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Last update 08 May 2025

Insulin-Like Growth Factor I, Resistance To

Last update 08 May 2025

Basic Info

Synonyms

Growth delay due to insulin-like growth factor 1 resistance, Growth delay due to insulin-like growth factor I resistance, Growth delay due to insulin-like growth factor I resistance (disorder)

+ [18]

Introduction

Tissue unresponsiveness to insulin-like growth factor-I.

Drugs associated with Insulin-Like Growth Factor I, Resistance To

AZD9362

Target

IGF-1R

Mechanism

IGF-1R antagonists

Active Org.-

Originator Org.

AstraZeneca PLC

Active Indication-

Inactive Indication

Insulin-Like Growth Factor I, Resistance To

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with Insulin-Like Growth Factor I, Resistance To

IRCT20190218042751N1

/ CompletedNot ApplicableIIT

Effect of 12 Weeks Selected Rubber Band Resistance Training on Serum Fibroblast Growth Factor 23 and Insulin Resistance in Older Women

Start Date18 Feb 2019

Sponsor / Collaborator

Shahrekord University

100 Clinical Results associated with Insulin-Like Growth Factor I, Resistance To

100 Translational Medicine associated with Insulin-Like Growth Factor I, Resistance To

0 Patents (Medical) associated with Insulin-Like Growth Factor I, Resistance To

Literatures (Medical) associated with Insulin-Like Growth Factor I, Resistance To

01 Nov 2024·International Journal of Obesity

Likely causal effects of insulin resistance and IGF-1 bioaction on childhood and adult adiposity: a Mendelian randomization study

Article

Author: Vaudel, Marc ; Perry, John R. B. ; Perry, John R B ; Kaisinger, Lena R ; Kentistou, Katherine A ; Stankovic, Stasa ; Njølstad, Pål R ; Kaisinger, Lena R. ; Day, Felix R ; Olwi, Duaa I. ; Kentistou, Katherine A. ; Ong, Ken K ; Day, Felix R. ; Johansson, Stefan ; Njølstad, Pål R. ; Ong, Ken K. ; Olwi, Duaa I

AbstractBackgroundCirculating insulin and insulin-like growth factor-1 (IGF-1) concentrations are positively correlated with adiposity. However, the causal effects of insulin and IGF-1 on adiposity are unclear.MethodsWe performed two-sample Mendelian randomization analyses to estimate the likely causal effects of fasting insulin and IGF-1 on relative childhood adiposity and adult body mass index (BMI). To improve accuracy and biological interpretation, we applied Steiger filtering (to avoid reverse causality) and ‘biological effect’ filtering of fasting insulin and IGF-1 associated variants.ResultsFasting insulin-increasing alleles (35 variants also associated with higher fasting glucose, indicative of insulin resistance) were associated with lower relative childhood adiposity (P = 3.8 × 10−3) and lower adult BMI (P = 1.4 × 10−5). IGF-1-increasing alleles also associated with taller childhood height (351 variants indicative of greater IGF-1 bioaction) showed no association with relative childhood adiposity (P = 0.077) or adult BMI (P = 0.562). Conversely, IGF-1-increasing alleles also associated with shorter childhood height (306 variants indicative of IGF-1 resistance) were associated with lower relative childhood adiposity (P = 6.7 × 10−3), but effects on adult BMI were inconclusive.ConclusionsGenetic causal modelling indicates negative effects of insulin resistance on childhood and adult adiposity, and negative effects of IGF-1 resistance on childhood adiposity. Our findings demonstrate the need to distinguish between bioaction and resistance when modelling variants associated with biomarker concentrations.

01 Feb 2024·Journal of Feline Medicine and Surgery

Feline comorbidities: hypersomatotropism-induced diabetes in cats

Review

Author: Scudder, Christopher ; Church, David

Practical relevance: Diabetes mellitus is the second-most common feline endocrinopathy, affecting an estimated 1/200 cats. While the underlying causes vary, around 15-25% of cats with diabetes mellitus develop the condition secondarily to progressive growth hormone (GH)-induced insulin resistance. This typically results in a form of diabetes that is challenging to manage, whereby the response to insulin is very variable or high doses are required to achieve even minimal diabetic control. Clinical challenges: Although uncontrolled chronic excessive GH may result in phenotypic changes that raise suspicion for acromegaly, many cats with hypersomatotropism (HST) do not have these changes. In these situations, a clinician's index of suspicion may be increased by the presence of less dramatic changes such as marked polyphagia, stertor or uncontrolled diabetes mellitus. The current diagnostic test of choice is demonstration of a markedly increased serum insulin-like growth factor 1 (IGF1) concentration, but some affected cats will have only a marginal increase; additionally, chronic insulin administration in cats results in an increase in serum IGF1, making the diagnosis less clear cut and requiring additional confirmatory tests. Evidence base: Over the past two decades, HST has increasingly been recognised as an underlying cause of diabetes mellitus in cats. This review, which focuses on diagnosis and treatment, utilises data from observational studies, clinical trials and case series, as well as drawing on the experience of the authors in managing this condition.

01 Aug 2023·Neurobiology of Disease

Prenatal stress aggravates age-dependent cognitive decline, insulin signaling dysfunction, and the pro-inflammatory response in the APPNL-F/NL-F mouse model of Alzheimer's disease

Article

Author: Graff, Johannes ; Trojan, Ewa ; Basta-Kaim, Agnieszka ; Lasoń, Władysław ; Curzytek, Katarzyna ; Saito, Takashi ; Cieślik, Paulina ; Wierońska, Joanna M ; Saido, Takaomi C

Accumulating evidence indicates that early adverse life experiences may be involved in the pathogenesis of Alzheimer's disease (AD). Prenatal stress (PS) can affect brain maturation and neuroimmune and metabolic interactions, leading to age-dependent cognitive deficits in offspring. However, a multi-faceted cause-and-effect impact of PS on the development of cognitive deficits in the process of physiological ageing and in the APP^NL-F/NL-F mouse model of Alzheimer's disease has not yet been evaluated. We have identified age-dependent cognitive learning and memory deficits using male C57BL/6 J (wild type, WT) and the knock-in APP^NL-F/NL-F (KI) aged 12, 15, and 18 months. An increase in the Aβ42/Aβ40 ratio and mouse ApoE levels in the hippocampus and frontal cortex preceded the onset of cognitive deficits in the KI mice. Moreover, dysfunction in insulin signaling, including increased IRS-1 serine phosphorylation in both brain areas and the tyrosine phosphorylation deficit in the frontal cortex, suggested age-dependent insulin/IGF-1 resistance. Resistance was reflected by disturbances in mTOR or ERK1/2 kinase phosphorylation and excessive pro-inflammatory (TNF-α, IL-6, and IL-23) status in the KI mice. Importantly, our study has provided insights into the higher vulnerability to PS-induced exacerbation of age-dependent cognitive deficits and biochemical dysfunction in KI mice than in WT animals. We anticipate our study will lead to future investigation of a multi-faceted cause-and-effect relationship between stress during neurodevelopment and the onset of AD pathology, distinguishing it from changes in the course of dementia during normal ageing.

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