Abnormalities of glucose metabolism in spontaneously hypertensive rats

Abstract

Abnormalities in glucose metabolism and insulin action are frequently detected in patients with essential hypertension. Spontaneously hypertensive rats (SHR) have been used as an experimental model to understand this pathological condition. The objective of the present study was to assess glucose metabolism and insulin action in SHR and Wistar rats under fed and fasting conditions. Peripheral glucose utilization was estimated by kinetic studies with [6-3 H]-glucose and gluconeogenetic activity was measured during continuous [ 14 C]-bicarbonate infusion. Plasma glucose levels were higher in the SHR group. Plasma insulin levels in the fed state were higher in the SHR group (99.8 ± 6.5 µM) than in the control group (70.4 ± 3.6 µM). Muscle glycogen content was reduced in SHR compared to control under the various experimental conditions. Peripheral glucose utilization was slightly lower in the SHR group in the fed state (8.72 ± 0.55 vs 9.52 ± 0.80 mg kg -1 min -1 in controls). Serum free fatty acid levels, hepatic glycogen levels, hepatic phosphoenolpyruvate carboxykinase activity and gluconeogenetic activity were similar in the two groups. The presence of hyperglycemia and hyperinsulinemia and the slightly reduced peripheral glucose utilization suggest the presence of resistance to the action of insulin in peripheral tissues of SHR. Hepatic gluconeogenesis does not seem to contribute to the metabolic alterations detected in these animals.

Hepatic parasympathetic role in insulin resistance on an animal model of hypertension

“…That is consistent with the results of other studies where insulin sensitivity was measured before and after feeding [21,23]. There, skeletal muscle glycogen content, identical between WKY and SHR in the fasted state, increased from fasting to refeeding in WKY, whereas in SHR it remained similar to fasting levels [21].…”

“…In addition, feeding increased muscle glycogen content much more in WIS than in SHR [23]. However, in both studies, liver glycogen accumulation increased similarly in both strains and liver glycogen total content was similar [21,23], which indicates that the difference in postprandial insulin sensitivity between the strains is specific to the skeletal muscle. This supports our concept that, in the postprandial state, the skeletal muscle is further sensitized to glucose uptake and glycogen synthesis by a mechanism that is unable to properly function in the SHR.…”

“…There, skeletal muscle glycogen content, identical between WKY and SHR in the fasted state, increased from fasting to refeeding in WKY, whereas in SHR it remained similar to fasting levels [21]. In addition, feeding increased muscle glycogen content much more in WIS than in SHR [23]. However, in both studies, liver glycogen accumulation increased similarly in both strains and liver glycogen total content was similar [21,23], which indicates that the difference in postprandial insulin sensitivity between the strains is specific to the skeletal muscle.…”

Circadian Rhythm of Glucose Uptake in Cultures of Skeletal Muscle Cells and Adipocytes in Wistar-Kyoto, Wistar, Goto-Kakizaki, and Spontaneously Hypertensive Rats

“…However, this effect was not present in cells of hypertensive and diabetic animals. Existing studies are ambiguous with respect to insulin resistance in SHR (Gouveia et al, 2000;Natalucci et al, 2000;Swislocki et al, 1999). A decreased glucose uptake after insulin stimulation was shown in muscle (Swislocki et al, 1997) and fat (Caldiz and Cingolani, 1999) cells of SHR.…”

Angiotensin II or epinephrine hemodynamic and metabolic responses in the liver of L-NAME induced hypertension and spontaneous hypertensive rats

“…Gouveia et al[44] described increased glycemia and insulinemia values for fasted or fed SHRs. We observed normal glycemia and insulinemia in both hypertension models in fed state, which contrasts with the studies that show changes in these metabolic parameters.…”