The Effects Of Sucrose And ’Free Fructose And Glucose’ On Glucose And Lipid Metabolism In The Rat

High fructose corn syrup (HFCS), as a new nutritional sweetener, has replaced thedominant position of sucrose, and this aroused large concern about free fructose (i.e. HFCS,pure fructose) and bound fructose (i.e. sucrose). However, the different effects of free fructose(HFCS) and bound fructose (sucrose) were a critical research gap but also in dispute. Giventhis, forty male rats were fed different diets for11weeks in this paper to explore the effects ofhigh fructose on diabetes, insulin resistance, inflammatory and fatty liver, more importantly,to compare the long-termeffects of ‘free’ fructose and ‘bound’ fructose (as part of sucrose) onglucose and lipid metabolism in the rat. It will make sacrifice for the study of fructosemetabolism, and provide theoretical basis for the prevention and dia gnosis for metabolicsyndrome.Methods: Forty male rats were randomly and averagely divided into four experimentalgroups and a control group according to their body weight after feeding normal diet for twoweeks: Control group (ST group, starch), Fructose bound glucose group (SU group, sucrose),free fructose and glucose group (F/G group, fructose/glucose), positive control group1(F/STgroup, fructose/starch), positive control group2(G/ST group, glucose/starch). Each groupwas fed a diet containing68%of total calories as different composition of carbohydrate for11weeks. Daily food intake was calculated and body mass was weighted every week. Fastingserum glucose (FSG), insulin (FINS), triglyceride (TG), total cholesterol (TC) and free fattyacid (FFA) levels were measured at the end of7weeks and11weeks respectively. An oralglucose tolerance test (OGTT) was administered5days before sacrifice at11weeks. At theend of the experiment, rats were sacrificed by anesthesia and were autopsied, then perirenaland epididymal fat were peeled and weighed. Serum and liver monocyte chemoattractantprotein-1(MCP-1) and tumor necrosis factor-α (TNF-α) as well as liver TG were detected byELISA method. The pathological changes of liver, kidney and pancreas were directed withhematoxylin&eosin (HE) staining.Results:1) In the case of similar total food intake, fructose-fed rats (SU, F/G and F/STgroup) did not show significant increase in body weight compared to the control group, whileSU group tended to have higher weight gain and significantly higher than the F/G and F/STgroup (P <0.05).2) Long-term intake of free fructose and bound fructose can developdifferent levels of glucose dysfunction: the SU, F/G and F/ST group showed higher fastingserum glucose (FSG), insulin, AUCgluand lower insulin sensitivity index (ISI) at7and11weeks. In particular, there are significant differences between SU and F/G group (P <0.05) at11weeks.3) Long-term intake of free fructose and bound fructose can develop differentlevels of lipid dysfunction: fructose-fed rats, especially the SU and F/ST group, showed significantly higher serum triglycerides (TG), total cholesterol (TC) and free fatty acids (FFA),as well as liver index, visceral fat, hepatic TG accumulation and fatty liver (P <0.05)compared to the control. The SU group tended to have higher levels of serum TG, TC andFFA, as well as fatty liver than the F/G group.4) High dose fructose could triggerinflammation，especially the SU group showed higher serum and liver TNF-α and MCP-1than the F/G group (P <0.05).5) The level of key gluconeogenic enzyme in liver (PEPCK)was higher in rats fed fructose diets (SU, F/G and F/ST group) after11weeks, especially theSU and F/ST group (P <0.01). Besides, the SU group showed significantly higher level ofPEPCK than the F/G group.6) Fructose fed rats (SU, F/G and F/ST group) showed differentlevels of kidney and pancreas damage, but there is no obvious difference between SU and F/Ggroup.Conclusions:1) These data confirmed fructose rather than glucose is the primary nutrientmediator of sucrose or high fructose corn syrup (HFCS)-induced metabolic syndrome.2)Long-term intake of free fructose or bound fructose can both lead to different levels ofdyslipidemia, impaired glucose tolerance, inflammatory, fatty liver and other metabolicsyndrome.3) Observably, sucrose disrupted glucose and lipids homeostasis more than didfree fructose and glucose with more weight gain, more serious impaired fasting glucose,impaired glucose tolerance, reduced insulin sensitivity, dyslipidemia, fatty liver, and higherlevels of inflammatory cytokines and hepatic gluconeogenesis, possessing greater potential toinduce type2diabetes.To sum up, the intake of high fructose corn syrup (i.e. free fructose and glucose) wasmore secure than the same mount of sucrose in our daily life.