scholarly journals Central insulin‐like growth factor‐1 ( IGF ‐1) restores whole‐body insulin action in a model of age‐related insulin resistance and IGF ‐1 decline

Aging Cell ◽  
2015 ◽  
Vol 15 (1) ◽  
pp. 181-186 ◽  
Author(s):  
Derek M. Huffman ◽  
Gabriela Farias Quipildor ◽  
Kai Mao ◽  
Xueying Zhang ◽  
Junxiang Wan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Growth Factor ◽  
Insulin Action ◽  
Whole Body ◽  
Insulin Like Growth Factor ◽  
Age Related

scholarly journals Association between insulin-like growth factor 1 and insulin resistance in obese prepubertal boys:a cross-sectional study

2020 ◽  
Author(s):  
Jiangying Kuang ◽  
Li Zhang ◽  
Yueqin Xu ◽  
Jiang Xue ◽  
Shuang Liang
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Cardiovascular Risk ◽  
Growth Factor ◽  
Cardiovascular Risk Factors ◽  
Whole Body ◽  
Sensitivity Index ◽  
Insulin Like Growth Factor ◽  
Prepubertal Boys ◽  
The Relationship

Abstract Background As one of the most common features of obesity, insulin resistance is central to the pathogenesis of the metabolic syndrome. Low insulin-like growth factor 1(IGF-1) levels have been proven to be associated with many traditional cardiovascular risk factors, but it still remains controversy with the relationship between IGF-1 and insulin resistance. Accordingly, the main purpose of this study is to investigate the relationship between IGF-1 and insulin resistance in obese prepubertal boys.Methods We used whole body insulin sensitivity index (WBISI) to represent insulin resistance. 70 obese prepubertal boys were included in this study, and the obese subjects were divided into two groups by using 1.285 as a threshold value for WBISI. Clinical examination and laboratory examinations were assessed for all participants.Results Among obese boys, the group of children with WBISI ≤ 1.285 had lower IGF-1 standard deviation scores (SDS) (p = 0.021) than WBISI > 1.285 group. The results of multivariate stepwise regression analysis show that WBISI was positively correlated with IGF-1 SDS (β = 1.726, p = 0.002) after adjusting for traditional cardiovascular risk factors.Conclusion IGF-1 SDS was negatively associated with insulin resistance in obese prepubertal boys, independent of other traditional cardiovascular disease risk markers.

scholarly journals Association Between Insulin-like Growth Factor 1 and Insulin Resistance in Obese Prepubertal Boys: A Cross-sectional Study

2020 ◽  
Author(s):  
Jiangying Kuang ◽  
Li Zhang ◽  
Yueqin Xu ◽  
Jiang Xue ◽  
Shuang Liang
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Cardiovascular Risk ◽  
Growth Factor ◽  
Cardiovascular Risk Factors ◽  
Whole Body ◽  
Sensitivity Index ◽  
Insulin Like Growth Factor ◽  
Prepubertal Boys ◽  
The Relationship

Abstract Background: As one of the most common features of obesity, insulin resistance is central to the pathogenesis of the metabolic syndrome. Low insulin-like growth factor 1(IGF-1) levels have been proven to be associated with many traditional cardiovascular risk factors, but it still remains controversy with the relationship between IGF-1 and insulin resistance. Accordingly, the main purpose of this study is to investigate the relationship between IGF-1 and insulin resistance in obese prepubertal boys.Methods: We used whole body insulin sensitivity index (WBISI) to represent insulin resistance. 70 obese prepubertal boys were included in this study, and the obese subjects were divided into two groups by using 1.285 as a threshold value for WBISI. Clinical examination and laboratory examinations were assessed for all participants.Results: Among obese boys, the group of children with WBISI ≤1.285 had lower IGF-1 standard deviation scores (SDS) (p = 0.021) than WBISI >1.285 group. The results of multivariate stepwise regression analysis show that WBISI was positively correlated with IGF-1 SDS (β =1.726, p = 0.002) after adjusting for traditional cardiovascular risk factors.Conclusion: IGF-1 SDS was negatively associated with insulin resistance in obese prepubertal boys, independent of other traditional cardiovascular disease risk markers.

scholarly journals Disruption of Hepatocyte Jak2 leads to Spontaneous NASH in Aged Mice and Uncouples Metabolic Liver Disease from Insulin Resistance

2016 ◽  
Author(s):  
Camella G. Wilson ◽  
Aras N. Mattis ◽  
Jennifer L. Tran ◽  
Kevin Corbit ◽  
Ethan J. Weiss
Keyword(s):  
Insulin Resistance ◽  
Growth Hormone ◽  
Fatty Acid ◽  
Liver Disease ◽  
Insulin Sensitivity ◽  
Growth Factor ◽  
Whole Body ◽  
Aged Mice ◽  
Age Related ◽  
Specific Deletion

ABSTRACTGrowth Hormone (GH) is a master regulator of metabolic homeostasis and longevity. Whole body GH insensitivity (GHI) augments insulin sensitivity, age-related disease resistance, adiposity, and occurrence of NAFLD. Conversely, acromegalic patients are prone to diabetes and increased mortality due to constitutive high levels of circulating GH. However, which tissues control the various metabolic aspects of GH physiology are unknown. Therefore, we determined the role of GH in age-related metabolic dysfunction by inducing hepatocyte- (JAK2L) or adipocyte-specific (JAK2A) GHI individually or combinatorially (JAK2LA) via deletion of Jak2, an obligate transducer of GH signaling. Aged JAK2L mice were insulin resistant but lean and had significant NASH, hepatic inflammation, and fibrosis. In contrast, JAK2A animals had increased adiposity and were completely resistant to age-associated hepatic steatosis, NASH, and insulin resistance. Interestingly, while JAK2LA mice retained enhanced whole-body insulin sensitivity, they still developed NASH to an almost identical degree as JAK2L mice but with a substantial reduction in the degree of microvesicular steatosis. Collectively, loss of adipocyte Jak2 conferred whole body insulin sensitivity even in the face of obesity and NASH. Deletion of hepatocyte Jak2 promoted NASH in aged mice without any dietary or drugs perturbations. The effect appears to be liver autonomous and cannot be overcome by the insulin sensitizing effect of adipocyte Jak2 deletion. Here, we describe the first model of spontaneous NASH that is coupled to augmented insulin sensitivity. Further, there was an inverse correlation between insulin sensitivity and the degree of microvesicular steatosis. Therefore, GH signaling independently mediates insulin/glucose and lipid homeostasis and directly regulates the development of NASH in aged mice.Financial Support:This study was supported by National Institutes of Health (NIH) Grants 1R01DK091276 (to E.J.W.). We also acknowledge the support of the University of California, San Francisco (UCSF) Cardiovascular Research Institute, the UCSF Diabetes Center (P30 DK063720), the UCSF Liver Center (P30 DK026743, and the James Peter Read Foundation.AbbreviationsNASHnon-alcoholic steato-hepatitisNAFLDnon-alcoholic fatty liver diseaseGHgrowth hormoneJAK2Janus kinase 2CONCON miceJAK2Lhepatocyte-specific deletion of JAK2JAK2Aadipocyte-specific deletion of JAK2JAK2LAhepatocyte and adipocyte JAK2 knockoutTGtriglycerideASTaspartate aminotransferaseALTalanine transaminaseStat5signal transducer and activator of transcription 5qRT-PCRquantitative reverse-transcription polymerase chain reactionMcp1monocyte chemoattractant protein-1Cd11bcluster of differentiation molecule 11bF4/80EGF-like module-containing mucin-like hormone receptor-like 1FcgR1high affinity immunoglobulin gamma Fc receptor IL-Fabpliver fatty acid binding proteinPPARγperoxisome proliferator-activated receptor gammaFATPfatty acid transport proteinCD36/FATFatty Acid TranslocaseITTinsulin tolerance test.Lpllipoprotein lipaseIL-interleukin-FcgR1Fc receptor IgGTnfαtumor necrosis factor alphaTgfβ1transforming growth factor beta 1αSMA, alpha 2smooth muscle actinIGF-1insulin-like growth factor 1.

scholarly journals Association between insulin-like growth factor 1 and insulin resistance in obese prepubertal boys: a cross-sectional study

2020 ◽  
Author(s):  
Jiangying Kuang ◽  
Li Zhang ◽  
Yueqin Xu ◽  
Jiang Xue ◽  
shuang liang
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Cardiovascular Risk ◽  
Growth Factor ◽  
Cardiovascular Risk Factors ◽  
Whole Body ◽  
Sensitivity Index ◽  
Insulin Like Growth Factor ◽  
Prepubertal Boys ◽  
The Relationship

Abstract Background As one of the most common features of obesity, insulin resistance is central to the pathogenesis of the metabolic syndrome. Low insulin-like growth factor 1(IGF-1) levels have been proven to be associated with many traditional cardiovascular risk factors, but it still remains controversy with the relationship between IGF-1 and insulin resistance. Accordingly, the main purpose of this study is to investigate the relationship between IGF-1 and insulin resistance in obese prepubertal boys. Methods We used whole body insulin sensitivity index (WBISI) to represent insulin resistance. 70 obese prepubertal boys were included in this study, and the obese subjects were divided into two groups by using 1.285 as a threshold value for WBISI. Clinical examination and laboratory examinations were assessed for all participants. Results Among obese boys, the group of children with WBISI ≤ 1.285 had lower IGF-1 standard deviation scores (SDS) (p = 0.021) than WBISI > 1.285 group. The results of multivariate stepwise regression analysis show that WBISI was positively correlated with IGF-1 SDS (β = 1.726, p = 0.002) after adjusting for traditional cardiovascular risk factors. Conclusion IGF-1 SDS was negatively associated with insulin resistance in obese prepubertal boys, independent of other traditional cardiovascular disease risk markers.

scholarly journals Reduced Insulin-Like Growth Factor 1 Is Associated with Insulin Resistance in Obese Prepubertal Boys

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Jiangying Kuang ◽  
Li Zhang ◽  
Yueqin Xu ◽  
Jiang Xue ◽  
Shuang Liang ◽  
...  
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Cardiovascular Risk ◽  
Growth Factor ◽  
Cardiovascular Risk Factors ◽  
Whole Body ◽  
Sensitivity Index ◽  
Insulin Like Growth Factor ◽  
Prepubertal Boys ◽  
The Relationship

As one of the most common features of obesity, insulin resistance is central to the pathogenesis of the metabolic syndrome. Low insulin-like growth factor 1 (IGF-1) levels have been proven to be associated with many traditional cardiovascular risk factors, but it still remains controversial with the relationship between IGF-1 and insulin resistance. Accordingly, the main purpose of this study is to investigate the relationship between IGF-1 and insulin resistance in obese prepubertal boys. We used the whole-body insulin sensitivity index (WBISI) to represent insulin resistance. 70 obese prepubertal boys were included in the study, and the obese subjects were divided into two groups by using 1.285 as a threshold value for WBISI. Clinical examination and laboratory examinations were assessed for all participants. Among obese boys, the group of children with WBISI ≤ 1.285 had lower IGF-1 standard deviation scores (SDS) ( p = 0.021 ) than the WBISI > 1.285 group. The results of multiple linear analyses show that lg WBISI was positively correlated with IGF-1 SDS ( p = 0.031 ) after adjusting for traditional cardiovascular risk factors. IGF-1 SDS was negatively associated with insulin resistance in obese prepubertal boys, independent of other traditional cardiovascular disease risk markers.

scholarly journals Adipokine Protein Expression Pattern in Growth Hormone Deficiency Predisposes to the Increased Fat Cell Size and the Whole Body Metabolic Derangements

2008 ◽  
Vol 93 (6) ◽  
pp. 2255-2262 ◽  
Author(s):  
Jozef Ukropec ◽  
Adela Penesová ◽  
Martina Škopková ◽  
Mikuláš Pura ◽  
Miroslav Vlček ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Growth Factor ◽  
Glucose Tolerance ◽  
Protein Expression ◽  
Expression Pattern ◽  
Insulin Action ◽  
Whole Body ◽  
Protein Expression Pattern ◽  
Chemotactic Protein

Abstract Context: GH deficiency (GHD) in adults is associated with central adiposity, dyslipidemia, and insulin resistance. Objective: The objective of the study was to test the hypothesis that GHD might change the spectrum of adipokines and thus influence the adipose tissue and the whole-body metabolic and inflammatory status leading to development of insulin resistance. Design: This was a single-center observational study with a cross-sectional design. Participants and Methods: Protein arrays were used to characterize adipokines expressed in the sc adipose tissue obtained from young GHD adults and compared with age-, gender-, and body mass index (BMI)-matched group of healthy individuals. All subjects underwent an oral glucose tolerance test, euglycemic hyperinsulinemic clamp, and magnetic resonance imaging examination. Results: Presence of abdominal obesity, enlarged adipocytes, increased circulating high-sensitivity C-reactive protein, impaired glucose tolerance, and decreased insulin action were found in GHD. Changes in adipokine protein expression due to GHD were highly dependent on the obesity phenotype. Lean GHD individuals (BMI ∼23 kg/m2) had decreased protein levels for stem cell factor and epithelial growth factor, indicating a possible defect in adipocyte differentiation and proliferation. Decrease of vascular endothelial growth factor, stromal cell-derived factor, angiopoietin-2, and brain-derived neurotrophic factor advocated for attenuated angiogenesis and neurogenesis. Presence of obesity (BMI ∼31 kg/m2) eliminated these inhibitory effects. However, adipose tissue expansion in GHD individuals was paralleled by an elevation of adipose tissue proinflammatory cytokines (IL-1β, interferon-γ) and chemoattractants (interferon-inducible T cell α-chemoattractant, monocyte chemotactic protein-2, monocyte chemotactic protein-3, eotaxin). Conclusion: Our data demonstrate that GHD modulates adipokine and cytokine protein expression pattern, which might influence the adipose tissue growth and differentiation and predispose to tissue hypoxia, inflammation, and a defect in the whole-body insulin action.

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