scholarly journals Insulin resistance per se drives early and reversible dysbiosis-mediated gut barrier impairment and bactericidal dysfunction

2022 ◽  
pp. 101438
Author(s):  
Dalale Gueddouri ◽  
Michèle Caüzac ◽  
Véronique Fauveau ◽  
Fadila Benhamed ◽  
Wafa Charifi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gut Barrier ◽  
Per Se

Glucocorticoids produce whole body insulin resistance with changes in cardiac metabolism

2007 ◽  
Vol 292 (3) ◽  
pp. E654-E667 ◽  
Author(s):  
Dake Qi ◽  
Brian Rodrigues
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Glucose Utilization ◽  
Experimental Studies ◽  
Cardiac Metabolism ◽  
Multiple Organ ◽  
Whole Body ◽  
Metabolic Abnormalities ◽  
Organ Systems ◽  
Per Se

Insulin resistance is viewed as an insufficiency in insulin action, with glucocorticoids being recognized to play a key role in its pathogenesis. With insulin resistance, metabolism in multiple organ systems such as skeletal muscle, liver, and adipose tissue is altered. These metabolic alterations are widely believed to be important factors in the morbidity and mortality of cardiovascular disease. More importantly, clinical and experimental studies have established that metabolic abnormalities in the heart per se also play a crucial role in the development of heart failure. Following glucocorticoids, glucose utilization is compromised in the heart. This attenuated glucose metabolism is associated with altered fatty acid supply, composition, and utilization. In the heart, elevated fatty acid use has been implicated in a number of metabolic, morphological, and mechanical changes and, more recently, in “lipotoxicity”. In the present article, we review the action of glucocorticoids, their role in insulin resistance, and their influence in modulating peripheral and cardiac metabolism and heart disease.

scholarly journals Aging per se Increases the Susceptibility to Free Fatty Acid-Induced Insulin Resistance

2010 ◽  
Vol 65A (8) ◽  
pp. 800-808 ◽  
Author(s):  
F. H. Einstein ◽  
D. M. Huffman ◽  
S. Fishman ◽  
E. Jerschow ◽  
H. J. Heo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Per Se

In vivo insulin action in genetic models of hypertension

1992 ◽  
Vol 262 (2) ◽  
pp. E191-E196 ◽  
Author(s):  
S. Frontoni ◽  
L. Ohman ◽  
J. R. Haywood ◽  
R. A. DeFronzo ◽  
L. Rossetti
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Hepatic Glucose Production ◽  
High Dose ◽  
Rat Models ◽  
Genetic Hypertension ◽  
Per Se

Insulin resistance has been described in nonobese subjects with essential hypertension. At present it is unknown whether hypertension per se may lead to the onset of insulin resistance. To examine this question we studied in vivo insulin action in two rat models of genetic hypertension. Four groups of conscious rats were studied: Milan hypertensive (MHS), Milan normotensive (MNS), spontaneously hypertensive (SHR), and Wistar-Kyoto (WKY). Mean arterial pressure was increased in SHR vs. WKY in both the fed (184 +/- 5 vs. 126 +/- 6 mmHg; P less than 0.001) and fasting (160 +/- 5 vs. 129 +/- 5; P less than 0.001) states. During high-dose insulin clamps, total body glucose uptake (mg.kg-1.min-1) was similar in MNS (28.7 +/- 1.4) vs. MHS (33.6 +/- 3.0) and in WKY (34.6 +/- 1.8) vs. SHR (35.7 +/- 2.4). During low-dose insulin clamps, suppression of hepatic glucose production (3.5 +/- 0.6 vs. 3.0 +/- 0.5 mg.kg-1.min-1) and stimulation of glycolysis (12.9 +/- 0.8 vs. 14.4 +/- 1.5 mg.kg-1.min-1) were similar in WKY vs. SHR, whereas glucose uptake (24.6 +/- 1.9 vs. 18.3 +/- 1.2 mg.kg-1.min-1; P less than 0.01) and muscle glycogenic rate (10.2 +/- 1.1 vs. 6.5 +/- 1.1 mg.kg-1.min-1; P less than 0.05) were increased in SHR vs. WKY. In conclusion, 1) feeding markedly augments blood pressure in hypertensive but not in normotensive rats, and 2) hepatic and muscle insulin sensitivity are normal or increased in two different rat models of genetic hypertension. These results provide evidence that high blood pressure per se does not invariably lead to the development of insulin resistance.

scholarly journals Lipodystrophy HIV-related and FGF21: A new marker to follow the progression of lipodystrophy?

2016 ◽  
Vol 4 (4) ◽  
pp. 150-154 ◽  
Author(s):  
Stefano Benedini ◽  
Livio Luzi
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Body Composition ◽  
Pharmaceutical Formulations ◽  
Hepatic Insulin Resistance ◽  
Fibroblast Growth Factor 21 ◽  
Per Se ◽  
New Evidence ◽  
Hiv 1

Abstract Recently new evidence about fibroblast growth factor 21 (FGF21) highlights the opportunities to use this molecule in new pharmaceutical formulations to combat type 2 diabetes and metabolic syndrome. It is well known that HIV is per se a condition of insulin resistance and in particular the patient with HIV-related lipodystrophy has a condition strictly related to metabolic syndrome. Lipodystrophy is associated with severe metabolic side effects, including dyslipidemia, hepatic insulin resistance, and lipid oxidation impairment. Research carried out showed that FGF21 levels were significantly increased in untreated HIV-1-infected patients and the increase was much marked in HIV-1-infected antiretroviral-treated patients that have developed lipodystrophy and in the patients with greatest metabolic alterations. FGF21 is expressed mainly by the liver, but also by other tissues such as the thymus, adipose tissue, and skeletal muscle. Therefore, many researchers have considered the investigation of possible variations of FGF21 in patients with significant alterations in body composition both in regard to fat mass and lean mass. In the light of the possible interactions between FGF21 and metabolic syndrome, it seems interesting to evaluate the implication of this hormone in patients with HIV-related lipodystrophy who have a severe metabolic picture of insulin resistance with important alterations in body composition.

scholarly journals Increase in visceral fat per se does not induce insulin resistance in the canine model

Obesity ◽  
2014 ◽  
Vol 23 (1) ◽  
pp. 105-111 ◽  
Author(s):  
Ana V.B. Castro ◽  
Orison O. Woolcott ◽  
Malini S. Iyer ◽  
Morvarid Kabir ◽  
Viorica Ionut ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Visceral Fat ◽  
Canine Model ◽  
Induce Insulin Resistance ◽  
Per Se

scholarly journals Ectopic Fat and Insulin Resistance: Pathophysiology and Effect of Diet and Lifestyle Interventions

2012 ◽  
Vol 2012 ◽  
pp. 1-18 ◽  
Author(s):  
M. Snel ◽  
J. T. Jonker ◽  
J. Schoones ◽  
H. Lamb ◽  
A. de Roos ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Ectopic Fat ◽  
Lifestyle Interventions ◽  
Organ Function ◽  
Per Se ◽  
Diet And Lifestyle

The storage of triglyceride (TG) droplets in nonadipose tissues is called ectopic fat storage. Ectopic fat is associated with insulin resistance and type 2 diabetes mellitus (T2DM). Not the triglycerides per se but the accumulation of intermediates of lipid metabolism in organs, such as the liver, skeletal muscle, and heart seem to disrupt metabolic processes and impair organ function. We describe the mechanisms of ectopic fat depositions in the liver, skeletal muscle, and in and around the heart and the consequences for each organs function. In addition, we systematically reviewed the literature for the effects of diet-induced weight loss and exercise on ectopic fat depositions.

scholarly journals New Insights on the Interactions Between Insulin Clearance and the Main Glucose Homeostasis Mechanisms

2021 ◽  
Author(s):  
Roberto Bizzotto ◽  
Domenico Tricò ◽  
Andrea Natali ◽  
Amalia Gastaldelli ◽  
Elza Muscelli ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Glucose Homeostasis ◽  
Insulin Clearance ◽  
Oral Glucose ◽  
Β Cell ◽  
Euglycemic Clamp ◽  
Glucose Ingestion ◽  
Per Se

<i>Objective</i> Endogenous insulin clearance (EIC) is physiologically reduced at increasing insulin secretion rate (ISR). Computing EIC at the prevailing ISR does not distinguish the effects of hypersecretion from those of other mechanisms of glucose homeostasis. We aimed to measure EIC in standardized ISR conditions (i.e., at fixed ISR levels) and to analyze its associations with relevant physiologic factors. <p><i>Research Design and Methods</i> We estimated standardized EIC (EIC<sub>ISR</sub>) by mathematical modelling in 9 different studies with insulin and glucose infusions (N=2067). EIC<sub>ISR</sub> association with various traits was analyzed by stepwise multivariable regression, in studies with euglycemic clamp and OGTT (N=1410). We also tested whether oral glucose ingestion, as opposed to intravenous infusion, has an independent effect on EIC (N=1555).</p> <p><i>Results</i> Insulin sensitivity (as M/I from the euglycemic clamp) is the strongest determinant of EIC<sub>ISR</sub>, ~4 times more influential than insulin-resistance related hypersecretion. EIC<sub>ISR</sub> independently associates positively with M/I, fasting and mean OGTT glucose or type 2 diabetes, and β-cell glucose sensitivity, and negatively with African American or Hispanic race, female sex, and female age. With oral glucose ingestion, an ISR-independent ~10% EIC reduction is necessary to explain the observed insulin concentration profiles.</p> <p><i>Conclusions</i> Based on EIC<sub>ISR</sub>, we posit the existence of two adaptive processes involving insulin clearance: the first reduces EIC<sub>ISR</sub> with insulin resistance (not with higher BMI <i>per se</i>) and is more relevant than the concomitant hypersecretion; the second reduces EIC<sub>ISR</sub> with β-cell dysfunction. These processes are dysregulated in type 2 diabetes. Finally, oral glucose ingestion <i>per se</i> reduces insulin clearance.<br> </p>

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