Michael Kruse

Publications (2)7.45 Total impact

• Article: Maternal substrate utilization programs the development of the metabolic syndrome in male mice exposed to high fat in utero.

  Kirsten Hartil, Patricia M Vuguin, Michael Kruse, Esther Schmuel, Ariana Fiallo, Carlos Vargas, Matthew J Warner, Jorge L Durand, Linda A Jelicks, Maureen J Charron
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  ABSTRACT: Studies were conducted to determine whether maternal substrate utilization during pregnancy affects fetal growth and predisposes offspring to metabolic disease. Female wild-type (WT) and glucose transporter 4 heterozygous mice (G4+/-, a model of altered peripheral substrate utilization) were fed high-fat diet (HFD, 35.5% fat) or control chow (C, 9.5% fat) for 2 wk before mating, throughout pregnancy and lactation (IU/L). WT HFD females exhibited increased serum nonesterified fatty acid and lactate levels and increased hepatic mRNA expression of peroxisome proliferator-activated receptor gamma coactivator-1-beta and SREBP-1c, consistent with increased lipogenesis. G4+/- HFD females exhibited enhanced lipid clearance, and exposure to HFD did not increase hepatic gene expression. HFD independent of maternal genotype decreased fetal growth and birth weight. WT offspring were weaned onto a low-fat diet (5.6% fat). Male offspring of WT mothers exposed to HFD exhibited "catch-up" growth accompanied by increased adiposity, impaired glucose tolerance, and insulin sensitivity. In contrast, male offspring of G4+/- HFD mothers did not exhibit any characteristics of metabolic syndrome. These data suggest that differences in maternal substrate utilization influence offspring metabolic phenotype.
  Pediatric Research 08/2009; 66(4):368-73. · 2.70 Impact Factor
• Article: Hepatic response to restoration of GLUT4 in skeletal muscle of GLUT4 null mice.

  Mollie Ranalletta, Xiu Quan Du, Yoshinori Seki, Alan S Glenn, Michael Kruse, Ariana Fiallo, Irma Estrada, Tsu-Shuen Tsao, Antine E Stenbit, Ellen B Katz, Maureen J Charron
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  ABSTRACT: Expression of GLUT4 in fast-twitch skeletal muscle fibers of GLUT4 null mice (G4-MO) normalized glucose uptake in muscle and restored peripheral insulin sensitivity. GLUT4 null mice exhibit altered carbohydrate and lipid metabolism in liver and skeletal muscle. To test the hypothesis that increased glucose utilization by G4-MO muscle would normalize the changes seen in the GLUT4 null liver, serum metabolites and hepatic metabolism were compared in control, GLUT4 null, and G4-MO mice. The fed serum glucose and triglyceride levels of G4-MO mice were similar to those of control mice. In addition, the alternations in liver metabolism seen in GLUT4 nulls including increased GLUT2 expression and fatty acid synthesis accompanied by an increase in the oxidative arm of the pentose phosphate pathway were absent in G4-MO mice. The transgene used for GLUT4 restoration in muscle was specific for fast-twitch muscle fibers. The mitochondria hypertrophy/hyperplasia in all GLUT4 null skeletal muscles was absent in transgene-positive extensor digitorum longus muscle but present in transgene-negative soleus muscle of G4-MO mice. Results of this study suggest that the level of muscle GLUT4 expression influences mitochondrial biogenesis. These studies also demonstrate that the type and amount of substrate that muscle takes up and metabolizes, determined in part by GLUT4 expression levels, play a major role in directing hepatic carbohydrate and lipid metabolism.
  AJP Endocrinology and Metabolism 12/2007; 293(5):E1178-87. · 4.75 Impact Factor