Insulin resistance induced by hydrocortisone is increased in patients with abdominal obesity

2006 ◽  
Vol 291 (5) ◽  
pp. E995-E1002 ◽  
Author(s):  
Patrice Darmon ◽  
Frédéric Dadoun ◽  
Sandrine Boullu-Ciocca ◽  
Michel Grino ◽  
Marie-Christine Alessi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Free Fatty Acids ◽  
Abdominal Obesity ◽  
Visceral Fat ◽  
Mild Stress ◽  
Model Assessment ◽  
Obese Women ◽  
Pai 1

Glucocorticoids hypersensitivity may be involved in the development of abdominal obesity and insulin resistance. Eight normal weight and eight obese women received on two occasions a 3-h intravenous infusion of saline or hydrocortisone (HC) (1.5 μg·kg−1·min−1). Plasma cortisol, insulin, and glucose levels were measured every 30 min from time−30(min) (time−30) to time240. Free fatty acids, adiponectin, and plasminogen activator inhibitor-1 (PAI-1) levels were measured at time−30, time180, and time240. At time240, subjects underwent an insulin tolerance test to obtain an index of insulin sensitivity (KITT). Mean30–240cortisol level was similar in control and obese women after saline (74 ± 16 vs. 75 ± 20 μg/l) and HC (235 ± 17 vs. 245 ± 47 μg/l). The effect of HC on mean180–240insulin, mean180–240insulin resistance obtained by homeostasis model assessment (HOMA-IR), and KITTwas significant in obese (11.4 ± 2.0 vs. 8.2 ± 1.3 mU/l, P < 0.05; 2.37 ± 0.5 vs. 1.64 ± 0.3, P < 0.05; 2.81 ± 0.9 vs. 3.32 ± 1.02%/min, P < 0.05) but not in control women (3.9 ± 0.6 vs. 2.8 ± 0.5 mU/l; 0.78 ± 0.1 vs. 0.49 ± 0.1; 4.36 ± 1.1 vs. 4.37 ± 1.2%/min). In the whole population, the quantity of visceral fat, estimated by computerized tomography scan, was correlated with the increment of plasma insulin and HOMA-IR during HC infusion [Δmean30–240insulin ( r = 0.61, P < 0.05), Δmean30–240HOMA-IR ( r = 0.66, P < 0.01)]. The increase of PAI-1 between time180and time240after HC was higher in obese women (+25%) than in controls (+12%) ( P < 0.05), whereas no differential effect between groups was observed for free fatty acids or adiponectin. A moderate hypercortisolism, equivalent to that induced by a mild stress, has more pronounced consequences on insulin sensitivity in abdominally obese women than in controls. These deleterious effects are correlated with the amount of visceral fat.

scholarly journals Circulating Plasma Free Fatty Acids, Insulin Resistance and Metabolic Markers in Obese Women

2020 ◽  
Vol 13 (4) ◽  
pp. 1595-1600
Author(s):  
Moushira Zaki ◽  
Jihan Hussein ◽  
Amr M.M. Ibrahim ◽  
Eman R. Youness
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Anthropometric Measurements ◽  
Model Assessment ◽  
Obese Women ◽  
Metabolic Markers ◽  
The Metabolic Syndrome ◽  
The Relationship

Objectives:Elevation of free fatty acids (FFAs) in serum is an importantrisk factor for metabolic changes.Conversely, the relationship between obesity and metabolic abnormalities, and FFAsis not yet completely understood.Thus,we aimed in this study to explore the relationship and the association between insulin resistance (IR), metabolic markers and the variation inplasmaFFAs among the obese women. Methods:This study included fifty obese women aged 25–35 years and has insulin resistance (IR)in addition to fifty age-matched healthy normal weightwomen served as control group.Blood was withdrawn after twelve hours fasting;fasting blood glucose, lipidsand plasma insulinwere estimated;IR was assessedvia the Homeostasis Model Assessment-Insulin Resistance (HOMA-IR).Fatty acids in plasma were measured by HPLC using UV detector that was set at 200 nm.Indeed, anthropometric measurements was performed . Results:Lipid profile, fasting blood sugar, insulin resistance, oleic acids (OA), linoleic acid (LA), arachidonic acid (AA) and anthropometric measurements were significantly increased in IR women compared to control. Whereas, the mean value levels of alpha-linolenicacid(ALA)was significantly decreased in IR women compare to controls. Conclusion:lower plasma levels of ALA and higher levels of AA, OA, LA were significantly associated with risk of IR and metabolic disorder markers in obese women.These results might explain the positive benefits of foods rich with poly unsaturated fatty acids (PUFA).Obesity and IR may be associated with the alterations in composition of the circulating fatty acid.These findings underscore the potential role of PUFA in the metabolic syndrome pathogenesis.

Sex-dependent nutritional programming: fish oil intake during early pregnancy in rats reduces age-dependent insulin resistance in male, but not female, offspring

2013 ◽  
Vol 304 (4) ◽  
pp. R313-R320 ◽  
Author(s):  
Fatima L. C. Sardinha ◽  
Flavia S. Fernandes ◽  
Maria G. Tavares do Carmo ◽  
Emilio Herrera
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Early Pregnancy ◽  
Adult Life ◽  
Male Offspring ◽  
Oral Glucose ◽  
Sensitivity Index ◽  
Standard Diet ◽  
Model Assessment

Prenatal and early postnatal nutritional status may predispose offspring to impaired glucose tolerance and changes in insulin sensitivity in adult life. The long-term consequences of changes in maternal dietary fatty acid composition were determined in rats. From day 1 until day 12 of pregnancy, rats were given isocaloric diets containing 9% nonvitamin fat based on soybean, olive, fish (FO), linseed, or palm oil. Thereafter, they were maintained on the standard diet; offspring were studied at different ages. Body weight at 4, 8, and 12 mo and lumbar adipose tissue and liver weights at 12 mo did not differ between females on the different diets, whereas in males the corresponding values were all lower in the offspring from the FO group compared with the other dietary groups. Plasma glucose concentrations (both basal and after an oral glucose load) did not change with sex or dietary group, but plasma insulin concentrations were lower in females than in males and, in males, were lowest in the FO group. Similar relations were found with both the homeostasis model assessment of insulin resistance and insulin sensitivity index. In conclusion, the intake of more n–3 fatty acids (FO diet) during early pregnancy reduced both fat accretion and age-related decline in insulin sensitivity in male offspring but not in females. It is proposed that the lower adiposity caused by the increased n–3 fatty acids during the intrauterine life was responsible of the lower insulin resistance in male offspring.

From Obesity to Diabetes

2006 ◽  
Vol 76 (4) ◽  
pp. 172-177 ◽  
Author(s):  
Keller
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Free Fatty Acids ◽  
Vegetable Consumption ◽  
Prediabetic State ◽  
The Metabolic Syndrome ◽  
Life Style Changes

The prevalence of obesity has been increasing dramatically in the last decades in the whole world, not only in industrialized countries but also in developing areas. A major complication of obesity is insulin resistance and type 2 diabetes. Diabetes is also rapidly increasing world-wide – reaching a prevalence in adults of approx. 5–6% in Central Europe and in the US, and more than 50% in specific, genetically prone populations. This article reviews pathogenetic mechanisms linking obesity and type 2 diabetes. Emphasis is placed on the observation that excessive amounts of adipocytes are associated with an impairment of insulin sensitivity, a key feature of the "metabolic syndrome". This is a cluster of metabolic abnormalities such as type 2 diabetes, hypertension and dyslipidemia; all of them are enhanced by the presence of visceral (abdominal) obesity and all contribute to the increased cardiovascular risk observed in these patients. Besides release of free fatty acids, adipocytes secrete substances that contribute to peripheral insulin resistance, including adiponectin, resistin, TNF-α and interleukin 6. Increased turnover of free fatty acids interferes with intracellular metabolism of glucose in the muscle, and they exert lipotoxic effect on pancreatic β-cells. The pre-receptor metabolism of cortisol is enhanced in visceral adipose tissue by activation of 11 β-hydroxysteroid dehydrogenase type 1. A new class of anti-diabetic drugs (thiazolidinediones, or glitazones) bind to peroxisome proliferator activated receptor (PPAR-γ) and lower thereby plasma free fatty acids and cytokine production in adipocytes, in addition to a decrease of resistin and an increase in adiponectin observed in animals, resulting in an overall increase in insulin sensitivity and in an improvement of glucose homeostasis. However, the first step to avoid insulin resistance and prevent the development of diabetes should be a reduction in body weight in overweight subjecs, and an increase in physical activity. There are now three published randomized controlled trials demonstrating that in high risk individuals, life style changes with modest weight lost, associated with diminished fat intake and an increase in fruit and vegetable consumption result in marked inhibition of the transition from the prediabetic state to manifest type 2 diabetes.

scholarly journals Role of adiponectin and free fatty acids on the association between abdominal visceral fat and insulin resistance

2015 ◽  
Vol 14 (1) ◽  
pp. 20 ◽  
Author(s):  
Aida Medina-Urrutia ◽  
Carlos Posadas-Romero ◽  
Rosalinda Posadas-Sánchez ◽  
Esteban Jorge-Galarza ◽  
Teresa Villarreal-Molina ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Visceral Fat ◽  
Abdominal Visceral Fat

scholarly journals Serum Vascular Endothelial Growth Factor in Egyptian Obese Women with Insulin Resistance

2019 ◽  
Vol 7 (8) ◽  
pp. 1330-1334
Author(s):  
Moushira Erfan Zaki ◽  
Walaa Basha ◽  
Rasha Nazih Yousef ◽  
Mona Awad
Keyword(s):  
Insulin Resistance ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Visceral Fat ◽  
Control Group ◽  
Vascular Endothelial ◽  
Model Assessment ◽  
Obese Women ◽  
Metabolic Complications ◽  
Endothelial Growth Factor

BACKGROUND: Obesity is a major factor in the development of several sub-clinical anomalies. Insulin resistance (IR) is associated with obesity. Vascular endothelial growth factor (VEGF) plays a significant role in inflammation and vascular neogenesis. However the precise relationships of its levels with clinical, lipid, and metabolic profiles are unknown. AIM: This study aimed to examine the association between serum VEGF concentrations with IR risk and metabolic and lipid parameters in obese women. METHODS: Serum VEGF, metabolic biomarkers and anthropometry were measured in 83 obese women with IR and 50 healthy women. Fat distributions in the abdominal, subcutaneous and visceral area were assessed. Homeostasis model assessment for insulin resistance index (HOMA-IR) was calculated. For analytical purposes, VEGF levels were categorised into three tertiles groups. RESULTS: Obese women with IR showed significantly higher levels of serum VEGF as compared with the control group. Moreover, obese women in the highest VEGF tertile had significantly higher values of obesity indices, visceral fat index, abnormal lipid levels and HOMA-IR compared to with those in the lower tertile. CONCLUSION: Elevated VEGF levels are associated with IR and high visceral fat index in obese women which in turn increased the risk for metabolic complications.

scholarly journals Metabolomics Identifies Distinctive Metabolite Signatures for Measures of Glucose Homeostasis: The Insulin Resistance Atherosclerosis Family Study (IRAS-FS)

2018 ◽  
Vol 103 (5) ◽  
pp. 1877-1888 ◽  
Author(s):  
Nicholette D Palmer ◽  
Hayrettin Okut ◽  
Fang-Chi Hsu ◽  
Maggie C Y Ng ◽  
Yii-Der Ida Chen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Glucose Homeostasis ◽  
Cell Function ◽  
Insulin Response ◽  
Model Assessment ◽  
Homeostatic Model Assessment ◽  
Β Cell Function ◽  
Homeostatic Model

Abstract Context Metabolomics provides a biochemical fingerprint that, when coupled with clinical phenotypes, can provide insight into physiological processes. Objective Survey metabolites associated with dynamic and basal measures of glucose homeostasis. Design Analysis of 733 plasma metabolites from the Insulin Resistance Atherosclerosis Family Study. Setting Community based. Participants One thousand one hundred eleven Mexican Americans. Main Outcome Dynamic measures were obtained from the frequently sampled intravenous glucose tolerance test and included insulin sensitivity and acute insulin response to glucose. Basal measures included homeostatic model assessment of insulin resistance and β-cell function. Results Insulin sensitivity was associated with 99 metabolites (P &lt; 6.82 × 10−5) explaining 28% of the variance (R2adj) beyond 28% by body mass index. Beyond branched chain amino acids (BCAAs; P = 1.85 × 10−18 to 1.70 × 10−5, R2adj = 8.1%) and phospholipids (P = 3.51 × 10−17 to 3.00 × 10−5, R2adj = 14%), novel signatures of long-chain fatty acids (LCFAs; P = 4.49 × 10−23 to 4.14 × 10−7, R2adj = 11%) were observed. Conditional analysis suggested that BCAA and LCFA signatures were independent. LCFAs were not associated with homeostatic model assessment of insulin resistance (P &gt; 0.024). Acute insulin response to glucose was associated with six metabolites; glucose had the strongest association (P = 5.68 × 10−16). Homeostatic model assessment of β-cell function had significant signatures from the urea cycle (P = 9.64 × 10−14 to 7.27 × 10−6, R2adj = 11%). Novel associations of polyunsaturated fatty acids (P = 2.58 × 10−13 to 6.70 × 10−5, R2adj = 10%) and LCFAs (P = 9.06 × 10−15 to 3.93 × 10−7, R2adj = 10%) were observed with glucose effectiveness. Assessment of the hyperbolic relationship between insulin sensitivity and secretion through the disposition index revealed a distinctive signature of polyunsaturated fatty acids (P = 1.55 × 10−12 to 5.81 × 10−6; R2adj = 3.8%) beyond that of its component measures. Conclusions Metabolomics reveals distinct signatures that differentiate dynamic and basal measures of glucose homeostasis and further identifies new metabolite classes associated with dynamic measures, providing expanded insight into the metabolic basis of insulin resistance.

Insulin Sensitivity in Post-Obese Women

1994 ◽  
Vol 87 (4) ◽  
pp. 407-413 ◽  
Author(s):  
Søren Toubro ◽  
Philip Western ◽  
Jens Bülow ◽  
Ian Macdonald ◽  
Anne Raben ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Lipid Oxidation ◽  
Free Fatty Acids ◽  
Plasma Concentrations ◽  
Glucose Disposal ◽  
Obese Women ◽  
Basal Plasma ◽  
Obese Subjects ◽  
Glucose Disposal Rate

1. Both increased and decreased sensitivity to insulin has been proposed to precede the development of obesity. Therefore, insulin sensitivity was measured during a 2 h hyperinsulinaemia (100 m-units min−1 m−2) euglycaemic (4.5 mmol/l) glucose clamp combined with indirect calorimetry in nine weight-stable post-obese women and in nine matched control women preceded by 12 h fasting after 48 h on a standardized diet. 2. Both glucose disposal rate (post-obese women, 9.5 ± 2.2 mg min−1 kg−1, control women, 11.2 ± 1.4 mg min−1 kg−1, not significant) and glucose oxidation (3.6 ± 0.5 mg min−1 kg−1 versus 4.0 ± 0.7 mg min−1 kg−1, not significant) were similar in the two groups during the last 30 min of the clamp. Lipid oxidation also decreased similarly during the clamp in the post-obese women (from 30.4 ± 12 to 2.0 ± 7 J min−1 kg−1) and in the control women (from 33.6 ± 11 to 5.4 ± 8 J min−1 kg−1, not significant). Basal plasma concentrations of free fatty acids were similar, but at the end of the clamp free fatty acids were lower in the post-obese women than in the control women (139 ± 19 and 276 ± 48 μmol/l, P = 0.02). 3. We conclude that the insulin sensitivity of glucose metabolism is unaltered in the post-obese state. The study, however, points to an increased antilipolytic insulin action in post-obese subjects, which may favour fat storage and lower lipid oxidation rate post-prandially. The results suggest that alterations in lipid metabolism may contribute to the explanation of the propensity to obesity in susceptible individuals.

scholarly journals The Relationship between Abdominal Fat Phenotypes and Insulin Resistance in Non-Obese Individuals after Acute Pancreatitis

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2883 ◽  
Author(s):  
Juyeon Ko ◽  
Loren Skudder-Hill ◽  
Jaelim Cho ◽  
Sakina H. Bharmal ◽  
Maxim S. Petrov
Keyword(s):  
Insulin Resistance ◽  
Acute Pancreatitis ◽  
Insulin Sensitivity ◽  
Visceral Fat ◽  
Abdominal Fat ◽  
Model Assessment ◽  
Healthy Controls ◽  
Tyg Index ◽  
Pancreatic Fat ◽  
Matsuda Index

Both type 2 prediabetes/diabetes (T2DM) and new-onset prediabetes/diabetes after acute pancreatitis (NODAP) are characterized by impaired tissue sensitivity to insulin action. Although the outcomes of NODAP and T2DM are different, it is unknown whether drivers of insulin resistance are different in the two types of diabetes. This study aimed to investigate the associations between abdominal fat phenotypes and indices of insulin sensitivity in non-obese individuals with NODAP, T2DM, and healthy controls. Indices of insulin sensitivity (homeostasis model assessment of insulin sensitivity (HOMA-IS), Raynaud index, triglyceride and glucose (TyG) index, Matsuda index) were calculated in fasting and postprandial states. Fat phenotypes (intra-pancreatic fat, intra-hepatic fat, skeletal muscle fat, visceral fat, and subcutaneous fat) were determined using magnetic resonance imaging and spectroscopy. Linear regression and relative importance analyses were conducted. Age, sex, and glycated hemoglobin A1c were adjusted for. A total of 78 non-obese individuals (26 NODAP, 20 T2DM, and 32 healthy controls) were included. Intra-pancreatic fat was significantly associated with all the indices of insulin sensitivity in the NODAP group, consistently in both the unadjusted and adjusted models. Intra-pancreatic fat was not significantly associated with any index of insulin sensitivity in the T2DM and healthy controls groups. The variance in HOMA-IS was explained the most by intra-pancreatic fat (R2 = 29%) in the NODAP group and by visceral fat (R2 = 21%) in the T2DM group. The variance in the Raynaud index was explained the most by intra-pancreatic fat (R2 = 18%) in the NODAP group and by visceral fat (R2 = 15%) in the T2DM group. The variance in the TyG index was explained the most by visceral fat in both the NODAP group (R2 = 49%) and in the T2DM group (R2 = 25%). The variance in the Matsuda index was explained the most by intra-pancreatic fat (R2 = 48%) in the NODAP group and by visceral fat (R2 = 38%) in the T2DM group. The differing association between intra-pancreatic fat and insulin resistance can be used to differentiate NODAP from T2DM. Insulin resistance in NODAP appears to be predominantly driven by increased intra-pancreatic fat deposition.

scholarly journals Distribution of Fasting Plasma Insulin, Free Fatty Acids, and Glucose Concentrations and of Homeostasis Model Assessment of Insulin Resistance in a Representative Sample of Quebec Children and Adolescents

2003 ◽  
Vol 49 (4) ◽  
pp. 644-649 ◽  
Author(s):  
Pierre Allard ◽  
Edgard E Delvin ◽  
Gilles Paradis ◽  
James A Hanley ◽  
Jennifer O’Loughlin ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Representative Sample ◽  
Plasma Insulin ◽  
Model Assessment ◽  
Fasting Insulin ◽  
Homeostasis Model Assessment ◽  
Fasting Plasma ◽  
Fasting Plasma Insulin

Abstract Background: Plasma fasting insulin and the homeostasis model assessment of insulin resistance (HOMA-IR) are markers of IR, which, at least in part, mediates the relation of obesity to increased cardiovascular risk. Increased free fatty acids (FFAs) may be involved in the pathogenesis of IR. Our objectives were to describe the distributions of fasting plasma insulin, glucose, and FFAs and HOMA-IR in youth and to assess the relationship between FFAs and markers of IR. Methods: Fasting plasma insulin, glucose, and FFAs were measured in a representative sample of Quebec youth comprising 2244 individuals 9, 13, and 16 years of age. Results: In all age and sex groups, glucose exhibited remarkably tight distributions (median CV, 7.1%) in contrast to insulin, HOMA-IR, and FFAs (median CVs, 52%, 54% and 45%, respectively). For every percentile examined, 9-year-olds had lower insulin concentrations and HOMA-IR values than 13- and 16-year-olds. We observed strong correlations between insulin concentrations and HOMA-IR values, as well as close similarity in their rankings of individuals. The mean concentrations of glucose were higher in our population than in other Caucasian pediatric populations. No positive correlations were detected between FFAs and markers of IR. Conclusions: We report some of the first data on the distributions of fasting plasma insulin, HOMA-IR, and FFAs from a representative sample of youth. HOMA-IR does not appear more informative than fasting insulin as a marker of IR. Our findings on higher mean glucose concentrations in this population require confirmation in other representative samples of youth to assess whether the North American distribution of glucose concentrations is shifting positively.

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