Insulin resistance, hyperinsulinemia, hypertriglyceridemia, and hypertension. Parallels between human disease and rodent models.
There is considerable evidence that abnormalities of glucose, insulin, and lipoprotein metabolism occur more frequently in untreated hypertensive patients than in normotensive control subjects. More recently, it has also become apparent that similar metabolic abnormalities occur in rodent models of hypertension. One purpose of this article is to review the experimental data that have led to the above generalizations. The second goal is to address the significance of these findings, which is certainly not clear. For example, it could be argued that the relationship between high blood pressure and the associated metabolic defects is incidental. On the other hand, there is evidence that the changes in glucose, insulin, and lipoprotein metabolism may play a role in the etiology and/or clinical course of patients with high blood pressure. Although it is impossible at this point to definitively choose between these possibilities, an effort is made to marshal the evidence in support of the latter alternative.
Reaven
G M
GM
Department of Medicine, Stanford University School of Medicine, Palo Alto, California.
D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D006946:Hyperinsulinism / Q000503:physiopathology*; D006973:Hypertension / Q000503:physiopathology*; D015228:Hypertriglyceridemia / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains