Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q7LGC8 (HSD)
 3,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diets high in fat and/or sucrose decrease whole bone mechanical properties and mineralization. This study examines the impact on rat bone mechanical properties and composition of age and diets (a) low in fat, (b) high in sucrose, and (c) high in fat. Sprague-Dawley rats aged 3 weeks (weanling [W]; n = 42), 8 weeks (young [Y]; n = 42), 16 weeks (teenage [T]; n = 39) and 56 weeks (old [O]; n = 40) were randomly assigned to groups: low fat, high sucrose and high fat with n = 12-16 per group. All animals were fed a purified low-fat, high starch diet for two weeks, and fed a low fat (STD), high sucrose (HSD), or high-fat (HFD) for five additional weeks. After sacrifice, the femurs were harvested and non-osseous tissue was removed. The bones were dried at 25 degrees C for 48 hours. Length and the periosteal minimum and maximum diameter (D-min and D-max) at the mid-diaphysis of the femurs were measured with Vernier calipers. The femurs were rehydrated and tested via three-point flexure. Bones were weighed after drying at 105 degrees C (48 hours; Dry-M) and 800 degrees C (24 hours; Ash-M). Percent mineralization (%Min) was calculated as Ash-M/Dry-M X 100%. Length, D-min and D-max, Dry-M and Ash-M all significantly (p < 0.05) increased with age (W < Y < T < O) within each group. %Min and stiffness were significantly greater in [O] than in the younger femurs. No significant results were seen in any age group due to varying diet. These results indicate that five weeks of high fat or high sucrose diet feeding does not affect whole bone size, composition or mechanical properties. Whether a longer dietary period or different diet composition would elicit changes requires further study.
 ...
PMID:Effects of high fat or high sucrose diets on rat femora mechanical and compositional properties. 1083 63

Sucrose- and fructose-enriched diets produce hepatic insulin resistance in rats independently of obesity. In humans, fructose infusion results in impaired insulin regulation of glucose production. The aim of the present study was to identify intrahepatic mediators of sucrose- and fructose-induced hepatic insulin resistance. In study 1, male rats were fed a control diet (STD, 68% of energy from corn starch, 12% from corn oil) or a sucrose-enriched diet (HSD, 68% sucrose, 12% corn oil) for 1, 2, or 5 wk. HSD produced hepatic insulin resistance at all time points. Hepatic protein tyrosine phosphatase 1B protein levels and activity were increased at 5 wk only, whereas c-jun NH(2)-terminal kinase (JNK) activity was increased at all time points. Normalization of JNK activity in hepatocytes isolated from HSD rats improved insulin-stimulated tyrosine phosphorylation of insulin receptor substrate (IRS) proteins and insulin suppression of glucose release. In study 2, male rats were provided STD for 1 wk and then were either fasted or fasted and refed either STD or HSD for 3 or 6 h. Rats refed HSD were characterized by increased hepatic JNK activity and phosphorylation of IRS1 on Ser(307) after 6 h only. In study 3, hyperglycemic, hyperinsulinemic pancreatic clamps were performed for 3 or 6 h in the presence or absence of low or high intraportal fructose infusions. High intraportal fructose infusions, which increased portal vein fructose concentration to approximately 1 mM, increased hepatic JNK activity and phosphorylation of IRS1 on Ser(307) at 6 h only. These data suggest that sucrose- and fructose-induced hepatic insulin resistance are mediated, in part, via activation of JNK activity. Thus high rates of fructose metabolism in the liver appear to acutely activate stress pathways.
 ...
PMID:Hepatospecific effects of fructose on c-jun NH2-terminal kinase: implications for hepatic insulin resistance. 1519 36