Adrenergic overactivity and insulin resistance in nonobese hereditary hypertriglyceridemic rats
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Epinephrine blood MeSH
- Receptors, Adrenergic, beta physiology MeSH
- Dihydroalprenolol metabolism MeSH
- Glucose metabolism MeSH
- Glucose Clamp Technique MeSH
- Hypertriglyceridemia genetics physiopathology MeSH
- Insulin blood MeSH
- Insulin Resistance * MeSH
- Blood Glucose metabolism MeSH
- Blood Pressure MeSH
- Rats MeSH
- Homovanillic Acid urine MeSH
- Vanilmandelic Acid urine MeSH
- Rats, Wistar MeSH
- Muscles metabolism MeSH
- Adipose Tissue metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Epinephrine MeSH
- Receptors, Adrenergic, beta MeSH
- Dihydroalprenolol MeSH
- Glucose MeSH
- Insulin MeSH
- Blood Glucose MeSH
- Homovanillic Acid MeSH
- Vanilmandelic Acid MeSH
Nonobese, hereditary hypertriglyceridemic (HTG) rats provide an interesting model of hypertriglyceridemia, glucose intolerance, and hypertension. In age-matched 15 HTG and 16 control Wistar rats fed on a high sucrose diet (70 cal%) for 6 weeks, we measured insulin sensitivity in vivo and some parameters of sympatoadrenal system. Using euglycemic clamps with administration of 2-deoxy[1-3H]glucose, we found whole body insulin resistance and decreased glucose metabolic index Rg' in soleus muscle, epitrochlearis muscle, diaphragm, and white adipose tissue in HTG rats. We found higher levels of plasma epinephrine and higher excretion of vanilmandelic and homovanilic acids in HTG rats. The binding of [3H]-dihydroalprenol to the heart membrane fraction was similar in both groups, but the dissociation constant Kd was increased by 75% in the heart of HTG rats.
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