Effects of high fructose diet on lipid metabolism and the hepatic NF-κB/ SIRT-1 pathway

The liver is the primary site for fructose metabolism; therefore, the liver is susceptible to fructose related metabolic disturbances including metabolic insulin dysfunction, dyslipidemia and inflammation. We investigated whether astaxanthin (ASX) can modify hepatic nuclear factorkappa B (NF-κB)/sirtuin-1 (SIRT-1) expression to alter oxidative stress caused by ingestion of excess fructose in rats. The animals were divided randomly into two x two factorially arranged groups: two regimens were given either water (W) or 30% fructose in drinking water (F). These two groups were divided further into two subgroups each: two treatments, either orally with 0.2 ml olive oil (OO) or 1 mg ASX/kg/day in 0.2 ml olive oil (ASX). Fructose administration increased serum glucose, triglycerides and very low density lipoproteins, and decreased serum concentration of high density lipoproteins; fructose did not alter serum total cholesterol. Excess fructose decreased hepatic superoxide dismutase (SOD) and increased hepatic NF-κB and MDA levels. ASX treatment increased hepatic SIRT-1 and decreased hepatic NF-κB and malondialdehyde (MDA) levels. ASX treatment decreased hepatic NF-κB and increased SOD levels, but did not alter MDA level in rats fed high fructose. ASX administration ameliorated oxidative stress caused by excess fructose by increasing hepatic NF-κB and SIRT-1 expression

Astaxanthin alleviates renal damage of rats on high fructose diet through modulating NF kappa B/SIRT1 pathway and mitigating oxidative stress

Coordinator of Scientific Research Projects at Artvin Coruh University: 2016.M80.02.08This study was conducted to determine the effect of astaxanthin (ASX) treatment on alleviation ofrenal damage in high fructose induced nephrotoxicity in rats. Treatments were arranged in a 2 2 fac-torial fashion: administrations of fructose (30%, via drinking water) and ASX (1 mg/kg/day, within0.2ml olive oil) for 8 weeks. Data were analyzed by two-way ANOVA. The ASX treatment decreasedserum urea (p<.01) and blood urea–N concentrations (p<.02) at a lower extent in rats receiving fruc-tose than those not receiving fructose. Moreover, the ASX treatment reversed the increases in malon-dialdehyde (MDA) (p<.0001) and nuclear factor kappa B (NF-jB) (p<.0003) levels and the decreasesin superoxide dismutase (SOD) activity (p<.0001) and sirtuin-1 (SIRT1) level (p<.0004), in the kidneyupon high fructose consumption. The data suggest that ASX supplementation alleviates renal damageinduced by high fructose consumption through modulating NF-jB/SIRT1 pathway and mitigating oxi-dative stress

Effects of oleanolic acid on inflammation and metabolism in diabetic rats

This work was supported by Coordinator of Scientific Research Projects [2018.M83.02.02] at Artvin Coruh University.Diabetes mellitus (DM) is a chronic metabolic disease that threatens the health of the world population. We investigated the effects of oleanolic acid (OA) administration on inflammation status and metabolic profile in streptozotocin (STZ) induced diabetic rats. Four experimental groups were established: healthy rats not administered OA, healthy rats administered OA, diabetic rats not administered OA, diabetic rats administered OA. OA, 5 mg/kg, was administered by oral gavage for 21 days. Serum samples collected at the end of the experiment and analyzed for toll-like receptor-9, interleukin-18, nuclear factor kappa B, malondialdehyde MDA, glucose, total cholesterol, triglycerides, high-density lipoprotein, low-density lipoprotein, calcium, phosphorus, magnesium and potassium. Pancreas tissue was examined for pathology. Induction of DM caused increased serum concentrations of inflammation and oxidative damage markers. DM also caused hyperglycemia-hyperlipidemia and decreased serum concentration of minerals. The islets of Langerhans were degenerated and necrotic. Administration of OA reversed the adverse effects of DM. OA treatment can ameliorate inflammation and oxidative damage due to DM by normalizing hyperglycemia and decreasing TLR-9, IL-18, NF-kappa B and MDA levels