W09.264 Metabolic syndrome: Insulin resistant, proinflammatory and prothrombogennic

2004 ◽  
Vol 5 (1) ◽  
pp. 61
Author(s):  
H VAVERKOVA
Keyword(s):  
Metabolic Syndrome ◽  
Insulin Resistant

scholarly journals Female offspring born to obese and insulin-resistant dams are not at increased risk for obesity and metabolic dysfunction during early development

2018 ◽  
Vol 96 (1) ◽  
pp. 97-102 ◽  
Author(s):  
Hanin Aburasayn ◽  
Rami Al Batran ◽  
Keshav Gopal ◽  
Malak Almutairi ◽  
Amina Eshreif ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Female Offspring ◽  
Metabolic Dysfunction ◽  
Insulin Resistant ◽  
The Metabolic Syndrome ◽  
Rate Versus ◽  
Increased Risk ◽  
Study Completion ◽  
Reduced Rate

The percentage of women who are obese at the time of conception or during pregnancy is increasing, with animal and human studies demonstrating that offspring born to obese dams or mothers are at increased risk for obesity and the metabolic syndrome. Our goal was to confirm in an experimental model of metabolic syndrome in the dam, whether the offspring would be at increased risk of obesity. Conversely, we observed that male offspring born to dams with metabolic syndrome had no alterations in their body mass profiles, whereas female offspring born to dams with metabolic syndrome were heavier at weaning, but exhibited no perturbations in energy metabolism. Moreover, they gained weight at a reduced rate versus female offspring born to healthy dams, and thus weighed less at study completion. Hence, our findings suggest that factors other than increased adiposity and insulin resistance during pregnancy are responsible for the increased risk of obesity in children born to obese mothers.

scholarly journals Circulating Apolipoprotein L1 is associated with insulin resistance-induced abnormal lipid metabolism

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kenji Nishimura ◽  
Taichi Murakami ◽  
Toshihiro Sakurai ◽  
Masashi Miyoshi ◽  
Kiyoe Kurahashi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Insulin Resistant ◽  
Cell Dysfunction ◽  
Fractionation Analysis ◽  
Abnormal Lipid Metabolism ◽  
Hdl Metabolism ◽  
Relationship Of

Abstract Circulating ApolipoproteinL1 (ApoL1) is a component of pre-β-high-density lipoprotein (HDL), however little is known about the relationship of ApoL1 with cardiometabolic factors. Considering previous studies reporting the correlation of ApoL1 to triglyceride, we have hypothesized that ApoL1 associates with insulin-related metabolism. The current study examined their associations in 126 non-diabetic subjects and 36 patients with type 2 diabetes (T2DM). Non-diabetic subjects demonstrated triglyceride (standardized coefficients [s.c.] = 0.204, p < 0.05), body mass index (s.c. =0.232, p < 0.05) and HDL cholesterol (s.c. = −0.203, p < 0.05) as independent determinant of ApoL1 levels, and the significant elevation of ApoL1 in metabolic syndrome. Lipoprotein fractionation analysis revealed the predominant distribution of ApoL1 in large HDL fraction, and the significant increase of ApoL1 in large LDL fraction in high ApoL1 samples with insulin resistance. In T2DM, ApoL1 was higher in T2DM with metabolic syndrome, however ApoL1 was lower with β cell dysfunction. Insulin significantly promotes ApoL1 synthesis and secretion in HepG2 cells. In conclusion, circulating ApoL1 may be associated with abnormal HDL metabolism in insulin resistant status. This may suggest a regulation of insulin signal on the ApoL1 level, leading to offer a novel insight to the ApoL1 biology.

scholarly journals Donor metabolic characteristics drive effects of faecal microbiota transplantation on recipient insulin sensitivity, energy expenditure and intestinal transit time

Gut ◽  
2019 ◽  
Vol 69 (3) ◽  
pp. 502-512 ◽  
Author(s):  
Pieter de Groot ◽  
Torsten Scheithauer ◽  
Guido J Bakker ◽  
Andrei Prodan ◽  
Evgeni Levin ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Bile Acids ◽  
Transit Time ◽  
Intestinal Transit ◽  
Faecal Microbiota ◽  
Intestinal Transit Time ◽  
Insulin Resistant

ObjectiveBariatric surgery improves glucose metabolism. Recent data suggest that faecal microbiota transplantation (FMT) using faeces from postbariatric surgery diet-induced obese mice in germ-free mice improves glucose metabolism and intestinal homeostasis. We here investigated whether allogenic FMT using faeces from post-Roux-en-Y gastric bypass donors (RYGB-D) compared with using faeces from metabolic syndrome donors (METS-D) has short-term effects on glucose metabolism, intestinal transit time and adipose tissue inflammation in treatment-naïve, obese, insulin-resistant male subjects.DesignSubjects with metabolic syndrome (n=22) received allogenic FMT either from RYGB-D or METS-D. Hepatic and peripheral insulin sensitivity as well as lipolysis were measured at baseline and 2 weeks after FMT by hyperinsulinaemic euglycaemic stable isotope (2H2-glucose and 2H5-glycerol) clamp. Secondary outcome parameters were changes in resting energy expenditure, intestinal transit time, faecal short-chain fatty acids (SCFA) and bile acids, and inflammatory markers in subcutaneous adipose tissue related to intestinal microbiota composition. Faecal SCFA, bile acids, glycaemic control and inflammatory parameters were also evaluated at 8 weeks.ResultsWe observed a significant decrease in insulin sensitivity 2 weeks after allogenic METS-D FMT (median rate of glucose disappearance: from 40.6 to 34.0 µmol/kg/min; p<0.01). Moreover, a trend (p=0.052) towards faster intestinal transit time following RYGB-D FMT was seen. Finally, we observed changes in faecal bile acids (increased lithocholic, deoxycholic and (iso)lithocholic acid after METS-D FMT), inflammatory markers (decreased adipose tissue chemokine ligand 2 (CCL2) gene expression and plasma CCL2 after RYGB-D FMT) and changes in several intestinal microbiota taxa.ConclusionAllogenic FMT using METS-D decreases insulin sensitivity in metabolic syndrome recipients when compared with using post-RYGB-D. Further research is needed to delineate the role of donor characteristics in FMT efficacy in human insulin-resistant subjects.Trial registration numberNTR4327.

scholarly journals A Possible Role for Pioglitazone in the Management of Depressive Symptoms in Metabolic Syndrome Patients (EPICAMP Study): A Double Blind, Randomized Clinical Trial

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Hamidreza Roohafza ◽  
Pedram Shokouh ◽  
Masoumeh Sadeghi ◽  
Zahra Alikhassy ◽  
Nizal Sarrafzadegan
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
General Health Questionnaire ◽  
Depression Scale ◽  
Depression Score ◽  
Model Assessment ◽  
Double Blind ◽  
Resistance Level ◽  
Insulin Resistant ◽  
Present Trial

The present trial aimed to evaluate the effects of pioglitazone on the mental status of nondiabetic metabolic syndrome patients. From 145 patients screened, 104 eligible volunteers (57% female; age 20–70 years) were enrolled and randomly assigned to receive either pioglitazone (uptitrated to 30 mg/day; P=53) or matching placebo (P=51) for 24 weeks. Depression and anxiety were quantified using the hospital anxiety and depression scale and stress level using the general health questionnaire 12 at baseline, week 12, and endpoint. Homeostasis model assessment was used to estimate insulin resistance. At week 24, pioglitazone was superior in mitigating depression score (P=0.011). In trend analysis, the effect of time (P<0.001) and group (P=0.023) as well as the time by group interaction (P=0.032) on the mean depression score was considerable. In contrast, significant decrements in anxiety and stress levels (P<0.001 and P=0.012, resp.) were comparable between two groups. With respect to our findings, alterations in depression severity were not correlated with changes in insulin resistance level (P=0.145). In conclusion, our findings suggest that pioglitazone might be able to improve mood in nondiabetic insulin resistant patients. (Registered at Australian New Zealand Clinical Trials Registry; ACTRN12611000351910.)

scholarly journals Insulin Resistance, the Metabolic Syndrome, and Nonalcoholic Fatty Liver Disease

2005 ◽  
Vol 90 (3) ◽  
pp. 1578-1582 ◽  
Author(s):  
F. Angelico ◽  
M. Del Ben ◽  
R. Conti ◽  
S. Francioso ◽  
K. Feole ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Oral Glucose ◽  
Nonalcoholic Fatty Liver ◽  
Insulin Resistant ◽  
The Metabolic Syndrome

Background/Aims: An association of nonalcoholic fatty liver disease with the insulin-resistant metabolic syndrome has been suggested. The aim of the study was to assess the association of fatty liver to different degrees of insulin resistance and secretion. Methods and Results: The study was performed in 308 alcohol- and virus-negative consecutive patients attending a metabolic clinic, who underwent a complete clinical and biochemical work-up including oral glucose tolerance test and routine liver ultrasonography. Steatosis was graded as absent/mild, moderate, and severe. In nondiabetic subjects, a progressive (P &lt; 0.05) increase in mean homeostasis model of insulin resistance was recorded from the group without steatosis to the groups with mild/moderate and severe steatosis. Severe steatosis was associated with the clustering of the five clinical and biochemical features proposed for the clinical diagnosis of the metabolic syndrome. Subjects with the metabolic syndrome with a more pronounced insulin resistance had a higher prevalence of severe steatosis (P &lt; 0.01) compared with those with homeostasis model of insulin resistance below the median. Conclusions: The findings stress the heterogeneous presentation of patients with the metabolic syndrome when the diagnosis is based on the broad Adult Treatment Panel III clinical criteria and demonstrate that those who are more insulin resistant have a higher prevalence of severe steatosis.

Generalized impairment of vasodilator reactivity during hyperinsulinemia in patients with obesity-related metabolic syndrome

2010 ◽  
Vol 299 (6) ◽  
pp. E947-E952 ◽  
Author(s):  
Francesca Schinzari ◽  
Manfredi Tesauro ◽  
Valentina Rovella ◽  
Angelica Galli ◽  
Nadia Mores ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Vitamin C ◽  
Vascular Reactivity ◽  
Vascular Complications ◽  
Glucose Disposal ◽  
Vascular Abnormalities ◽  
Insulin Resistant ◽  
The Metabolic Syndrome ◽  
Before And After

Defective insulin-dependent vasodilation might contribute importantly to metabolic and vascular abnormalities of the metabolic syndrome (MetS). However, despite extensive investigation, the precise mechanisms involved in insulin's vasoactive effects have not been fully elucidated. Therefore, this study sought to better characterize insulin's physiological actions on vascular reactivity and their potential derangement in the MetS. Forearm blood flow responses to graded doses of acetylcholine, sodium nitroprusside, and verapamil were assessed by strain-gauge plethysmography in patients with obesity-related MetS ( n = 20) and in matched controls ( n = 18) before and after intra-arterial infusion of insulin (0.2 mU·kg−1·min−1). Possible involvement of increased oxidative stress in the impaired insulin-stimulated vasodilator responsiveness of patients with MetS ( n = 12) was also investigated using vitamin C (25 mg/min). In control subjects, significant potentiation of the vasodilator responses to acetylcholine, nitroprusside, and verapamil was observed after insulin infusion (all P < 0.05). However, no significant change in vasodilator reactivity to either of these drugs was observed following hyperinsulinemia in patients with MetS (all P > 0.05). Interestingly, administration of vitamin C to patients with MetS during hyperinsulinemia significantly enhanced the vasodilator responsiveness to acetylcholine, nitroprusside, and verapamil (all P < 0.05 vs. hyperinsulinemia alone). In conclusion, insulin exerts a generalized facilitatory action on vasodilator reactivity, and this effect is impaired in patients with MetS likely because of increased oxidative stress. Given the importance of vasodilator reactivity in affecting glucose disposal and vascular homeostasis, this defect may then contribute to the development of metabolic and vascular complications in insulin-resistant states.

scholarly journals Whole Blood Gene Expression Profiles in Insulin Resistant Latinos with the Metabolic Syndrome

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e84002 ◽  
Author(s):  
Samantha E. Tangen ◽  
Darwin Tsinajinnie ◽  
Martha Nuñez ◽  
Gabriel Q. Shaibi ◽  
Lawrence J. Mandarino ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Whole Blood ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Blood Gene Expression ◽  
Insulin Resistant ◽  
The Metabolic Syndrome

scholarly journals Metabolic syndrome identifies normal weight insulin-resistant stroke patients at risk for recurrent vascular disease

2018 ◽  
Vol 14 (6) ◽  
pp. 639-645 ◽  
Author(s):  
Jennifer L Dearborn ◽  
Catherine M Viscoli ◽  
Silvio E Inzucchi ◽  
Lawrence H Young ◽  
Walter N Kernan
Keyword(s):  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Obesity Paradox ◽  
Normal Weight ◽  
Diabetic Patients ◽  
Insulin Resistant ◽  
Increased Risk ◽  
All Cause Mortality ◽  
Patients At Risk

Background The obesity paradox refers to the finding in observational studies that patients with obesity have a better prognosis after stroke than normal weight patients. Aim To test the hypothesis that there might be important heterogeneity within the obese stroke population, such that those with metabolic syndrome would be at higher risk for stroke or myocardial infarction and all-cause mortality compared to patients without metabolic syndrome. Methods The Insulin Resistance Intervention after Stroke trial enrolled non-diabetic patients with a recent ischemic stroke or transient ischemic attack and insulin resistance. We examined the association between metabolic syndrome and outcome risk in patients with normal weight at entry (body mass index (BMI) = 18.5–24.9 kg/m2), overweight (BMI = 25–29.9 kg/m2), or obesity (BMI ≥ 30 kg/m2). Analyses were adjusted for demographic features, treatment assignment, smoking, and major comorbid conditions. Results Metabolic syndrome was not associated with greater risk for stroke or myocardial infarction among 1536 patients who were overweight (adjusted hazard ratio (HR), 0.95; 95% confidence interval (CI): 0.69–1.31) or 1626 obese patients (adjusted HR, 1.00; 95% CI: 0.70–1.41). However, among 567 patients with a normal BMI, metabolic syndrome was associated with increased risk for stroke or myocardial infarction (adjusted HR, 2.05; 95% CI: 1.25–3.37), and all-cause mortality (adjusted HR, 1.70; 95% CI: 1.03–2.81) compared to patients without metabolic syndrome. Conclusions The presence of metabolic syndrome identified normal weight patients with insulin resistance but no diabetes who have a higher risk of adverse cardiovascular outcomes, compared with patients without metabolic syndrome.

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