Intra-uterine growth restriction differentially regulates perinatal brain and skeletal muscle glucose transporters

Sadiq, Heena; Das, Utpala G.; Tracy, Thomas F.; Devaskar, Sherin U.

doi:10.1016/s0006-8993(99)01145-2

Cited by 60 publications

(40 citation statements)

References 40 publications

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“…Altered fetal and neonatal GLUT gene expression has been reported for non-cardiac tissues from growthretarded animals exposed to uteroplacental insufficiency, though altered adult myocardial gene expression of GLUT1 and GLUT4 has not been previously reported in this or other models of IUGR (Simmons et al 1992, Sadiz et al 1999. However, rat models that induce IUGR by maternal malnutrition, particularly those employing isocaloric low-protein maternal diets, provide insights into the significance of our findings.…”

Section: Discussionmentioning

confidence: 55%

Myocardial gene expression of glucose transporter 1 and glucose transporter 4 in response to uteroplacental insufficiency in the rat

Tsirka

Gruetzmacher²,

Kelley³

et al. 2001

Journal of Endocrinology

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Uteroplacental insufficiency causes intrauterine growth retardation (IUGR) and subsequent low birth weight, which predisposes the affected newborn towards adult Syndrome X. Individuals with Syndrome X suffer increased morbidity from adult ischemic heart disease. Myocardial ischemia initiates a defensive increase in cardiac glucose metabolism, and individuals with Syndrome X demonstrate reduced insulin sensitivity and reduced glucose uptake. Glucose transporters GLUT1 and GLUT4 facilitate glucose uptake across cardiac plasma membranes, and hexokinase II (HKII) is the predominant hexokinase isoform in adult cardiac tissue. We therefore hypothesized that GLUT1, GLUT4 and HKII gene expression would be reduced in heart muscle of growth-retarded rats, and that reduced gene expression would result in reduced myocardial glucose uptake. To prove this hypothesis, we measured cardiac GLUT1 and GLUT4 mRNA and protein in control IUGR rat hearts at day 21 and at day 120 of life. HKII mRNA quantification and 2-deoxyglucose-uptake studies were performed in day-120 control and IUGR cardiac muscle. Both GLUT1 and GLUT4 mRNA and protein were significantly reduced at day 21 and at day 120 of life in IUGR hearts. HKII mRNA was also reduced at day 120. Similarly, both basal and insulin-stimulated glucose uptake were significantly reduced in day-120 IUGR cardiac muscle. We conclude that adult rats showing IUGR as a result of uteroplacental insufficiency express significantly less cardiac GLUT1 and GLUT4 mRNA and protein than control animals (which underwent sham operations), and that this decrease in gene expression occurs in parallel with reduced myocardial glucose uptake. We speculate that this reduced GLUT gene expression and glucose uptake contribute towards mortality from ischemic heart disease seen in adults born with IUGR.

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Section: Discussionmentioning

confidence: 55%

Myocardial gene expression of glucose transporter 1 and glucose transporter 4 in response to uteroplacental insufficiency in the rat

Tsirka

Gruetzmacher²,

Kelley³

et al. 2001

Journal of Endocrinology

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“…= [214] ↓4-23% [79,87,88,[93][94][95][96] = [201,215] ↓7-52% [91,92,[97][98][99][100][101]216] ↓9.5-14% [83,89] = [84] ↓[128, 129,131,146] ↓8-40% [99,112,114,115,160,203,217,218] ↓36-42% [145,162] ↓18-44% [102, 116-118, 163, 212] ↓42-48% [122,124,125] ↓17-28% [132,[134][135][136][137][138][139][140][141] Brain size = [214] ↓cerebrum, 11% [79] ↓11-66% [90,…”

Section: Birth Weightmentioning

confidence: 99%

Programming the brain: Common outcomes and gaps in knowledge from animal studies of IUGR

Hunter

Hazel

Kind

et al. 2016

Physiology & Behavior

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“…The glucose transporter molecule GLUT1 has been proposed as a candidate to mediate those cellular effects of glucose (56). Recent animal studies showed that intrauterine growth retardation induced by uterine artery ligation is associated with an increased hepatic (57) and skeletal muscle (58) expression of GLUT1 in the neonatal period. Although it is not known whether these changes persist into adulthood, it may be speculated that parallel or similar compensatory changes in expression patterns of glucose transporters may occur as a result of altered organ programming in men who had LBW.…”

Section: Subject Characteristicsmentioning

confidence: 99%

Early Differential Defects of Insulin Secretion and Action in 19-Year-Old Caucasian Men Who Had Low Birth Weight

et al. 2002

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Several studies have linked low birth weight (LBW) and type 2 diabetes. We investigated hepatic and peripheral insulin action including intracellular glucose metabolism in 40 19-year-old men (20 LBW, 20 matched control subjects), using the hyperinsulinemic-euglycemic clamp technique at two physiological insulin levels (10 and 40 mU/m 2 per min), indirect calorimetry, and [3-3 H]glucose. Insulin secretion was examined during an oral and intravenous glucose tolerance test. Fasting p-glucose was higher in the LBW group (5.6 ؎ 0.1 vs. 5.4 ؎ 0.1; P < 0.05). Basal plasma glycerol concentrations were significantly lower in the LBW group. Insulin-stimulated glycolytic flux was significantly reduced, and suppression of endogenous glucose production was enhanced in the LBW group. Nevertheless, basal and insulin-stimulated rates of whole-body peripheral glucose disposal, glucose oxidation, lipid oxidation, exogenous glucose storage, and nonoxidative glucose metabolism were similar in the two groups. Insulin secretion was reduced by 30% in the LBW group, when expressed relative to insulin sensitivity (disposition index ‫؍‬ insulin secretion ؋ insulin action). We propose that reduced insulin-stimulated glycolysis precedes overt insulin resistance in LBW men. A lower insulin secretion may contribute to impaired glucose tolerance and ultimately lead to diabetes.

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Intra-uterine growth restriction differentially regulates perinatal brain and skeletal muscle glucose transporters

Cited by 60 publications

References 40 publications

Myocardial gene expression of glucose transporter 1 and glucose transporter 4 in response to uteroplacental insufficiency in the rat

Myocardial gene expression of glucose transporter 1 and glucose transporter 4 in response to uteroplacental insufficiency in the rat

Programming the brain: Common outcomes and gaps in knowledge from animal studies of IUGR

Early Differential Defects of Insulin Secretion and Action in 19-Year-Old Caucasian Men Who Had Low Birth Weight

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