Impact of Fish Oil Supplementation and Interruption of Fructose Ingestion on Glucose and Lipid Homeostasis of Rats Drinking Different Concentrations of Fructose

Abstract

Background. Continuous fructose consumption may cause elevation of circulating triacylglycerol. However, how much of this alteration is reverted after the removal of fructose intake is not known. We explored this question and compared the efficacy of this approach with fish oil supplementation. Methods. Male Wistar rats were divided into the following groups: control (C), fructose (F) (water intake with 10% or 30% fructose for 9 weeks), fish oil (FO), and fructose/fish oil (FFO). Fish oil was supplemented only for the last 33 days of fructose ingestion. Half of the F group remained for additional 8 weeks without fructose ingestion (FR). Results. Fructose ingestion reduced food intake to compensate for the increased energy obtained through water ingestion, independent of fructose concentration. Fish oil supplementation exerted no impact on these parameters, but the removal of fructose from water recovered both ingestion behaviors. Plasma triacylglycerol augmented significantly during the second and third weeks (both fructose groups). Fish oil supplementation did not attenuate the elevation in triacylglycerol caused by fructose intake, but the interruption of sugar consumption normalized this parameter. Conclusion. Elevation in triacylglyceridemia may be recovered by removing fructose from diet, suggesting that it is never too late to repair improper dietary habits.

Moderate-intensity exercise training improves long-term memory in fructose-fed rats

“…Eating behavior was modified by fructose intake as SDF and TRF had lower food intake and higher drinking than SD and TR, which had water to drink. A similar result was observed in a previous study carried out with the same animal lineage and fructose solution concentration 32 . Exercise training carried out three days a week, did not affect eating behavior.…”

A fish oil-rich diet leads to lower adiposity and serum triglycerides but increases liver lipid peroxidation in fructose-fed rats

“…Even though water intake data was not available in these previous studies, it can be hypothesized that the extent to which fructose can lead to hepatic injury and lipid accumulation depends heavily on the experiment's duration and water intake, which directly impacts fructose intake. As discussed previously, since water intake was not increased in the Fr group, as opposed to what is seen in similar experiments [20,21], fructose intake was limited. Other methods that circumvent this limitation can be used to induce NAFLD and obesity in animals, such as including fructose in the actual diet alongside saturated fat [36][37][38], leading to an increased fructose intake and a stronger stimulus to provoke metabolic alterations, given the effects of saturated fats on the onset of inflammation and weight gain in animal models [39,40].…”

“…Also, water intake remained the same between CT and Fr groups, and decreased slightly in the FOFr group, leading to marginally smaller fructose intake. In similar studies, animals receiving water in fructose tend to have increased water intake, which in turn leads to a higher daily fructose intake [20,21]. It is unclear why water intake did not increase in our experiment; however, that may have protected animals from developing more serious metabolic complications, such as liver steatosis.…”

“…In the present study, fructose consumption in water led to lower diet intake, causing caloric intake to be very similar between experimental groups. Indeed, previous research has shown that animals are capable of altering their food intake to maintain similar energy intake when consuming fructose in water [20,21], although not always being sufficient to compensate for the additional calories from fructose [22,23]. Equal energy ingestion may suggest that differences in weight gain and biochemical parameters seen in this study were due to fructose and fish oil's significant effects on lipid metabolism and not due to a more energy-dense diet.…”

“…In contrast, fish oil and marine n-3 fatty acids have been shown to reduce fatty acid synthesis by suppressing SREBP-1c expression and preventing LXRα activation [28,29] and increase lipolysis by upregulating hepatic PPAR-α [30], therefore hindering TG synthesis and fat storage. In a similar experiment, the addition of fish oil in the animal diet failed to attenuate an increase in serum TGs due to fructose consumption 30 days after fructose ingestion in water was initiated [21]. It would seem therefore that fish oil is more efficient at preventing the development of elevated serum TGs rather than treating it, since in the aforementioned experiment fish oil ingestion started alongside fructose addition in water.…”