ArticleDiabetologia2003
Peripheral insulin resistance develops in transgenic rats overexpressing phosphoenolpyruvate carboxykinase in the kidney.
Article in Diabetologia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 24 citations in OpenAlex.
- The neglected PCK1/glucagon (inter)action in nutrient homeostasis beyond gluconeogenesis: Disease pathogenesis and treatment.Molecular metabolism · 2025Review
- Whole body glucoregulation and tissue-specific glucose uptake in a novel Akt substrate of 160 kDa knockout rat model.PloS one · 2019Article
- Impaired glucose metabolism and exercise capacity with muscle-specific glycogen synthase 1 (gys1) deletion in adult mice.Molecular metabolism · 2016Article
- Article
- Transgenic modifications of the rat genome.Transgenic research · 2005Review
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Authors and funding
9 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisTo study the secondary consequences of impaired suppression of endogenous glucose production (EGP) we have created a transgenic rat overexpressing the gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK) in the kidney. The aim of this study was to determine whether peripheral insulin resistance develops in these transgenic rats.
methodsWhole body rate of glucose disappearance (R(d)) and endogenous glucose production were measured basally and during a euglycaemic/hyperinsulinaemic clamp in phosphoenolpyruvate carboxykinase transgenic and control rats using [6-(3)H]-glucose. Glucose uptake into individual tissues was measured in vivo using 2-[1-(14)C]-deoxyglucose.
resultsPhosphoenolpyruvate carboxykinase transgenic rats were heavier and had increased gonadal and infrarenal fat pad weights. Under basal conditions, endogenous glucose production was similar in phosphoenolpyruvate carboxykinase transgenic and control rats (37.4+/-1.1 vs 34.6+/-2.6 micromol/kg/min). Moderate hyperinsulinaemia (810 pmol/l) completely suppressed EGP in control rats (-0.6+/-5.5 micromol/kg/min, p<0.05) while there was no suppression in phosphoenolpyruvate carboxykinase rats (45.2+/-7.9 micromol/kg/min). Basal R(d) was comparable between PEPCK transgenic and control rats (37.4+/-1.1 vs 34.6+/-2.6 micromol/kg/min) but under insulin-stimulated conditions the increase in R(d) was greater in control compared to phosphoenolpyruvate carboxykinase transgenic rats indicative of insulin resistance (73.4+/-11.2 vs 112.0+/-8.0 micromol/kg/min, p<0.05). Basal glucose uptake was reduced in white and brown adipose tissue, heart and soleus while insulin-stimulated transport was reduced in white and brown adipose tissue, white quadriceps, white gastrocnemius and soleus in phosphoenolpyruvate carboxykinase transgenic compared to control rats. The impairment in both white and brown adipose tissue glucose uptake in phosphoenolpyruvate carboxykinase transgenic rats was associated with a decrease in GLUT4 protein content. In contrast, muscle GLUT4 protein, triglyceride and long-chain acylCoA levels were comparable between PEPCK transgenic and control rats. CONCLUSIONS/
interpretationA primary defect in suppression of EGP caused adipose tissue and muscle insulin resistance.
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