We are analyzing https://link.springer.com/article/10.1007/s00125-005-1669-7.

Title:
Low birthweight is associated with specific changes in muscle insulin-signalling protein expression | Diabetologia
Description:
Aims/hypothesis People with low birthweight have an increased risk of developing type 2 diabetes mellitus in adulthood. The mechanistic basis of this phenomenon is not known. Here we investigate the effect of early growth restriction on the expression of insulin-signalling proteins in skeletal muscle in a human cohort and a rat model. Methods We recruited 20 young men with low birthweight (mean birthweight 2702±202 g) and 20 age-matched control subjects (mean birthweight 3801±99 g). Biopsies were obtained from the vastus lateralis muscle and protein expression of selected insulin-signalling proteins was determined. Rats used for this study were male offspring born to dams fed a standard (20%) protein diet or a low (8%) protein diet during pregnancy and lactation. Protein expression was determined in soleus muscle from adult offspring. Results Low-birthweight subjects showed reduced muscle expression of protein kinase C (PKC)ζ, p85α, p110β and GLUT4. PKCζ, GLUT4 and p85 were also reduced in the muscle of rats fed a low-protein diet. Other proteins studied were unchanged in low-birthweight humans and in rats fed a low-protein diet when compared with control groups. Conclusions/interpretation We found decreased expression of specific insulin-signalling proteins in low-birthweight subjects compared to controls. These changes precede the onset of impaired glucose tolerance. The similarity of protein expression profile in the men with low birthweight compared to that of the offspring of rats fed a low-protein diet suggests that the rodent model is an accurate representation of the human situation. It also provides a potential mechanistic explanation as to why the fetal environment plays an important role in determining risk of developing type 2 diabetes.
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Keywords {🔍}

muscle, expression, insulin, protein, diabetes, lowbirthweight, glucose, control, subjects, google, scholar, article, low, insulinsignalling, observed, birthweight, kinase, tissue, type, resistance, rat, rats, subunit, glut, proteins, human, reduced, table, early, growth, fat, samples, diet, restriction, skeletal, offspring, determined, lowprotein, compared, diabetic, receptor, ozanne, men, pkcζ, humans, adipose, studies, molecular, plasma, antibody,

Topics {✒️}

horseradish-peroxidase-coupled secondary antibodies extensive genome-wide scans hand-held glass homogeniser hetero-dimeric enzyme consisting significant pre-diabetic condition poor maternal nutrition high-intensity interval training ice-cold solubilisation buffer mouse anti-peptide antibodies post-load plasma glucose insulin-signalling pathway proteins sheep anti-peptide antibody selected insulin-signalling proteins protein-restricted rat dams specific insulin-signalling proteins low-birthweight muscle samples low-protein rat model low-birthweight subjects compared rabbit anti-peptide antibody young low-birthweight subjects low-protein diet suggests poor fetal nutrition irs-1 signalling system low-protein offspring compared privacy choices/manage cookies early growth restriction vastus lateralis muscle p85/p110 phosphatidylinositol 3′-kinase muscle glucose uptake insulin-signalling proteins birth weight related poor early growth strenuous physical activity normal glucose tolerance fasting plasma glucose fasting plasma insulin insulin-signalling intermediates overt diabetic state british heart foundation human muscle biopsy medical research council insulin-signalling pathway impaired glucose tolerance poor glucose tolerance muscle biopsy samples insulin-signalling molecules rat fatty tissue low-birthweight subjects low-birthweight subjects [13] insulin-signalling defects

Questions {❓}

Newsome CA, Shiell AW, Fall CH, Phillips DI, Shier R, Law CM (2003) Is birth weight related to later glucose and insulin metabolism?

Schema {🗺️}

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         description:People with low birthweight have an increased risk of developing type 2 diabetes mellitus in adulthood. The mechanistic basis of this phenomenon is not known. Here we investigate the effect of early growth restriction on the expression of insulin-signalling proteins in skeletal muscle in a human cohort and a rat model. We recruited 20 young men with low birthweight (mean birthweight 2702±202 g) and 20 age-matched control subjects (mean birthweight 3801±99 g). Biopsies were obtained from the vastus lateralis muscle and protein expression of selected insulin-signalling proteins was determined. Rats used for this study were male offspring born to dams fed a standard (20%) protein diet or a low (8%) protein diet during pregnancy and lactation. Protein expression was determined in soleus muscle from adult offspring. Low-birthweight subjects showed reduced muscle expression of protein kinase C (PKC)ζ, p85α, p110β and GLUT4. PKCζ, GLUT4 and p85 were also reduced in the muscle of rats fed a low-protein diet. Other proteins studied were unchanged in low-birthweight humans and in rats fed a low-protein diet when compared with control groups. We found decreased expression of specific insulin-signalling proteins in low-birthweight subjects compared to controls. These changes precede the onset of impaired glucose tolerance. The similarity of protein expression profile in the men with low birthweight compared to that of the offspring of rats fed a low-protein diet suggests that the rodent model is an accurate representation of the human situation. It also provides a potential mechanistic explanation as to why the fetal environment plays an important role in determining risk of developing type 2 diabetes.
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