Oral solution of fructose promotes SREBP-1c high-expression in the hypothalamus of Wistar rats.

Objective: We evaluate whether the consumption of fructose for 8 weeks affects enzymes and transcription factors of the lipogenic and inflammatory pathways in the hypothalamus of Wistar rats. Methods: At 30 days, the animals were divided into groups: Control (C) and Fructose (F) and maintained with free access to feed and filtered water (C) or aqueous solution of purified fructose at 20% (F). RT-PCR and Western blotting were performed for the target genes and proteins. Results: In F group, results showed a lower feed intake, an increase in glycemia (146.20 ± 6.09 vs. 102.32 ± 4.58; n: 9) and triacylglycerol (F: 191.65 ± 13.51 vs. C: 131.69 ± 6.49; n: 9) and there was no difference in water and energy consumption. We identified a higher content of acetyl-CoA carboxylase (ACC) (F: 133.93 ± 5.58 vs. C: 100 ± 0.0; n: 9-10) and NFκB (F: 125.5 ± 8.85 vs. C: 100 ± 0; n: 14) in group F, whereas fatty acid synthase (FAS) was lower (F: 85.90 ± 4.81 vs. C: 100 ± 0.0; n: 4-6). SREBP-1c gene expression was higher in F vs. C group (F: 4.08 ± 0.44 vs. C: 1.13 ± 0.15; n: 5-6), although we did not found difference between groups in the gene expression for ACC, SREBP-2, and NFκB. Discussion: Dietary fructose can change important lipogenic and inflammatory factors in the hypothalamus of rats and it leads to regulation of transcription factors before changes in body mass are evident.

High-monosaccharide intake inhibits anorexigenic hypothalamic insulin response in male rats.

OBJECTIVE: The aim of this research is to evaluate if intake of 20% fructose solution is able to change the anorexigenic hypothalamic insulin action. METHODS: Thirty day-old male Wistar rats were randomly assigned to one of the following groups: standard chow and water for the rats (Control group, C) and standard chow and 20% fructose solution for the rats (Fructose group, F).These treatments lasted 8 weeks. Three-month-old rats from group C and F received insulin or saline intracerebroventricular injections for evaluation of 24 h food intake, phosphorylated forms of the IR (p-IR) and Akt (p-Akt) proteins and quantified hypothalamic insulin receptor (IR) and insulin receptor substrate 1 (IRS-1) proteins. RESULTS: Insulin injection was able to decrease food intake in group C compared to 0.9% saline. However, insulin infusion failed to inhibit 24 h food intake in group F compared to 0.9% saline. The hypothalamic content of the IRS-1 was 37% higher in group F as well as p-Akt protein was significant higher vs. group C. CONCLUSION: We concluded that the 20% fructose solution compromised insulin signaling considering that it inhibited the anorexigenic hypothalamic response to acute injection of this hormone and increase of IRS-1 and p-Akt content.

Intermittent food restriction in female rats induces SREBP high expression in hypothalamus and immediately postfasting hyperphagia.

OBJECTIVE: We investigated the effect of intermittent food restriction (IFR) cycles on hypothalamic expression of lipogenic proteins and induction of overeating. METHODS: Female Wistar rats were distributed in three groups: free access to feed (control, C), 2 d feed restriction at 50% of C intake followed by 3 d (restricted 3, R3) or 5 d (restricted 5, R5) ad libitum feeding. After 6 wk, the rats were submitted to euthanasia and collected the hypothalamus and blood. The deposits of retroperitoneal, mesenteric, and gonadal fat were weighed. The expression of the mRNA for sterol regulatory element binding protein (SREBP) 1c and 2 and acetyl-CoA carboxylase in the hypothalamus were determined by real-time polymerase chain reaction, and glucose and triacylglycerol were evaluated by a commercial kit. Body mass and food intake were measured daily. RESULTS: IFR promoted increased expression of SREBP-2 in both treated groups and, in R5, increased expression of SREBP-1c. The serum triacylglycerol, mesenteric deposit, and total fat content were higher in R3. Neither of the treatment intervals altered the expression of the mRNA of acetyl-CoA carboxylase enzyme but induced hyperglycemia and higher food intake immediately after food restriction. CONCLUSION: IFR affected the expression of SREBP-1c in R5 and SREBP-2 in the hypothalamus and caused overeating immediately after fasting in both groups. We suggest that hypothalamic and peripheral alterations, coupled with compulsive eating behavior in the ad libitum period, indicate risks for diabetes mellitus and recovery of body mass after interruption of IFR.

Effects of fructose consumption on food intake and biochemical and body parameters in Wistar rats. / Efeitos do consumo de frutose sobre ingestão alimentar, parâmetros bioquímicos e corporais em ratos Wistar.

INTRODUTION AND OBJECTIVE: Increased fructose consumption is associated with various metabolic changes that favor the onset of obesity and related comorbidities. The objective of this study was to assess the effects of chronic fructose consumption on body weight and adipose tissue, as well as on serum glucose and triglyceride levels. METHODS: Thirty-day-old Wistar rats were divided into two groups: fructose (F) and control (C), which had free access to commercial chow and either water or a 20% fructose solution. Body mass was measured weekly and food consumption at 30, 60 and 90 days. At 90 days, the animals were killed by decapitation and fat deposits (mesenteric, epididymal and retroperitoneal) were removed and blood collected for measurement of glucose and triglyceride levels. RESULTS: There was no significant difference in body weight gain, but the percentage of body fat was higher in group F. This group also consumed less feed at 60 and 90 days and had higher consumption of fructose solution than water in group C at 30 and 60 days. This meant higher calorie intake in group F and lower feed efficiency. Retroperitoneal and epididymal fat deposits and triglycerides were higher in group F than in group C. CONCLUSION: Consumption of fructose solution for eight weeks, while not directly reflected in body weight gain, did increase abdominal fat in group F compared to group C, as well as changing triglyceride levels. These two factors increase risk of cardiovascular disease.