Control of Adipose Tissue Expandability in Response to High Fat Diet by the Insulin-like Growth Factor-binding Protein-4

Gealekman, Olga; Gurav, Kunal; Chouinard, My T.; Straubhaar, Juerg R.; Thompson, Michael; Malkani, Samir; Hartigan, Celia; Corvera, Silvia

doi:10.1074/jbc.m113.545798

Cited by 56 publications

(54 citation statements)

References 49 publications

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“…Thymosin beta 10 ( TMSB10 ) was shown to be correlated with haematological, biochemical and body composition traits, and the transcript levels of TMSB10 were positively correlated with leukocytes and negatively correlated with erythrocytes, ALB, BUN and all fat traits. This finding is consistent with previous reports of the correlation of TMSB10 with insulin-stimulated sprouting and adipose tissue expansion67.…”

Section: Discussionsupporting

confidence: 94%

Genetically regulated hepatic transcripts and pathways orchestrate haematological, biochemical and body composition traits

Ponsuksili

Trakooljul

Hadlich

et al. 2016

Sci Rep

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The liver is the central metabolic organ and exhibits fundamental functions in haematological traits. Hepatic expression, haematological, plasma biochemical, and body composition traits were assessed in a porcine model (n = 297) to establish tissue-specific genetic variations that influence the function of immune-metabolism-correlated expression networks. At FDR (false discovery rate) <1%, more than 3,600 transcripts were jointly correlated (r = |0.22–0.48|) with the traits. Functional enrichment analysis demonstrated common links of metabolic and immune traits. To understand how immune and metabolic traits are affected via genetic regulation of gene expression, eQTLs were assessed. 20517 significant (FDR < 5%) eQTLs for 1401 transcripts were identified, among which 443 transcripts were associated with at least one of the examined traits and had cis-eQTL (such as ACO1 (6.52 × 10−7) and SOD1 (6.41 × 10−30). The present study establishes a comprehensive view of hepatic gene activity which links together metabolic and immune traits in a porcine model for medical research.

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Section: Discussionsupporting

confidence: 94%

Genetically regulated hepatic transcripts and pathways orchestrate haematological, biochemical and body composition traits

Ponsuksili

Trakooljul

Hadlich

et al. 2016

Sci Rep

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“…Adipose tissue expansion in response to high-fat feeding requires an expanded vasculostromal network. The angiogenic response was increased by insulin, which decreased IGFBP4 as well as altering expression of other genes (Gealekman et al 2014).…”

Section: Insulin-like Growth Factor-binding Proteinsmentioning

confidence: 99%

Endothelial cells and the IGF system

Bach¹

2014

Journal of Molecular Endocrinology

156

118

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Endothelial cells line blood vessels and modulate vascular tone, thrombosis, inflammatory responses and new vessel formation. They are implicated in many disease processes including atherosclerosis and cancer. IGFs play a significant role in the physiology of endothelial cells by promoting migration, tube formation and production of the vasodilator nitric oxide. These actions are mediated by the IGF1 and IGF2/mannose 6-phosphate receptors and are modulated by a family of high-affinity IGF binding proteins. IGFs also increase the number and function of endothelial progenitor cells, which may contribute to protection from atherosclerosis. IGFs promote angiogenesis, and dysregulation of the IGF system may contribute to this process in cancer and eye diseases including retinopathy of prematurity and diabetic retinopathy. In some situations, IGF deficiency appears to contribute to endothelial dysfunction, whereas IGF may be deleterious in others. These differences may be due to tissue-specific endothelial cell phenotypes or IGFs having distinct roles in different phases of vascular disease. Further studies are therefore required to delineate the therapeutic potential of IGF system modulation in pathogenic processes.

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“…A fragment of collagen VI has also been reported to confer metabolic dysfunction in adipose tissue 101 . Since IGF-1 is a potent stimulator of collagen expression, perhaps high insulin levels stimulate the IGF-1 receptor or cause IGF binding protein degradation 110 to strongly promote collagen synthesis in fibroblasts of adipose tissue. Thus, this pathway could represent another mechanism through which hyperinsulinemia causes insulin resistance.…”

Section: Cellular and Molecular Causes Of Impaired Insulin Responsivementioning

confidence: 99%

Insulin action and resistance in obesity and type 2 diabetes

Czech

2017

Nat Med

982

692

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Nutritional excess is a major forerunner of type 2 diabetes and enhances the secretion of insulin but attenuates its metabolic actions in the liver, skeletal muscle and adipose tissue. However, conflicting evidence indicates a lack of knowledge of the timing of these events during the development of obesity and diabetes and is a key gap in our understanding of metabolic disease. This Perspective reviews alternate viewpoints and recent results on the temporal and mechanistic connections between hyperinsulinemia, obesity and insulin resistance. Although much attention has addressed early steps in the insulin signaling cascade, insulin resistance in obesity appears to be largely elicited downstream of these steps. New findings also connect insulin resistance to extensive metabolic crosstalk between liver, adipose, pancreas and skeletal muscle. These and other advances over the last 5 years offer both exciting opportunities and daunting challenges in developing new therapeutic strategies for the treatment of type 2 diabetes.

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Control of Adipose Tissue Expandability in Response to High Fat Diet by the Insulin-like Growth Factor-binding Protein-4

Cited by 56 publications

References 49 publications

Genetically regulated hepatic transcripts and pathways orchestrate haematological, biochemical and body composition traits

Genetically regulated hepatic transcripts and pathways orchestrate haematological, biochemical and body composition traits

Endothelial cells and the IGF system

Insulin action and resistance in obesity and type 2 diabetes

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