Key result
Experimental diabetes increases regional blood flows, whereas genetic obesity reduces fat perfusion and relative cardiac output.
Why the study?
The effects of experimental diabetes and genetic obesity on regional blood flow across various rat tissues were investigated using a radioisotopically labeled microsphere technique.
Answers are grounded in this paper and cite their sources.
These rat findings should not change clinical practice; leaves open relevance of regional hemodynamics to human diabetes or obesity.
Blood flow through various tissues of streptozotocin- and alloxan-diabetic and genetically obese rats was compared with that of controls by a radioisotopically labeled microsphere technique. Total cardiac output per unit body weight was unchanged in the diabetic group but decreased in the obese animals. The proportion of cardiac output received by the kidney and organs of the gastrointestinal tract was increased in the diabetic animals. Tissue hyperplasia appeared to be largely responsible. Blood flow per unit weight was markedly increased in the fat tissue of diabetic rats but was reduced in that of the obese rats, indicating a positive relationship between fat mobilization and blood flow. Blood flow in the hindlimbs, tail, skin, and spleen were all reduced in at least one diabetic group. Most of the changes observed appeared to progress with the duration of diabetes. Possible hormonal and metabolic causes are discussed. Some of the experimental changes observed may form useful models for diabetic vasculopathy.
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Lucas et al. (1977) studied Experimental diabetes and genetic obesity. Streptozotocin- or alloxan-induced diabetes and genetic obesity vs. Control rats was evaluated on Regional blood flow and total cardiac output per unit body weight. Experimental diabetes increased fat, renal, and GI blood flow in rats, whereas genetic obesity decreased fat blood flow and total cardiac output per unit weight.
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