Sucrose Access Differentially Modifies 11β-Hydroxysteroid Dehydrogenase-1 and Hexose-6-Phosphate Dehydrogenase Message in Liver and Adipose Tissue in Rats ,

Abstract

11Beta-hydroxysteroid dehydrogenase-1 (11beta-HSD-1) plays a key role in the regulation of intracellular glucocorticoid concentrations. Increased message and/or activity of adipose 11beta-HSD-1 are characteristics of human and animal models of obesity. Hexose-6-phosphate dehydrogenase (H6PDH) is colocalized with 11beta-HSD-1 and may be a critical factor in determining the oxo-reductase activity of 11beta-HSD-1. This study examined the effects of sucrose solution access on body weight, body composition, and message of 11beta-HSD-1 and H6PDH in mesenteric adipose and liver. Rats were assigned to 3 groups: 1) control (ad libitum intake of nonpurified diet and water only); 2) ad libitum intake of 16% sucrose solution (S16); or 3) ad libitum intake of 32% sucrose solution (S32) in addition to ad libitum intake of diet and water. The S32 group consumed more energy daily than the S16 and control groups, yet body weight did not differ among groups. Percentages of body fat did not differ between the S16 and S32 groups but were higher than in controls. Hepatic 11beta-HSD-1 message was suppressed by 46% in the S16 group and by 47% in the S32 group, whereas the H6PDH message nearly doubled in the S16 group compared to the control group. In mesenteric fat, 11beta-HSD-1 message increased 23-fold in the S16 group and 32-fold in the S32 group and the H6PDH message increased 3.5-fold in the S16 group compared to the control group. These data demonstrate that sucrose can promote increased 11beta-HSD-1 and H6PDH message in mesenteric fat while concomitantly decreasing 11beta-HSD-1 message and increasing H6PDH message in liver. These observations support the hypothesis that sucrose access causes obesity via its ability to increase adipose 11beta-HSD-1.

Diet and the role of 11β-hydroxysteroid dehydrogenase-1 on obesity

“…Voluntary sucrose solution intake also restores food intake, weight gain and circulating triglyceride, leptin and insulin levels in ADX rats suggesting that dietary sugar can trigger enhanced peripheral glucocorticoid production and/or affect behavior to compensate for the absence of adrenal activity. More recently, we have shown that rats given free access to 16% sucrose solution in addition to chow and water for 10 weeks have increased 11β-HSD-1 and H6PDH message in mesenteric adipose [45]. These changes in adipose are accompanied by a decrease in 11β-HSD-1 message and increase in H6PDH message in liver in comparison to controls given ad lib access to chow and water.…”

“…While there is evidence to suggest that diet and macronutrient composition can influence glucocorticoid metabolism and carbohydrate intake can impact pentose phosphate pathway flux [45], it is not clear how intake is involved in changing the activity or expression levels of these enzymes. Additionally, there is no clear mechanism to explain how 11β-HSD-1 or H6PDH expression and/or activity levels are increased or decreased in a tissue-specific manner in obesity.…”

Effects of sugar solutions on hypothalamic appetite regulation

“…Over time however this result washes out and total caloric intake returns to a level that resembles control (70,74).…”

“…Despite the extensive behavioral examinations of the rat"s avidity for sugar solutions, relatively little work has been focused on the impact of sugar intake on the hepatic and central mechanisms controlling intake. We have more recently added to this literature by reporting that fructose consumption can promote increased oxoreductase activity of 11 beta hydroxysteroid dehydrogenase -1, an enzyme that regulates intracellular glucocorticoids in adipose tissue (70,71).…”

The Modulatory Role of Artichoke leaves Water Extract on Lipid Status on Rats Fed High Fat Diet

“…Includes an increased mass of adipose tissue that may lead to hypertension (Klop, 2013) and cardiovascular diseases (London, 2007 andFantuzzi, 2005). Furthermore, obesity has hazardous effects on liver and antioxidant enzyme.…”