11,756 participants from NHANES cohort. Outcome MeasuresPercentage of LBP reported. MethodsLBP reported in the 1999-2004 miscellaneous pain NHANES questionnaire was the dependent variable examined. Covariates included HbA1c, BMI, age, and family income ratio to poverty as continuous variables as well as race, gender, and smoking as binary variables. Individuals were further subdivided by weight class and diabetes status. Regression and graphical analyses were performed on the study population as a whole and also on subpopulations. ResultsIncreasing HbA1c did not increase the odds of reporting LBP in the full cohort. However, multivariate logistic regression of the 6 subpopulations revealed that the odds of LBP significantly increased with increasing HbA1c levels in normal weight diabetics. No other subpopulations reported significant relationships between LBP and HbA1c. LBP was also significantly associated with BMI for normal weight diabetics and also for obese subjects regardless of their DM status. ConclusionsLBP is significantly related to DM status, but this relationship is complex and may interact with BMI. These results support the concept that LBP may be improved in normal weight diabetic subjects with improved glycemic control and weight loss, and that all obese LBP subjects may benefit from improved weight loss alone.

Serum obestatin level strongly correlates with lipoprotein subfractions in non-diabetic obese patients

BackgroundObestatin is a ghrelin-associated peptide, derived from preproghrelin. Although many of its effects are unclear, accumulating evidence supports positive actions on both metabolism and cardiovascular function. To date, level of obestatin and its correlations to the lipid subfractions in non-diabetic obese (NDO) patients have not been investigated.MethodsFifty NDO patients (BMI: 41.96 ± 8.6 kg/m2) and thirty-two normal-weight, age- and gender-matched healthy controls (BMI: 24.16 ± 3.3 kg/m2) were enrolled into our study. Obestatin level was measured by ELISA. Low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subfractions, intermediate density lipoprotein (IDL) and very low-density lipoprotein (VLDL) levels and mean LDL size were detected by nongradient polyacrylamide gel electrophoresis (Lipoprint).ResultsSerum level of obestatin was significantly lower in NDO patients compared to controls (3.01 ± 0.5 vs. 3.29 ± 0.6 μg/ml, p < 0.05). We found significant negative correlations between the level of obestatin and BMI (r = − 0.33; p < 0.001), level of serum glucose (r = − 0.27, p < 0.05), HbA1c (r = − 0.38; p < 0.001) and insulin (r = − 0.34; p < 0.05). Significant positive correlation was found between obestatin level and the levels of ApoA1 (r = 0.25; p < 0.05), large HDL subfraction ratio and level (r = 0.23; p < 0.05 and r = 0.24; p < 0.05), IDL (r = 0.25 p < 0.05) and mean LDL size (r = 0.25; p < 0.05). Serum VLDL ratio and level negatively correlated with obestatin (r = − 0.32; p < 0.01 and r = − 0.21; p = 0.05). In multiple regression analysis obestatin was predicted only by VLDL level.ConclusionsBased on our data, measurement of obestatin level in obesity may contribute to understand the interplay between gastrointestinal hormone secretion and metabolic alterations in obesity.

Age at onset of obesity, transcription factor 7-like 2 (TCF7L2) rs7903146 polymorphism, adiponectin levels and the risk of type 2 diabetes in obese patients.

IntroductionInteraction between obesity and genetic factors involved in the regulatory pathways of glucose homeostasis may play a significant role in diabetes development in the obese. The aim of this study was to investigate the associations between the TCF7L2 rs7903146 polymorphism, adiponectin levels, age at onset of obesity and the occurrence of type 2 diabetes (T2D) in a sample of obese Polish adults.Material and methodsA total of 474 unrelated obese subjects were included in this study. Real-time PCR was used to detect the TCF7L2 rs7903146 polymorphism. Serum level of adiponectin was determined by the ELISA method. Standard assays were used to measure total cholesterol, HDL cholesterol, triglycerides, glucose and HbA1c concentrations. We used multiple logistic regression to identify factors associated with type 2 diabetes.ResultsWe found that the T allele of rs7903146 was significantly associated with T2D risk (odds ratio of 1.59 for T allele, p = 0.005). This association persisted after adjusting for confounders in the recessive model (odds ratio of 3.54 for TT genotype, p = 0.011). Serum adiponectin levels were significantly lower in diabetic subjects than in nondiabetic individuals (3.6 vs. 5.6 µg/ml, p < 0.001). Participants who were obese at age ≥ 20 years had significantly higher odds of having T2D (OR = 4.94) than those with the onset of obesity before 20 years (p < 0.001).ConclusionsOur study highlights the significance of the relationship between the TCF7L2 polymorphism, a person’s age at onset of obesity and the prevalence of T2D, and confirms lower adiponectin levels in obese diabetics in comparison to obese nondiabetics.

Serum afamin level is strongly associated to the components of metabolic syndrome in non-diabetic obese patients

Aim: The human plasma vitamin E-binding protein afamin was reported to be highly significantly associated with the components for metabolic syndrome in three independent human general populations. Data from afamin-transgenic mice also suggest a role of afamin in the development of metabolic syndrome. To date, level of afamin and its correlations to the components of metabolic syndrome in non-diabetic obese (NDO) patients has not been investigated.

Obesity risk prediction among women of Upper Egypt: The impact of serum vaspin and vaspin rs2236242 gene polymorphism

BackgroundVaspin is an adipokine that is potentially linking obesity, insulin resistance, metabolic syndrome and type-2 diabetes. AimThe present study aimed to investigate the impact of vaspin rs2236242 gene polymorphism on the risk of obesity, diabetes, their metabolic traits, and serum vaspin levels in a sample of Upper Egyptian women. Subjects and methodsA total of 224 subjects, 112 obese (62 non diabetics, 50 diabetics) and 112 controls were included in this case control study. Vaspin gene rs2236242 polymorphism was performed using tetra-amplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) and serum vaspin levels were estimated by ELISA. ResultsThe minor (A) allele of vaspin rs2236242 gene polymorphism was significantly lower in obese (30.8%) than controls (43.7%) (P=0.005). The protective effect was evident in dominant and recessive inheritance models (TT vs TA+AA, P=0.004 and TT+TA vs AA, P=0.036). After adjusting genotypes for diabetes there were no significant association between vaspin rs2236242 gene polymorphism and obesity but significant association was maintained in the obese diabetics. Vaspin serum levels were found to be lower in minor protective (AA) genotype carriers than the other two genotypes (P<0.001). In the mean-time serum vaspin levels were significantly higher in obese diabetics and non-diabetics than controls (P<0.001 each).There were significant positive correlations between vaspin levels and hs-CRP, cholesterol, LDL-C, fasting glucose, HOMA-IR, insulin, and ALT values (P<0.05 each) and a negative correlation with HDL-C (P<0.01). ConclusionThe minor A allele of vaspin rs2236242 polymorphism plays a protective role against obesity and diabetes but this relation is largely ascribed to its effect on insulin resistance. The serum vaspin concentration was lower in minor protective allele carriers. To the best of our knowledge, this is the first study of vaspin SNP in Upper Egyptian women. The entire understanding of vaspin intimate mechanistic action might enable the development of novel etiology-based treatment strategies for obesity, the complex genetic trait.

RETRACTED ARTICLE: TREM-1 associated macrophage polarization plays a significant role in inducing insulin resistance in obese population

BackgroundTREM-1 acts as an amplifier of inflammation expressed on macrophages. The objective of this study was to evaluate the relationship between TREM-1 and macrophage polarization, and association of TREM-1 and M1 macrophage polarization with insulin resistance (IR) in obese population compared to non-obese population.MethodsWe enrolled 38 patients after obtaining IRB approval for this study. We evaluated the mRNA and protein expression levels of general macrophage marker (CD68), M1 marker (CD86, CCR7, iNOS, IFNγ, TNF-α and IL-6,), M2 marker (CD206, CD163, IL-10, IL-4) and chemokine axis (MCP-1, CCR2 and CCR5) along with TREM-1 and TREM-2 in omentum fat, subcutaneous fat, and liver biopsy tissues of non-obese (N = 5), obese non-diabetics, (N = 16) and obese diabetics (N = 17).ResultsThe results of our study showed over-expression of TREM-1, M1 markers and down-regulation of TREM-2 and M2 markers in the omentum, subcutaneous and liver biopsies of obese patients (diabetics and non-diabetics) compared to non-obese patients. Overall, the obese diabetic group showed a significant (p < 0.05) higher number of patients with over expression of M1 markers (TREM-1, CD68, CD86, CCR-7, iNOS, IFN-γ, TNF-α, IL-6, MCP-1, CCR-2 and CCR-5) and down-regulation of M2 markers (CD206, CD163 and IL-4) in liver biopsy compared to obese non-diabetics.ConclusionsTREM-1 expression is significantly increased along with the M1 markers in liver biopsy of obese diabetic (17/17) and obese non-diabetic patients (9/16). Our data suggests that TREM-1 overexpression and M1 macrophage polarization are associated with obesity-induced IR.

Association of 4-hydroxynonenal with classical adipokines and insulin resistance in a Chinese non-diabetic obese population.

The prevalence of obesity is increasing worldwide. Oxidative stress plays an etiological role in a variety of obesity-related metabolic disorders. 4-hydroxynonenal (4-HNE) is the most abundant and reactive aldehydic product derived from the peroxidation of n-6 polyunsaturated fatty acids with diverse biological effects that are not well detailed. Obesity is associated with decreased plasma adiponectin concentrations and increased production of lipid peroxidation products, including 4-HNE, in adipose tissue. There may be some association between the level of adipokines and 4-HNE. To analyze the associations between 4-HNE and classical adipokines, namely, adiponectin and leptin in a Chinese population, the plasma 4-HNE, adiponectin and leptin levels of 160 non-diabetic obese (NDO) patients and 160 healthy subjects were determined by ELISA, and their associations with adiposity, glucose, lipid profiles, insulin secretion and insulin sensitivity were studied. Plasma 4-HNE levels were significantly increased in patients with NDO compared with healthy controls (p < 0.01). 4-HNE was negatively correlated with adiponectin and positively correlated with leptin. The plasma levels of 4-HNE were significantly correlated to several parameters involved in body mass index (BMI) and insulin resistance (IR). The 4-HNE levels were positively correlated with BMI and negatively correlated with insulin sensitivity. We conclude that 4-HNE is associated with the secretion of adiponectin and leptin and is correlated with IR in NDO humans. These findings indicate a pro-inflammatory role of 4-HNE in NDO patients, which supports the potential role of 4-HNE in the development of obesity-related disorders.

Association of oral microbiome with type 2 diabetes risk.

The oral microbiome may help to maintain systemic health, including how it affects blood glucose levels; however, direct evidence linking the oral microbiome with diabetes is lacking. We compared the oral microbiome profiles of 98 participants with incident diabetes, 99 obese non-diabetics and 97 normal weight non-diabetics, via deep sequencing of the 16S rRNA gene. We found that the phylum Actinobacteria was present significantly less abundant among patients with diabetes than among the controls (p = 3.9 × 10-3 ); the odds ratio (OR) and 95% confidence interval (CI) was 0.27 (0.11-0.66) for those individuals who had relative abundance higher than the median value. Within this phylum, five families and seven genera were observed, and most of them were less abundant among patients with diabetes. Notably, genera Actinomyces and Atopobium were associated with 66% and 72% decreased risk of diabetes with p-values of 8.9 × 10-3 and 7.4 × 10-3 , respectively. Stratified analyses by race showed that most taxa in this phylum were associated with diabetes in both black and white participants. This phylum was also less abundant among non-diabetic obese subjects compared to normal weight individuals, particularly genera Mobiluncus, Corynebacterium and Bifidobacterium, which showed p < 0.05. Our study revealed that multiple bacteria taxa in the phylum Actinobacteria are associated with the risk of type 2 diabetes. Some are also associated with the prevalence of obesity, suggesting that the oral microbiome may play an important role in diabetes etiology.

Insulinotropic effects of GPR120 agonists are altered in obese diabetic and obese non-diabetic states.

G-protein-coupled receptor 120 (GPR120) is a putative target for obesity and diabetes therapies. However, it remains controversial whether resident GPR120 plays a direct regulatory role in islet β-cell insulin secretion. The present study examined this issue in isolated rodent islets and rat β-cell line INS-1E, and assessed the role of GPR120in islet insulin secretion in obese non-diabetic (OND) and diabetic states. GPR120 expression was detected in rodent islet β-cells. Docosahexaenoic acid (DHA) and synthetic GPR120 agonist GSK137647 (GSK) augmented insulin release from rat/mouse islets and INS-1E; DHA effects were partially mediated by GPR40. GPR120 knockdown and overexpression attenuated and enhanced DHA effects in INS-1E respectively. DHA and GSK improved postprandial hyperglycaemia of diabetic mice. Inhibition of calcium signalling in INS-1E reduced GPR120 activation-induced insulinotropic effects. The insulinotropic effects of DHA/GSK were amplified in OND rat islets, but diminished in diabetic rat islets. GPR120 and peroxisome proliferator-activated receptor γ (PPARγ) expression were elevated in OND islets and palmitic acid (PA)-treated INS-1E, but reduced in diabetic islets and high glucose-treated INS-1E. PPARγ activation increased GPR120 expression in rat islets and INS-1E. DHA and GSK induced protein kinase B (Akt)/extracellular signal-regulated kinase (ERK) phosphorylation in rodent islets and INS-1E, and these effects were altered in OND and diabetic states. Taken together, the present study indicates that (i) GPR120 activation has an insulinotropic influence on β-cells with the involvement of calcium signalling; (ii) GPR120 expression in β-cells and GPR120-mediated insulinotropic effects are altered in OND and diabetic states in distinct ways, and these alterations may be mediated by PPARγ.

Serum uric acid levels are associated with obesity but not cardio-cerebrovascular events in Chinese inpatients with type 2 diabetes

We aim to explore the associations between serum uric acid (SUA) and obesity and cardio-cerebrovascular events (CCEs) in Chinese inpatients with type 2 diabetes mellitus (T2DM). 2 962 inpatients with T2DM were stratified into quartile based on SUA concentrations. There were significant increases in the prevalence of both obesity (32.6%, 41.9%, 50.1%, and 62.8%, respectively, p < 0.001 for trend) and severe obesity (0.4%, 0.6%, 0.8%, and 1.3%, respectively, p < 0.001 for trend) across the SUA quartiles. A fully adjusted multiple logistic regression analysis revealed that SUA quartiles were independently associated with the presence of obesity (p < 0.001). The prevalence of CCEs was significantly higher in the obese diabetics than in the nonobese diabetics (16.8% vs. 13.2%, p = 0.027). After controlling for multiple confounding factors, BMI levels were also significantly correlated with the presence of CCEs (p = 0.020). However, there was no significant association of SUA quartiles/SUA levels with the presence of CCEs in T2DM. This study suggested that SUA levels were independently associated with obesity but not with CCEs in patients with T2DM. In selected populations such as subjects with T2DM, the role of uric acid in cardiovascular complications might be attributable to other cardiovascular risk factors, such as obesity.

Stratification of Obstructive Sleep Apnea Risk in Obese non-Diabetics and Obese Diabetics

Introduction: The prevalence of OSA and its consequences are likely to increase in light of the current obesity epidemic. Studies have shown that the prevalence of OSA is significantly higher in the diabetes population. Recent studies have revealed that BMI and diabetes as significant independent predictors of OSA. Owing to little research in this field and lack of data from Central India, the present study aims at assessing the risk of development of obstructive sleep apnoea in obese and obese diabetic patients. Objectives: To find out the prevalence of OSA risk in obese patients with Diabetes mellitus using Berlin Questionnaire, to find out the prevalence of OSA risk in obese non diabetic patients, correlation of OSA risk with Body Mass Index, fasting blood sugar, HbA1c and Blood Pressure. Methodology: Twenty four obese diabetic patients (Group I) and thirty-five obese – non- diabetic patients (Group II) were selected from medicine OPD randomly. Results were matched with thirty-one healthy non-obese nondiabetic controls (Group III). Risk of OSA was assessed using pre designed, validated Berlin questionnaire. HbA1C and fasting blood sugars were done. Results: As per Berlin Questionnaire Category 1 showed 19 (79.17%), 21 (60%) and 7 (22.58%) cases as positive in ‘DM and Obese’, ‘No DM but Obese’ and ‘Control’ groups respectively, P-value<0.0001 using Chi-square test, Category 2 had 7 (29.17%), 6 (17.14%) and 0 cases as positive in ‘DM and Obese’, ‘No DM but Obese’ and Control groups respectively with P-value of 0.008 (P<0.05) using Chi-square test and Category 3 had 18 (75%), 25 (71.4%) and 1(3.23%) positive cases in ‘DM and Obese’, ‘No DM but Obese’ and ‘Control’ groups respectively, and the difference in the proportions was statistically significant with P-value<0.0001 using Chi-square test. Age above 40 years, female sex increased the risk of OSA. HbA1C was found out to be an independent risk factor for OSA risk. After adjusting for covariates for HbA1C, the OR obtained was 6.20 [95% CI: 1.37-28.07], with a P-value of 0.018 (P<0.05). Conclusion: Our study shows that the risk of OSA is significantly increases with increasing BMI, fasting blood glucose levels, mean arterial pressure and HbA1c levels. High risk of OSA was 58.9% in our study.

Transcription factor 7-like 2 (TCF7L2) gene polymorphisms are strong predictorsof type 2 diabetes among nonobese diabetics in the Turkish population.

Type 2 diabetes (T2D) is1397645907a multifactorial disease, determined by environmental and genetic factors. Currently, the transcription factor 7-like 2 (TCF7L2) gene shows the strongest association with T2D. In this study, we investigated whether TCF7L2 gene polymorphisms are associated with T2D in a Turkish population. Using PCR-RFLP and PCR-SSCP, we genotyped six intronic polymorphisms in the TCF7L2 gene, commonly associated with T2D, in 169 individuals with diabetes and 119 healthy controls. We found that rs7903146 C → T substitution in intron 3 (OR: 1.9, P = 0.005) and rs12255372 G → T substitution in intron 4 (OR: 2.1, P = 0.002) were significantly associated with T2D while other SNPs were not associated (P > 0.05). We determined no association between TCF7L2 gene polymorphisms and fasting glucose, fasting insulin, HbA1c, or HOMA-IR levels (P > 0.05), except for rs7903146 C → T substitution, which was significantly associated with the fasting glucose level (P = 0.003). Our results indicate that, in the Turkish population, the T allele of the rs7903146 (C → T) and rs12255372 (G → T) polymorphisms in the TCF7L2 gene is an independent risk factor for the development of T2D.

The Relation between Periodontopathogenic Bacterial Levels and Resistin in the Saliva of Obese Type 2 Diabetic Patients

This study aims to investigate the relation between resistin and periodontopathogenic bacterial levels in the saliva of obese adults compared to healthy control and to examine whether salivary resistin can serve as a biomarker of type 2 diabetes in obese patients. A total of 78 saliva samples were collected from patients attending to the University Dental Hospital, Sharjah, UAE. The patients were divided into three equal groups: obese diabetics, obese nondiabetics, and nonobese nondiabetic control. Salivary resistin was measured using ELISA. The levels of bacterial species associated with periodontitis (Treponema denticola, Porphyromonas gingivalis, Tannerella forsythia, and Actinobacillus actinomycetemcomitans) and gingivitis (Fusobacterium spp.) were measured using real-time PCR. Both salivary resistin and periodontopathogenic bacteria including Fusobacterium spp., P. gingivalis, and T. forsythia were detected in significantly higher quantities in the obese patients (diabetics and nondiabetics) than nonobese nondiabetic control. Resistin concentrations were significantly correlated with BMI; however, its level was not correlated with the blood glucose. In this study, high salivary resistin was associated with obesity, which is a major predisposing factor for type 2 diabetes and also a risk factor for oral diseases. The high levels of salivary periodontopathogenic bacteria could upregulate the local release of salivary resistin in obese people.

Occurrence of Diabetes Mellitus in Obese Nondiabetic Patients, with Correlative Analysis of Visceral Fat, Fasting Insulin, and Insulin Resistance: A 3-year Follow-up Study (Mysore Visceral Adiposity in Diabetes Follow-up Study).

Objective:To assess the occurrence of diabetes in obese nondiabetic patients over a 3-year follow-up period with a correlative analysis of visceral fat (VF), fasting insulin levels, (FILs) and insulin resistance (IR).Material and Methods:Thirty-seven obese and nineteen nonobese nondiabetics of our previous study, Mysore Visceral Adiposity in Diabetes were followed for the next 3 years. Their blood pressure, body mass index, waist circumference (WC), fasting blood sugar (FBS), FIL, lipid profile and subcutaneous fat (SCF), and VF measurement by US method were repeated every 6 months for the next 3 years. The findings were analyzed with appropriate statistical methods.Results:Twenty-three obese and 18 nonobese nondiabetics completed the study. There were 17 dropouts. The changes in the physical and biochemical characteristics of the two groups before and after the study were not significant. SCF had no correlation with IR whereas VF correlated with FIL and IR. There were three diabetics in the obese group and two from the control group at the end of the study. There were 12 impaired glucose tolerance (IGT) in the test group and 2 in the control group. Those who developed diabetes had higher VF, WC, FBS, FIL, and IR. Those who showed IGT also had these at higher levels compared to others. There was no change in the VF at the end of the study.Conclusions:This follow-up study on South Indians has shown that VF is a significant risk factor for the development of IR. IR can develop without any increase in the volume of the VF, is the essential finding of this study. SCF has not shown any significant relationship with IR. We recommend FBS and FIL in all the obese nondiabetics to calculate IR, which has given much insight in the development of IGT and diabetes. Large multicentric, longitudinal studies are required to establish the cause of IR.

Somatic neural alterations in non-diabetic obesity: a cross-sectional study.

BackgroundReports on alterations in somatic neural functions due to non-diabetic obesity, a major risk factor for diabetes, are few and still a matter of debate. Nevertheless, to our knowledge, reports lack any comments on the type of somatic nerve fibers affected in non-diabetic obesity. Therefore, this study aimed to find out the alteration in somatic neural functions in non-diabetic obese persons if any.MethodsThe study was conducted on 30 adult non-diabetic obese persons (mean age 32.07 ± 7.25 years) with BMI > 30 Kg/m2 (mean BMI 30.02 ± 2.89 Kg/m2) and 29 age- and sex-matched normal weight controls (mean age 30.48 ± 8.01 years) with BMI: 18–24Kg/m2 (mean BMI 21.87 ± 2.40 Kg/m2). Nerve conduction study (NCS) variables of median, tibial and sural nerves were assessed in each subject using standard protocol. The data were compared by Mann Whitney ‘U’ test.ResultsIn comparison to normal weight persons, obese had lower compound muscle action potential (CMAP) amplitudes of right median [9.09(7.62–10.20) Vs 10.75(8.71–12.2) mV, p = 0.025] and bilateral tibial nerves [Right: 8.5(7.04–11.18) Vs 12.1(10.55–15) mV, p < 0.001 and left 9.08(6.58–11.65) Vs 13.05(10.2–15.6) mV, p = 0.002]. Furthermore, obese persons had prolonged CMAP durations of right and left median [10.5(9.62–12) Vs 10(8.4–10.3) ms, p = 0.02 and 10.85(10–11.88) Vs 10(9–10.57) ms, p = 0.019] and right tibial [10(9–11) 8.5(7.92–10) ms, p = 0.032] nerves. Sensory NCS (sural nerve) also showed diminished sensory nerve action potential (SNAP) amplitude [16(12.08–18.21) vs 22.8(18.3–31.08) μV, p < 0.001] and prolonged duration. However, onset latencies and conduction velocities for all nerves were comparable between the groups.ConclusionThis study documents subclinical peripheral nerve damage in non-diabetic obese with abnormal NCS parameters; shorter amplitudes and prolonged CMAP and SNAP durations. The reduced amplitudes of mixed and sensory nerves might be due to decreased axonal number stimulation or actual decrease in number of axonal fibers, or defect at NMJ in non-diabetic obese. Prolonged durations but normal onset latencies and conduction velocities strongly suggest involvement of slow conducting fibers.