Sucrose diet induced enzymatic and hormonal responses affecting carbohydrate, lipid and energy metabolism in two species differing in insulin availability: Spiny and ob/ob mice

Abstract

1. 1. The low-insulin responding spiny mice ( Acomys cahirinns), maintained on a 50% sucrose diet vs isocaloric regular diet, responded with an impressive increase in the activity of hepatic enzymes of glycolysis and lipogenesis and in hyperlipidemia. 2. 2. There was no hyperinsulinemia or hyperglycemia and spiny mice did not gain weight on sucrose due to loss of adipose tissue. 3. 3. Serum T 3 levels rose 1.8 fold and the activity of the hepatic mitochondrial FAD-glycerol-3-phosphate oxidase became induced 2.6 fold representing the enhancement of multiple, T 3-dependent, energy-consuming metabolic cycles. An increased TG lipolysis in adipose tissue was also observed. 4. 4. C57BL/6J ob/ob mice were markedly hyperinsulinemic and gained weight on sucrose almost as much as those on regular diet, without changes in serum glucose or insulin. Serum triglyceride level decreased, whereas liver triglycerides accumulated markedly. 5. 5. The extent of the increase in hepatic enzyme activities related to lipogenesis was much lower both in the ob/ob mice and their lean siblings, than in spiny mice, but the basal enzyme activities in ob/ob mice were remarkably elevated. 6. 6. Serum T 3 level was also elevated already on the regular diet and rose only slightly on sucrose. 7. 7. Basal glycerol phosphate oxidase activity in ob/ob mice exceeded that in spiny mice and rose only marginally on sucrose. 8. 8. Adipose tissue lipolysis was not increased. 9. 9. Thus, sucrose diet by enhancing the T 3 production appeared to activate protective mechanism against weight gain in normoinsulinemic spiny mice, whereas the full expression of these mechanisms appeared to be precluded by the hyperinsulinemia of ob/ob mice. 10. 10. The basally high T 3 levels and glycerol phosphate oxidase activity indicate that these animals are, from the start, close to the peak of their capacity to develop compensatory, energy-dissipating mechanisms.