Abstract
The purpose of this study was to demonstrate the accumulation and distribution of lipids in the liver of the adult Prague hereditary hypertriglyceridemic (HHTg) rats. They reveal an increased expression of 11beta-hydroxysteroid dehydrogenase 1 (11HSD1), which locally increases concentration of corticosterone in the liver. We studied the effect of the 11HSD1 inhibition on the lipid content. Samples of liver of three groups of adult female rats--HHTg, HHTg treated for 14 days with 50 mg/kg/day carbenoxolone (HHTg+CBX) and control Wistar rats, were examined histochemically. Cryosections of the samples were stained with Oil red O or Sudan black B to demonstrate different kinds of lipids. Extent and intensity of staining was evaluated semiquantitatively. The orientational analysis showed a higher extent and intensity of the staining of the liver of HHTg and HHTg+CBX rats (equal in both hypertriglyceridemic groups) than that of the control Wistar rats. Oil red O stained unsaturated fatty acids and neutral fats, mainly triglycerides. The difference was on average 30 per cent. Staining of phospholipids with Sudan black B showed similarly the higher positivity in the hypertriglyceridemic groups than in controls. Staining for triglycerides and phospholipids demonstrated a higher amount of lipids in the liver of HHTg and HHTg+CBX female rats than in controls. The inhibition of 11HSD1 activity had no effect on the lipid content in the liver of the HHTg rats.
Highlights
The increasing number of people in advanced countries suffers from a cluster of associated metabolic disorders that are collectively termed metabolic syndrome and that include hypertension, glucose intolerance, hyperinsulinemia, hypertriglyceridemia, hepatic steatosis and obesity
Experimental groups Lipid content was investigated in the liver of three experimental groups with 10 animals: adult Prague hereditary hypertriglyceridemic rats (HHTg), HHTg rats treated with carbenoxolone (14 days, 50 mg/kg/day dissolved in drinking water, HHTg +CBX), and Wistar rats as normotriglyceridemic controls
Histochemistry of lipids in the liver Animals were killed by decapitation, liver were removed, immediately frozen in liquid nitrogen and stored until use at – 84 °C. They were processed for cryosections 8 μm thick, fixed in Baker solution for 1 hour, rinsed in water, rinsed in 50 per cent ethanol and stained – either with Oil red O or Sudan black B4
Summary
The increasing number of people in advanced countries suffers from a cluster of associated metabolic disorders that are collectively termed metabolic syndrome and that include hypertension, glucose intolerance, hyperinsulinemia, hypertriglyceridemia, hepatic steatosis and obesity. 11β-hydroxysteroid dehydrogenase 1 (11HSD1) is an oxidoreductase highly expressed in liver and adipose tissue catalysing an interconversion of corticosterone into 11-dehydrocorticosterone and vice versa. Both activities, reductase and oxidase of 11HSD1, were found in vitro, conversion of 11-dehydrocorticosterone to corticosterone predominates in intact tissues[1]. Study on transgenic mice with selective overexpression of 11HSD1 in liver, a non-obese model of metabolic syndrome, showed enormous hepatic steatosis in these animals[2]. Prague hereditary hypertriglyceridemic rats (HHTg) were previously described as a genetic model of metabolic syndrome. They suffer from hypertriglyceridemia, insulin resistance and hypertension[3]. We examined the lipid content in the rat liver using lipid histochemistry
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