In vitro reversal of hyperglycemia normalizes insulin action in fat cells from type 2 diabetes patients: Is cellular insulin resistance caused by glucotoxicity in vivo?

Burén, Jonas; Lindmark, Stina; Renström, Frida; Eriksson, Jan W.

doi:10.1053/meta.2003.50041

Cited by 44 publications

(47 citation statements)

References 38 publications

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“…On the other hand, these hormones are obviously critical in emergency situations of urgent need for extra delivery of fuel to tissues, in prolonged fasting and also as a response against hypoglycemia (15). Nonetheless, the ability of counter-regulatory hormones, including glucagon, adrenaline, cortisol and growth hormone, to increase blood glucose can contribute to insulin resistance and development of type 2 diabetes if there is an inappropriately large response (13) Insulin resistance in the pathobiology of type 2 diabetes Insulin resistance is an important component of the pathophysiological processes that underlies the development of type 2 diabetes, and it is likely to play a role in development of other conditions such as dyslipidemia, hypertension and atherosclerosis.…”

Section: Page 5 Of 28mentioning

confidence: 99%

“…However, there is accumulating evidence suggesting that such cellular mechanisms are not primary phenomena in the development of whole-body insulin resistance. Accordingly, prediabetic subjects can display essentially normal cellular insulin sensitivity, and in insulin-responsive cells in type 2 diabetic patients, it seems that insulin resistance is largely reversible (15,17). Thus, perturbations in the extracellular environment may appear first and they may, in turn, lead to cellular insulin resistance.…”

Section: Page 5 Of 28mentioning

confidence: 99%

“…An imbalance in the autonomic nervous system, with an increase sympathetic and decreased parasympathetic activity, is associated with insulin resistance both following stress (15) and insulin infusion (39). A high sympathetic vs. parasympathetic reactivity is also strongly related to visceral adiposity as well as insulin resistance (40).…”

Section: The Parasympathetic Nervous System and Insulin Resistancementioning

confidence: 99%

“…The renin-angiotensin system (RAS) is yet another neurendocrine pathway that can be involved in the development of insulin resistance (15). Renin catalyses the conversion of angiotensinogen to angiotensin I and angiotensin converting enzyme (ACE) promotes the onward conversion into angiotensin II.…”

Section: Ras In Insulin Resistancementioning

confidence: 99%

“…Insulin resistance is characterized by low-grade inflammation and adipokines such M a n u s c r i p t 15 as TNFalpha decrease both insulin signalling, glucose uptake (88) and capillary recruitment (89).…”

Section: Neuroendocrine Effects On Endothelial Function and Muscle Glmentioning

confidence: 99%

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Neuroendocrine mechanisms in insulin resistance

Sjöstrand

Eriksson

2009

Molecular and Cellular Endocrinology

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Dysregulated hormonal, metabolic and neural signalling within and between organs can contribute to development of metabolic diseases including type 2 diabetes. Insulinantagonistic effects of hormones, cytokines and excess metabolic substrates such as glucose and fatty acids may be exerted via common mechanisms involving for example reactive oxygen species (ROS) accumulation and associated inflammatory responses.Visceral adiposity is a central component of the metabolic syndrome and it is also strongly associated with insulin resistance. Both visceral obesity and insulin resistance are important risk factors for the development of type 2 diabetes. In the development of insulin resistance, it is likely that intra-abdominal adipose tissue plays a critical role in a complex endocrine and neural network involving several tissues. This review paper focuses on neuroendocrine 'stress' factors that target insulin-responsive tissues, in particular adipose tissue. We propose that there are common pathways by which dysregulation in different endocrine systems may contribute to the development of type 2 diabetes.

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Section: Page 5 Of 28mentioning

confidence: 99%

Section: Page 5 Of 28mentioning

confidence: 99%

Section: The Parasympathetic Nervous System and Insulin Resistancementioning

confidence: 99%

Section: Ras In Insulin Resistancementioning

confidence: 99%

Section: Neuroendocrine Effects On Endothelial Function and Muscle Glmentioning

confidence: 99%

See 3 more Smart Citations

Neuroendocrine mechanisms in insulin resistance

Sjöstrand

Eriksson

2009

Molecular and Cellular Endocrinology

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Current literature in diabetes

2003

Diabetes Metabolism Res

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In order to keep subscribers up‐to‐date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of diabetes/metabolism. Each bibliography is divided into 17 sections: 1 Books, Reviews & Symposia; 2 General; 3 Genetics; 4 Epidemiology; 5 Immunology; 6 Prediction; 7 Prevention; 8 Intervention: a) General; b) Pharmacology; 9 Pathology: a) General; b) Cardiovascular; c) Neurological; d) Renal; 10 Endocrinology & Metabolism; 11 Nutrition; 12 Animal Studies; 13 Techniques. Within each section, articles are listed in alphabetical order with respect to author (4 Weeks journals ‐ Search completed at 5th March 2003)

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Is insulin resistance caused by defects in insulin's target cells or by a stressed mind?

Burén

Eriksson

2005

Diabetes Metab. Res. Rev.

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The importance of understanding insulin action is emphasized by the increasing prevalence of insulin resistance in various populations and by the fact that it plays an important pathophysiological role in many common disorders, for example, diabetes, obesity, hypertension and dyslipidemia. The primary factors responsible for the development of insulin resistance are so far unknown, although both genetic and environmental factors are involved. The genetic defects responsible for the common forms of insulin resistance, for example, in type 2 diabetes, are largely unidentified. Some studies from our group as well as by other investigators suggest that cellular insulin resistance is reversible and that it may be secondary to factors in the in vivo environment. These may include insulin-antagonistic action of hormones like catecholamines, glucocorticoids, sex steroids and adipokines as well as dysregulation of autonomic nervous activity and they could contribute to the early development of insulin resistance. Some of these factors can directly impair glucose uptake capacity and this might be due to alterations in key proteins involved in insulin's intracellular signaling pathways. This article briefly summarizes proposed mechanisms behind cellular and whole-body insulin resistance. In particular, we question the role of intrinsic defects in insulin's target cells as primary mechanisms in the development of insulin resistance in type 2 diabetes and we suggest that metabolic and neurohormonal factors instead are the main culprits.

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In vitro reversal of hyperglycemia normalizes insulin action in fat cells from type 2 diabetes patients: Is cellular insulin resistance caused by glucotoxicity in vivo?

Cited by 44 publications

References 38 publications

Neuroendocrine mechanisms in insulin resistance

Neuroendocrine mechanisms in insulin resistance

Current literature in diabetes

Is insulin resistance caused by defects in insulin's target cells or by a stressed mind?

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