Attenuation of hypertriglyceridemia-induced pressor effect in rats with fructose-induced insulin resistance.
This study was designed to compare the pressor response to hypertriglyceridemia under basal glucose and insulin condition as well as the decay pattern of this lipid-induced pressor effect in normal (NRs) and fructose-induced insulin resistant rats (FIRs). The rats were on a fructose-enriched or a regular chow diet for 8 wks and then were further divided into two subgroups (n = 8/group) with lipofundin (a 20% triglyceride emulsion) or saline infusion during the following clamp study. The acute clamp experiment contained a 30-min basal period, followed by a 120-min test period and a 90-min off period. After the basal period, somatostatin (1.3 microg/kg/min) combined with regular insulin (0.6 mU/kg/min) and variable glucose infusion were given to keep insulin and glucose levels basal throughout the experiment. The baseline triglyceride levels were about 6 folds higher in FIRs than those in NRs. During the test period, the lipofundin infusion (1.2 ml/kg/hr) increased plasma triglyceride levels by 368 +/- 39 and 489 +/- 38 mg/dL from baseline in NRs and FIRs, respectively. The elevated triglyceride level was dropped promptly while the lipofundin infusion was discontinued in the following off period. FIRs have higher mean arterial blood pressure (MAP) levels than those in NRs. During the test period, the hypertriglyceridemia-induced press responses were markedly delayed and attenuated in FIRs compared with those in NRs. Accordingly, the value of deltaMAP/deltaTG served as an index of the hypertriglyceridemia-induced increase in BP was significantly lower in FIRs than in NRs. This hypertriglyceridemia-induced pressor effect was sustained to the end of study even after removal of the lipid infusion for 60 min in NRs and FIRs. In rats without lipofundin infusion, MAP and plasma triglyceride levels failed to change throughout the study. The present results suggest that the prolonged pressor response induced by acute hypertriglyceridemia is attenuated in rats with fructose-induced insulin resistance.
Lin
Hung-Jung
HJ
Department of Emergency Medicine, Chi-Mei Medical Center, Tainan, ROC.
Loh
Ching-Hui
CH
Liao
Min-Tser
MT
Liu
Tse-Tsung
TT
Hsieh
Po-Shiuan
PS
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D001835:Body Weight; D004032:Diet; D004338:Drug Combinations; D005632:Fructose / Q000008:administration & dosage* / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D015228:Hypertriglyceridemia / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D007262:Infusions, Intravenous; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D009994:Osmolar Concentration; D010743:Phospholipids / Q000008:administration & dosage; D051381:Rats; D017207:Rats, Sprague-Dawley; D013012:Sorbitol / Q000008:administration & dosage; D014280:Triglycerides / Q000097:blood
D001786:Blood Glucose; D004338:Drug Combinations; D007328:Insulin; D010743:Phospholipids; D014280:Triglycerides; C008288:Lipofundin; D005632:Fructose; D013012:Sorbitol