(Q54117527)

English

Insulin action and insulin resistance: diseases involving defects in insulin receptors, signal transduction, and the glucose transport effector system.

scientific article published in October 1998

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scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

25 May 2018

http://europepmc.org/abstract/MED/9809695

1 reference

Europe PubMed Central

Insulin action and insulin resistance: diseases involving defects in insulin receptors, signal transduction, and the glucose transport effector system. (English)

1 reference

Europe PubMed Central

PubMed publication ID

25 May 2018

http://europepmc.org/abstract/MED/9809695

1 reference

based on heuristic

inferred from title

insulin resistance

1 reference

based on heuristic

inferred from title

author name string

Hunter SJ

1

1 reference

Europe PubMed Central

PubMed publication ID

25 May 2018

http://europepmc.org/abstract/MED/9809695

Garvey WT

2

1 reference

Europe PubMed Central

PubMed publication ID

25 May 2018

http://europepmc.org/abstract/MED/9809695

language of work or name

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publication date

1 October 1998

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Europe PubMed Central

PubMed publication ID

25 May 2018

http://europepmc.org/abstract/MED/9809695

American Journal of Medicine

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Europe PubMed Central

PubMed publication ID

25 May 2018

http://europepmc.org/abstract/MED/9809695

105

1 reference

Europe PubMed Central

PubMed publication ID

25 May 2018

http://europepmc.org/abstract/MED/9809695

4

1 reference

Europe PubMed Central

PubMed publication ID

25 May 2018

http://europepmc.org/abstract/MED/9809695

331-345

1 reference

Europe PubMed Central

PubMed publication ID

25 May 2018

http://europepmc.org/abstract/MED/9809695

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Insulin Resistance Caused by Massive Degradation of Subcutaneous Insulin

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Binding properties of chimeric insulin receptors containing the cysteine-rich domain of either the insulin-like growth factor I receptor or the insulin receptor related receptor

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Banting lecture 1989. Structure and function of insulin receptors

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Activation of protein kinase C alpha inhibits signaling by members of the insulin receptor family

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Structure of the insulin receptor substrate IRS-1 defines a unique signal transduction protein

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The 60-kDa phosphotyrosine protein in insulin-treated adipocytes is a new member of the insulin receptor substrate family

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Disruption of IRS-2 causes type 2 diabetes in mice

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Insulin second messengers.

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Expression of a constitutively active Akt Ser/Thr kinase in 3T3-L1 adipocytes stimulates glucose uptake and glucose transporter 4 translocation

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Insulin increases the association of Akt-2 with Glut4-containing vesicles

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Excess Insulin Binding to Insulin-Like Growth Factor Receptors: Proposed Mechanism for Acanthosis Nigricans

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The syndromes of insulin resistance and acanthosis nigricans. Insulin-receptor disorders in man.

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Mutant insulin receptors in syndromes of insulin resistance

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Profound peripheral insulin resistance, independent of obesity, in polycystic ovary syndrome

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The gonadotropic function of insulin

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Hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome: A common endocrinopathy with distinct pathophysiologic features

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Polycystic ovary syndrome as a form of functional ovarian hyperandrogenism due to dysregulation of androgen secretion.

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Suppression of hyperandrogenism does not improve peripheral or hepatic insulin resistance in the polycystic ovary syndrome

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Excessive insulin receptor serine phosphorylation in cultured fibroblasts and in skeletal muscle. A potential mechanism for insulin resistance in the polycystic ovary syndrome

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Tumor necrosis factor alpha-induced phosphorylation of insulin receptor substrate-1 (IRS-1). Possible mechanism for suppression of insulin-stimulated tyrosine phosphorylation of IRS-1

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IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance

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A molecular basis for insulin resistance. Elevated serine/threonine phosphorylation of IRS-1 and IRS-2 inhibits their binding to the juxtamembrane region of the insulin receptor and impairs their ability to undergo insulin-induced tyrosine phosphory

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Improvement in endocrine and ovarian function during dietary treatment of obese women with polycystic ovary syndrome

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Decreases in ovarian cytochrome P450c17 alpha activity and serum free testosterone after reduction of insulin secretion in polycystic ovary syndrome

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Thiazolidinediones block tumor necrosis factor-alpha-induced inhibition of insulin signaling

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From receptor to transporter: insulin signalling to glucose transport.

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Immunocytochemical evidence that GLUT4 resides in a specialized translocation post-endosomal VAMP2-positive compartment in rat adipose cells in the absence of insulin

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Identification and characterization of two distinct intracellular GLUT4 pools in rat skeletal muscle: evidence for an endosomal and an insulin-sensitive GLUT4 compartment

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Molecular actions of insulin on glucose transport

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gp160, a tissue-specific marker for insulin-activated glucose transport

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Molecular machinery mediating vesicle budding, docking and fusion

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Specificity and regulation of a synaptic vesicle docking complex

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Pathophysiology of insulin resistance in human disease.

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Pathogenesis of NIDDM. A balanced overview

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Skeletal muscle is a primary site of insulin resistance in essential hypertension

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Quantitation of muscle glycogen synthesis in normal subjects and subjects with non-insulin-dependent diabetes by 13C nuclear magnetic resonance spectroscopy.

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An in vitro human muscle preparation suitable for metabolic studies. Decreased insulin stimulation of glucose transport in muscle from morbidly obese and diabetic subjects

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Pretranslational suppression of a glucose transporter protein causes insulin resistance in adipocytes from patients with non-insulin-dependent diabetes mellitus and obesity

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In vivo stimulation of the insulin receptor kinase in human skeletal muscle. Correlation with insulin-stimulated glucose disposal during euglycemic clamp studies

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Insulin receptor phosphorylation, insulin receptor substrate-1 phosphorylation, and phosphatidylinositol 3-kinase activity are decreased in intact skeletal muscle strips from obese subjects

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Reversibility of defective adipocyte insulin receptor kinase activity in non-insulin-dependent diabetes mellitus. Effect of weight loss

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Gene expression of GLUT4 in skeletal muscle from insulin-resistant patients with obesity, IGT, GDM, and NIDDM

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7 January 2021

Evidence for defects in the trafficking and translocation of GLUT4 glucose transporters in skeletal muscle as a cause of human insulin resistance

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Insulin resistance in obese Zucker rat (fa/fa) skeletal muscle is associated with a failure of glucose transporter translocation

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Glucosamine induces insulin resistance in vivo by affecting GLUT 4 translocation in skeletal muscle. Implications for glucose toxicity

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based on heuristic

inferred from DOI database lookup

Identifiers

10.1016/S0002-9343(98)00300-3

1 reference

Europe PubMed Central

PubMed publication ID

25 May 2018

http://europepmc.org/abstract/MED/9809695

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

25 May 2018

http://europepmc.org/abstract/MED/9809695

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