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 Relationship between Serum Resistin Concentrations and Insulin Resistance in Nonobese, Obese, and Obese Diabetic Subjects

2004 ◽  
Vol 89 (4) ◽  
pp. 1844-1848 ◽  
Author(s):  
L. K. Heilbronn ◽  
J. Rood ◽  
L. Janderova ◽  
J. B. Albu ◽  
D. E. Kelley ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Human Subjects ◽  
Glucose Disposal ◽  
Fat Cell ◽  
Exact Function ◽  
Obese Subjects ◽  
Glucose Disposal Rate ◽  
Resistin Mrna

Abstract Early reports suggested that resistin is associated with obesity and insulin resistance in rodents. However, subsequent studies have not supported these findings. To our knowledge, the present study is the first assessment in human subjects of serum resistin and insulin sensitivity by the insulin clamp technique. Thirty-eight nonobese subjects [age, 23 ± 4 yr; body mass index (BMI), 25.4 ± 4.3 kg/m2], 12 obese subjects (age, 54 ± 8 yr; BMI, 33.0 ± 2.5 kg/m2), and 22 obese subjects with type 2 diabetes (age, 59 ± 7 yr; BMI, 34.0 ± 2.4 kg/m2) were studied. Serum resistin concentrations were not different among nonobese (4.1 ± 1.7 ng/ml), obese (4.2 ± 1.6 ng/ml), and obese diabetic subjects (3.7 ± 1.2 ng/ml), and were not significantly correlated to glucose disposal rate during a hyperinsulinemic glucose clamp across groups. Serum resistin was, however, inversely related to insulin sensitivity in nonobese subjects only (r = −0.35; P = 0.05), although this association was lost after adjusting for percent body fat. Serum resistin was not related to percent fat, BMI, or fat cell size. A strong correlation was observed between serum resistin and resistin mRNA expression from abdominal sc adipose tissue in a separate group of obese subjects (r = 0.62; P < 0.01; n = 56). Although the exact function of resistin is unknown, we demonstrated only a weak relationship between resistin and insulin sensitivity in nonobese subjects, indicating that resistin is unlikely to be a major link between obesity and insulin resistance in humans.

scholarly journals Effect of gender on lipid-induced insulin resistance in obese subjects

2008 ◽  
Vol 158 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Bodil Vistisen ◽  
Lars I Hellgren ◽  
Torill Vadset ◽  
Celena Scheede-Bergdahl ◽  
Jørn Wulff Helge ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Plasma Concentrations ◽  
Whole Body ◽  
Glucose Disposal ◽  
Muscle Lipid ◽  
Obese Subjects ◽  
Skeletal Muscle Insulin Sensitivity

ObjectiveIn obese subjects, chronically elevated plasma concentrations of non-esterified fatty acids (NEFAs) exert a marked risk to contract insulin resistance and subsequently type 2 diabetes. When NEFA is acutely increased due to i.v. infusion of lipid, glucose disposal during a hyperinsulinemic–euglycemic clamp is reduced. This effect has been explained by a NEFA-induced decrease in skeletal muscle insulin sensitivity caused by accumulation of the lipid intermediates such as ceramide and diacylglycerol in the myocytes. However, neither the lipid-induced reduction of glucose disposal nor the intramyocellular lipid deposition has been compared directly in obese females and males.DesignWe studied eight obese females and eight obese males (body mass index (BMI): 32.6±1.4 and 32.8±0.8 respectively, non significant (NS)) matched for cardiorespiratory fitness relative to lean body mass (43.7±1.6 and 47.6±1.3 ml/kg min respectively, NS).MethodsEach subject underwent two hyperinsulinemic–euglycemic clamps with infusion of lipid or saline respectively. Furthermore, the subjects exercised during the last half an hour of each clamp.ResultsThe lipid-induced reduction in glucose disposal during the clamp was similar in females and males (46±10 and 60±4% respectively, NS). However, whole-body insulin sensitivity as well as non-oxidative glucose disposal was higher in obese females compared with obese males both during lipid and saline infusion (P<0.001 andP=0.01 respectively). Muscle ceramide, triacylglycerol (TAG), diacylglycerol (DAG), and glycogen content were similar between sexes and remained unchanged during the clamp and when exercise was superimposed.ConclusionsThe lipid-induced inhibition of glucose disposal is similar in obese females and males. However, obese females are more insulin sensitive compared with obese males (both during saline and lipid infusion), which is not due to differences in the concentration of the muscle lipid intermediates such as ceramide and DAG.

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 Serum secreted frizzled-related protein 5 in relation to insulin sensitivity and its regulation by insulin and free fatty acids

Endocrine ◽  
2021 ◽  
Author(s):  
Marta Rydzewska ◽  
Agnieszka Nikołajuk ◽  
Natalia Matulewicz ◽  
Magdalena Stefanowicz ◽  
Monika Karczewska-Kupczewska
Keyword(s):  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Free Fatty Acids ◽  
Wnt Signaling Pathway ◽  
Normal Weight ◽  
Healthy Population ◽  
Related Protein ◽  
Heparin Infusion ◽  
Male Subjects ◽  
Contradictory Data

Abstract Purpose Secreted frizzled-related protein 5 (SFRP5) is an adipokine, which acts as an inhibitor of noncanonical WNT signaling pathway. It has been suggested to exert anti-inflammatory and insulin-sensitizing effects, however, contradictory data has also been reported. The aim of this study was to assess serum SFRP5 concentration in a young healthy population in relation to insulin sensitivity and its regulation by hyperinsulinemia and/or serum free fatty acids (FFA) elevation. Methods We examined 150 healthy subjects (83 normal-weight and 67 overweight/obese). Insulin sensitivity (M) was measured with hyperinsulinemic-euglycemic clamp. In 20 male subjects, clamp was prolonged to 6 h and after 1 week another clamp with the concurrent Intralipid/heparin infusion was performed. Independent group of 10 male subjects received infusions of Intralipid/heparin or saline in 1-week interval. Results Baseline SFRP5 was lower in the overweight/obese group (p = 0.01) and was positively associated with M (r = 0.23, p = 0.006) and serum adiponectin (r = 0.55, p < 0.001) and negatively with BMI (r = −0.18, p = 0.03). In multiple regression analysis, adiponectin was independently associated with SFRP5. Insulin infusion resulted in a decrease in serum SFRP5, both at 120′ (p = 0.02) and 360′ (p = 0.031). This effect was not observed during the clamp with Intralipid/heparin as well as during Intralipid/heparin alone or saline infusions. Conclusions The relation between SFRP5 and insulin sensitivity is mainly dependent on adiponectin. FFA abolish a decrease in circulating SFRP5 caused by insulin, but Intralipid/heparin infusion alone does not regulate SFRP5 concentration. Insulin seems to be more important factor in the regulation of circulating SFRP5 levels than FFA.

Influence of High Plasma Concentrations of Free Fatty Acids on Heart Rhythm in Healthy Fasting Men

2009 ◽  
Vol 205 (1-6) ◽  
pp. 299-301 ◽  
Author(s):  
Harald Wang ◽  
Knut Rasmussen ◽  
Harald Vik-Mo ◽  
Ole D. Mjøs ◽  
Helge Grendahl
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Plasma Concentrations ◽  
Heart Rhythm ◽  
High Plasma

The response of plasma minerals, free fatty acids and glucose to adrenaline and cortisol infusion in sheep

1986 ◽  
Vol 106 (2) ◽  
pp. 209-217 ◽  
Author(s):  
Sarah C. Bolton ◽  
T. E. C. Weekes
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Marked Decrease ◽  
Plasma Concentrations ◽  
Sodium Concentration ◽  
Plasma Calcium ◽  
Plasma Sodium ◽  
Plasma Phosphate ◽  
Plasma Sodium Concentration ◽  
Plasma Magnesium

SUMMARYAdrenaline was infused at three rates, 40, 15 or 3 μ/kg/h, in normal sheep and in sheep rendered hypercortisolaemic by infusion of cortisol at 150 μg/kg/h. In both normal and hypercortisolaemic animals, plasma concentrations of glucose and free fatty acids were increased by adrenaline treatment; plasma phosphate decreased with all treatments; plasma magnesium and potassium decreased on infusion of adrenaline at 40 or 15, but not at 3 μg/kg/h; plasma calcium decreased only on infusion of adrenaline in hypercortisolaemic animals, and plasma sodium concentration was unaffected by treatment.Induction of a degree of lipolysis likely to occur in the field was not associated with a marked decrease in plasma magnesium.

scholarly journals Circulating free fatty acids are increased independently of PPARγ activity after administration of poloxamer 407 to mice

2008 ◽  
Vol 86 (9) ◽  
pp. 643-649 ◽  
Author(s):  
Thomas P. Johnston ◽  
David J. Waxman
Keyword(s):  
Fatty Acids ◽  
Blood Glucose ◽  
Free Fatty Acids ◽  
Cholesterol Efflux ◽  
Plasma Insulin ◽  
Plasma Concentrations ◽  
Apolipoprotein A1 ◽  
Poloxamer 407 ◽  
Peroxisome Proliferator ◽  
Blood Glucose Concentrations

Poloxamer 407 (P-407) is a copolymer surfactant that induces a dose-controlled dyslipidemia in both mice and rats. Human macrophages cultured with P-407 exhibit a concentration-dependent reduction in cholesterol efflux to apolipoprotein A1 (apoA1) linked to downregulation of the ATP-binding cassette transporter A1 (ABCA1). Activators of peroxisome proliferator-activated receptor gamma (PPARγ), as well as PPARα, increase expression of liver X receptor alpha (LXRα) in macrophages and promote the expression of ABCA1, which, in turn, mediates cholesterol efflux to apoA1. The present study investigated whether P-407 interferes with this signaling pathway. A transactivation assay was used to evaluate whether P-407 can either activate or inhibit the transcriptional activity of PPARγ. Because thiazolidinedione drugs (PPARγ agonists) improve glycemic control in type 2 diabetes by reducing blood glucose concentrations, P-407 was also evaluated for its potential to alter plasma insulin and blood glucose concentrations in wild-type (C57BL/6) and PPARγ-deficient mice. Additionally, because thiazolidinediones attenuate release of free fatty acids (FFAs) from adipocytes and, consequently, decrease circulating plasma levels of FFAs, plasma concentrations of circulating FFAs were also determined in P-407-treated mice. P-407 was unable to modulate PPARγ activity in cell-based transactivation assays. Furthermore, P-407 did not perturb plasma insulin and blood glucose concentrations after administration to mice. However, by an as yet unidentified mechanism, P-407 caused a significant increase in the serum concentration of FFAs in mice beginning 3 h after administration and lasting more than 24 h postdosing. It is concluded that P-407 does not interfere with the functional activity of PPARγ after administration to mice.

scholarly journals Inhibition of Insulin Sensitivity by Free Fatty Acids Requires Activation of Multiple Serine Kinases in 3T3-L1 Adipocytes

2004 ◽  
Vol 18 (8) ◽  
pp. 2024-2034 ◽  
Author(s):  
Zhanguo Gao ◽  
Xiaoying Zhang ◽  
Aamir Zuberi ◽  
Daniel Hwang ◽  
Michael J. Quon ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Free Fatty Acids ◽  
Serine Kinases
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