scholarly journals Insulin Sensitizing and Antiatherogenic Role of Adiponectin: A Cross Sectional Study among the Healthy Subjects in Kerala

2021 ◽  
Vol 6 (12) ◽  
pp. 869-874
Author(s):  
Dr. Manju K Sudharmadevi ◽  
Dr. Leena K Balakumaran ◽  
Dr. Vijayalekshmi Lekshminarayan ◽  
Dr. Shenoy K Trivikrama
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Healthy Subjects ◽  
Calculated Data ◽  
Hdl Cholesterol ◽  
Serum Adiponectin ◽  
Healthy Population ◽  
Fat Percentage ◽  
Positive Correlation

Background of the study and objectives: Adiponectin, the most abundantly secreted adipokine plays a central role in energy homeostasis. Different studies have reported the protective role of adiponectin in obesity related complications such as insulin resistance, hypertension, dyslipidemia, atherosclerosis etc. Since not much studies were conducted to analyze the role of adiponectin in the metabolic homeostasis among the healthy population in Kerala, we designed this study. Materials and methods: This study included 170 healthy subjects of both gender in the age group of 20-60 years. Anthropometric measurements and blood pressure were recorded. BMI, WHR and BF% were calculated. Fasting blood sample was used to measure glucose, lipid profile, insulin and adiponectin. HOMA-IR, HOMA-β and QUICKI were calculated. Data was analyzed by student’s ‘t’ test and pearson’s correlation analysis. p <0.05 was considered statistically significant. Results: Serum adiponectin showed a negative correlation with BMI (r=-0.583) and body fat percentage (r=-0.369). An inverse significant correlation of adiponectin with serum triglycerides (p=0.01), fasting glucose (p=0.01) and HOMA-IR (p=0.001) was observed. But insulin sensitivity (QUICKI) (p=0.001) and serum HDL-cholesterol (p=0.01) showed a significant positive correlation with adiponectin. Analysis of the study subjects based on BMI showed a significant decrease in serum adiponectin (p=0.001) among obese group in comparison with normal weight subjects. Hypoadiponectinemia among obese subjects was also found to be associated with insulin resistance and decreased insulin sensitivity expressed as QUICKI. Conclusion: Serum adiponectin showed a positive correlation with insulin sensitivity and HDL-cholesterol. Adiponectin retains a significant role as a mediator of insulin resistance and atherosclerosis.

scholarly journals Detection of Insulin Resistance by Simple Quantitative Insulin Sensitivity Check Index QUICKI for Epidemiological Assessment and Prevention

2002 ◽  
Vol 87 (1) ◽  
pp. 144-144 ◽  
Author(s):  
Jiří Hřebíček ◽  
Vladimír Janout ◽  
Jana Malinčíková ◽  
Dagmar Horáková ◽  
Luděk Čížek
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Healthy Volunteers ◽  
Healthy Subjects ◽  
Clinical Manifestations ◽  
Hdl Cholesterol ◽  
Control Group ◽  
Confidence Limits ◽  
Obese Children ◽  
Prepubertal Age

The aim of the present study was to evaluate the recently defined simple insulin sensitivity check index QUICKI (Katz et al. 2000) for insulin resistance diagnostics in common clinical and epidemiological practice. Both the QUICKI (1/log insulin + log glycemia in mg/dL) and HOMA (insulin * glycemia in μmol/L/22.5) indexes were calculated from fasting values in 259 adult healthy volunteers and patients, and in 47 healthy and obese children of prepubertal age of both sexes. In adults, a fall in the QUICKI index (mean ± SEM in healthy subjects = 0.366 ± 0.029) as well as an increase in the HOMA index (in healthy subjects 1.57 ± 0.87) corresponded to metabolic and clinical manifestations of insulin resistance in various groups of outpatients. The QUICKI index had lower dispersion variances and the 95% confidence limits displayed a higher discrimination capacity. Patients with glucose intolerance or diabetes, hyperlipidemia typical for insulin resistance, or with combination of these metabolic disorders were characterized by QUICKI index values that were significantly lower than those of healthy volunteers. The QUICKI index in healthy prepubertal children indicated a higher insulin resistance compared to adults (mean 0.339 ± 0.020); an increase in the QUICKI index in obese children with BMI over 25 was not significant, although obese children showed a significant increase of serum leptin and triglycerides and a decrease of HDL-cholesterol. Adult patients with QUICKI index below 0.357 (which is at the lower limit of 95% confidence limits in healthy persons) represented a group with typical manifestations of metabolic syndrome, differing in these parameters significantly from the group of patients of comparable age with a QUICKI index greater than 0.357. The present study suggests suitability of the QUICKI index for diagnosis of insulin resistance in clinical and epidemiological practice. However, a normal QUICKI index range needs to be established for each laboratory with an appropriate control group because of significant interlaboratory variations in insulin determinations and/or possible differences in various populations.

Role of nutrition in preventing insulin resistance in children

2016 ◽  
Vol 29 (3) ◽  
Author(s):  
Annalisa Blasetti ◽  
Simone Franchini ◽  
Laura Comegna ◽  
Giovanni Prezioso ◽  
Francesco Chiarelli
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Fetal Development ◽  
Maternal Nutrition ◽  
Dietary Habits ◽  
Prenatal Period ◽  
Dietary Carbohydrates ◽  
Macro And Micronutrients

AbstractNutrition during prenatal, early postnatal and pubertal period is crucial for the development of insulin resistance and its consequences. During prenatal period fetal environment and nutrition seems to interfere with metabolism programming later in life. The type of dietary carbohydrates, glycemic index, protein, fat and micronutrient content in maternal nutrition could influence insulin sensitivity in the newborn. The effects of lactation on metabolism and nutritional behavior later in life have been studied. Dietary habits and quality of diet during puberty could prevent the onset of a pathological insulin resistance through an adequate distribution of macro- and micronutrients, a diet rich in fibers and vegetables and poor in saturated fats, proteins and sugars. We want to overview the latest evidences on the risk of insulin resistance later in life due to both nutritional behaviors and components during the aforementioned periods of life, following a chronological outline from fetal development to adolescence.

scholarly journals Susceptibility to oxidative stress, insulin resistance, and insulin secretory response in the development of diabetes from obesity

2007 ◽  
Vol 64 (6) ◽  
pp. 391-397 ◽  
Author(s):  
Radivoj Kocic ◽  
Dusica Pavlovic ◽  
Gordana Kocic ◽  
Milica Pesic
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Lipid Peroxidation ◽  
Insulin Sensitivity ◽  
Healthy Subjects ◽  
Critical Role ◽  
Secretory Response ◽  
Diabetic Patients ◽  
Apparent Difference ◽  
Insulin Secretory Response

Background/Aim. Oxidative stress plays a critical role in the pathogenesis of various diseases. Recent reports indicate that obesity may induce systemic oxidative stress. The aim of the study was to potentiate oxidative stress as a factor which may aggravate peripheral insulin sensitivity and insulinsecretory response in obesity in this way to potentiate development of diabetes. The aim of the study was also to establish whether insulin-secretory response after glucagonstimulated insulin secretion is susceptible to prooxidant/ antioxidant homeostasis status, as well as to determine the extent of these changes. Methods. A mathematical model of glucose/insulin interactions and C-peptide was used to indicate the degree of insulin resistance and to assess their possible relationship with altered antioxidant/prooxidant homeostasis. The study included 24 obese healthy and 16 obese newly diagnozed non-insulin dependent diabetic patients (NIDDM) as well as 20 control healthy subjects, matched in age. Results. Total plasma antioxidative capacity, erythrocyte and plasma reduced glutathione level were significantly decreased in obese diabetic patients, but also in obese healthy subjects, compared to the values in controls. The plasma lipid peroxidation products and protein carbonyl groups were significantly higher in obese diabetics, more than in obese healthy subjects, compared to the control healthy subjects. The increase of erythrocyte lipid peroxidation at basal state was shown to be more pronounced in obese daibetics, but the apparent difference was obtained in both the obese healthy subjects and obese diabetics, compared to the control values, after exposing of erythrocytes to oxidative stress induced by H2O2. Positive correlation was found between the malondialdehyde (MDA) level and index of insulin sensitivity (FIRI). Conclusion. Increased oxidative stress together with the decreased antioxidative defence seems to contribute to decreased insulin sensitivity and impaired insulin secretory response in obese diabetics, and may be hypothesized to favour the development of diabetes during obesity.

scholarly journals Duration of rise in free fatty acids determines salicylate's effect on hepatic insulin sensitivity

2013 ◽  
Vol 217 (1) ◽  
pp. 31-43 ◽  
Author(s):  
Sandra Pereira ◽  
Wen Qin Yu ◽  
María E Frigolet ◽  
Jacqueline L Beaudry ◽  
Yaniv Shpilberg ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Muscle Protein ◽  
Hepatic Insulin Resistance ◽  
Skeletal Muscle Protein ◽  
Protein Levels ◽  
Peripheral Insulin Resistance ◽  
Plasma Ffa ◽  
A Site

We have shown in rats that sodium salicylate (SS), which inhibits IkBa kinase B (IKKB), prevents hepatic and peripheral insulin resistance caused by short-term (7 h) i.v. administration of Intralipid and heparin (IH). We wished to further determine whether this beneficial effect of SS persisted after prolonged (48 h) IH infusion, which better mimics the chronic free fatty acid (FFA) elevation of obesity. Hence, we performed hyperinsulinemic euglycemic clamps with tritiated glucose methodology to determine hepatic and peripheral insulin sensitivity in rats infused with saline, IH, IH and SS, or SS alone. SS prevented peripheral insulin resistance (P<0.05) caused by prolonged plasma FFA elevation; however, it did not prevent hepatic insulin resistance. In skeletal muscle, protein levels of phospho-IkBa were augmented by prolonged IH administration and this was prevented by SS, suggesting that IH activates while SS prevents the activation of IKKB. Markers of IKKB activation, namely protein levels of phospho-IkBa and IkBa, indicated that IKKB is not activated in the liver after prolonged FFA elevation. Phosphorylation of serine 307 at insulin receptor substrate (IRS)-1, which is a marker of proximal insulin resistance, was not altered by IH administration in the liver, suggesting that this is not a site of hepatic insulin resistance in the prolonged lipid infusion model. Our results suggest that the role of IKKB in fat-induced insulin resistance is time and tissue dependent and that hepatic insulin resistance induced by prolonged lipid elevation is not due to an IRS-1 serine 307 kinase.

Impact of PPAR-α induction on glucose homoeostasis in alcohol-fed mice

2013 ◽  
Vol 125 (11) ◽  
pp. 501-511 ◽  
Author(s):  
Valérie Lebrun ◽  
Olivier Molendi-Coste ◽  
Nicolas Lanthier ◽  
Christine Sempoux ◽  
Patrice D. Cani ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Insulin Sensitivity ◽  
Alcohol Consumption ◽  
Insulin Signalling ◽  
Liver Steatosis ◽  
Hepatic Insulin Resistance ◽  
Alcoholic Fatty Liver ◽  
Glucose Homoeostasis

Alcohol consumption is a major cause of liver disease. It also associates with increased cardiovascular risk and Type 2 diabetes. ALD (alcoholic liver disease) and NAFLD (non-alcoholic fatty liver disease) share pathological features, pathogenic mechanisms and pattern of disease progression. In NAFLD, steatosis, lipotoxicity and liver inflammation participate to hepatic insulin resistance. The aim of the present study was to verify the effect of alcohol on hepatic insulin sensitivity and to evaluate the role of alcohol-induced steatosis and inflammation on glucose homoeostasis. C57BL/6J mice were fed for 20 days a modified Lieber–DeCarli diet in which the alcohol concentration was gradually increased up to 35% of daily caloric intake. OH (alcohol liquid diet)-fed mice had liver steatosis and inflammatory infiltration. In addition, these mice developed insulin resistance in the liver, but not in muscles, as demonstrated by euglycaemic–hyperinsulinaemic clamp and analysis of the insulin signalling cascade. Treatment with the PPAR-α (peroxisome-proliferator-activated receptor-α) agonist Wy14,643 protected against OH-induced steatosis and KC (Kupffer cell) activation and almost abolished OH-induced insulin resistance. As KC activation may modulate insulin sensitivity, we repeated the clamp studies in mice depleted in KC to decipher the role of macrophages. Depletion of KC using liposomes-encapsuled clodronate in OH-fed mice failed both to improve hepatic steatosis and to restore insulin sensitivity as assessed by clamp. Our study shows that chronic alcohol consumption induces steatosis, KC activation and hepatic insulin resistance in mice. PPAR-α agonist treatment that prevents steatosis and dampens hepatic inflammation also prevents alcohol-induced hepatic insulin resistance. However, KC depletion has little impact on OH-induced metabolic disturbances.

scholarly journals Prevalence and Clinical Characteristics of Children and Adolescents with Metabolically Healthy Obesity: Role of Insulin Sensitivity

Life ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 127 ◽  
Author(s):  
Federica Vinciguerra ◽  
Andrea Tumminia ◽  
Roberto Baratta ◽  
Alfredo Ferro ◽  
Salvatore Alaimo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Children And Adolescents ◽  
Metabolic Phenotype ◽  
Sensitivity Index ◽  
Insulinogenic Index ◽  
Model Assessment ◽  
Insulin Resistant ◽  
Metabolically Healthy

Obesity represents a major risk factor for metabolic disorders, but some individuals, “metabolically healthy” (MHO), show less clinical evidence of these complications, in contrast to “metabolically unhealthy” (MUO) individuals. The aim of this cross-sectional study is to assess the prevalence of the MHO phenotype in a cohort of 246 overweight/obese Italian children and adolescents, and to evaluate their characteristics and the role of insulin resistance. Homeostasis model assessment–insulin resistance (HOMA-IR), insulin sensitivity index (ISI), insulinogenic index (IGI) and disposition index (DI) were all calculated from the Oral Glucose Tolerance Test (OGTT). MHO was defined by either: (1) HOMA-IR < 2.5 (MHO-IRes), or (2) absence of the criteria for metabolic syndrome (MHO-MetS). The MHO prevalence, according to MHO-MetS or MHO-IRes criteria, was 37.4% and 15.8%, respectively. ISI was the strongest predictor of the MHO phenotype, independently associated with both MHO-IRes and MHO-MetS. The MHO-MetS group was further subdivided into insulin sensitive or insulin resistant on the basis of HOMA-IR (either < or ≥ 2.5). Insulin sensitive MHO-MetS patients had a better metabolic profile compared to both insulin resistant MHO-MetS and MUO-MetS individuals. These data underscore the relevance of insulin sensitivity to identifying, among young individuals with overweight/obesity, the ones who have a more favorable metabolic phenotype.

scholarly journals Adipocyte PU.1 knockout promotes insulin sensitivity in HFD-fed obese mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Denise E. Lackey ◽  
Felipe C. G. Reis ◽  
Roi Isaac ◽  
Rizaldy C. Zapata ◽  
Dalila El Ouarrat ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Target Genes ◽  
Obese Mice ◽  
Tissue Macrophage

Abstract Insulin resistance is a key feature of obesity and type 2 diabetes. PU.1 is a master transcription factor predominantly expressed in macrophages but after HFD feeding PU.1 expression is also significantly increased in adipocytes. We generated adipocyte specific PU.1 knockout mice using adiponectin cre to investigate the role of PU.1 in adipocyte biology, insulin and glucose homeostasis. In HFD-fed obese mice systemic glucose tolerance and insulin sensitivity were improved in PU.1 AKO mice and clamp studies indicated improvements in both adipose and liver insulin sensitivity. At the level of adipose tissue, macrophage infiltration and inflammation was decreased and glucose uptake was increased in PU.1 AKO mice compared with controls. While PU.1 deletion in adipocytes did not affect the gene expression of PPARg itself, we observed increased expression of PPARg target genes in eWAT from HFD fed PU.1 AKO mice compared with controls. Furthermore, we observed decreased phosphorylation at serine 273 in PU.1 AKO mice compared with fl/fl controls, indicating that PPARg is more active when PU.1 expression is reduced in adipocytes. Therefore, in obesity the increased expression of PU.1 in adipocytes modifies the adipocyte PPARg cistrome resulting in impaired glucose tolerance and insulin sensitivity.

Insulin sensitivity and big ET-1 conversion to ET-1 after ETA- or ETB-receptor blockade in humans

2002 ◽  
Vol 93 (6) ◽  
pp. 2112-2121 ◽  
Author(s):  
Gunvor Ahlborg ◽  
Jonas Lindström
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Healthy Subjects ◽  
Receptor Blockade ◽  
Receptor Stimulation ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Etb Receptor

Cardiovascular diseases are characterized by insulin resistance and elevated endothelin (ET)-1 levels. Furthermore, ET-1 induces insulin resistance. To elucidate this mechanism, six healthy subjects were studied during a hyperinsulinemic euglycemic clamp during infusion of (the ET-1 precursor) big ET-1 alone or after ETA- or ETB-receptor blockade. Insulin levels rose after big ET-1 with or without the ETB antagonist BQ-788 ( P < 0.05) but were unchanged after the ETA antagonist BQ-123 + big ET-1. Infused glucose divided by insulin fell after big ET-1 with or without BQ-788 ( P < 0.05). Insulin and infused glucose divided by insulin values were normalized by ETA blockade. Mean arterial blood pressure rose during big ET-1 with or without BQ-788 ( P < 0.001) but was unchanged after BQ-123. Skeletal muscle, splanchnic, and renal blood flow responses to big ET-1 were abolished by BQ-123. ET-1 levels rose after big ET-1 ( P< 0.01) in a similar way after BQ-123 or BQ-788, despite higher elimination capacity after ETA blockade. In conclusion, ET-1-induced reduction in insulin sensitivity and clearance as well as splanchnic and renal vasoconstriction are ETA mediated. ETA-receptor stimulation seems to inhibit the conversion of big ET-1 to ET-1.

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