Doses Of Fructose Research Articles

Interindividual Variability in Postprandial Plasma Fructose Patterns in Adults.

High fructose consumption is associated with an increased risk of cardiometabolic disease, and fructose feeding dose-dependently induces markers reflective of poor metabolic health. However, unlike glucose, surprisingly little is known about person-to-person differences in postprandial plasma fructose patterns. Herein, we performed post hoc analyses of two published studies to address this question. In the first cohort, 16 participants' all-day plasma fructose concentration patterns (08:00-23:30) were determined (8 women and 8 men) while consuming mixed meals (breakfast, lunch, and dinner) with a fructose-sweetened beverage at each meal (30% of calories). Individually plotted results demonstrate remarkably disparate fructose patterns with respect to peak concentration and timing. A secondary study confirmed substantial interindividual variability in plasma fructose patterns over 240 min in 16 adults consuming Ensure®, a commercially available mixed macronutrient drink containing a low dose of fructose. The health ramifications of interindividual variations in postprandial fructose metabolism and the underlying physiological mechanisms driving differences in post-meal blood patterns remain to be explored. Future research is warranted to determine if interindividual variability in fructose digestion, metabolism, and postprandial blood concentration patterns is associated with cardiometabolic health phenotypes and disease risk.

Effects of Prenatal Dexamethasone Treatment and Post-Weaning Moderate Fructose Intake on Synaptic Plasticity and Behavior in Adult Male Wistar Rat Offspring.

Early-life glucocorticoid overexposure induces diverse neurodevelopmental outcomes regarding stress reactivity and cognition. Increased fructose consumption has also been associated with alterations in cognitive capacity and behavior. The present study investigated the effects of prenatal dexamethasone exposure on synaptic plasticity, locomotion, anxiety, and recognition memory in adult male Wistar rat offspring, and whether these effects are potentiated by postnatal fructose consumption. Pregnant female rats were treated with dexamethasone during late gestation and male offspring were supplemented with a moderate dose of fructose. Recognition memory, locomotion, and anxiety-like behavior were assessed using a novel object recognition test, open-field test, and elevated plus maze, respectively. Hippocampal synaptic plasticity was estimated by the levels of growth-associated protein 43 (GAP-43), synaptophysin, postsynaptic density protein 95, calcium/calmodulin-dependent kinase IIα, and their activating phosphorylations. Additionally, protein levels of the glucocorticoid receptor (GR) and its transcriptionally active phosphorylated form were evaluated. Prenatal dexamethasone treatment induced an anxiolytic-like effect, stimulation of exploratory behavior, and novelty preference associated with an increase in GR and GAP-43 protein levels in the hippocampus. Fructose overconsumption after weaning did not modify the effects of prenatal glucocorticoid exposure. Applied prenatal dexamethasone treatment may induce changes in reactions to novel situations in male Wistar rats.

Effects of different doses of glucose and fructose on central carbon metabolic pathways and intercellular wireless communication networks in humans

Fructose and glucose are often widely used in food processing and may contribute to many metabolic diseases. To observe the effects of different doses of glucose and fructose on human metabolism and cellular communication, volunteers were given low, medium, and high doses of glucose and fructose. Serum cytokines, glucose, lactate, nicotinamide adenine dinucleotide (NADH) and metabolic enzymes were assayed, and central carbon metabolic pathway networks and cytokine communication networks were constructed. The results showed that the glucose and fructose groups basically maintained the trend of decreasing catabolism and increasing anabolism with increasing dose. Compared with glucose, low-dose fructose decreased catabolism and increased anabolism, significantly enhanced the expression of the inflammatory cytokine interferon-γ (IFN-γ), macrophage-derived chemokine (MDC), induced protein-10 (IP-10), and eotaxin, and significantly reduced the activity of isocitrate dehydrogenase (ICDH) and pyruvate dehydrogenase complexes (PDHC). Both medium and high doses of fructose increase catabolism and anabolism, and there are more cytokines and enzymes with significant changes. Furthermore, multiple cytokines and enzymes show strong relevance to metabolic regulation by altering the transcription and expression of enzymes in central carbon metabolic pathways. Therefore, excessive intake of fructose should be reduced to avoid excessive inflammatory responses, allergic reactions and autoimmune diseases.

Effects of fructose added to an oral glucose tolerance test on plasma glucose excursions in healthy adults

Background and objectivePrevious experimental studies have shown that fructose interacts with glucose metabolism by increasing hepatic glucose uptake. However, human studies investigating the effects of small (‘catalytic’) amounts of fructose, added to an oral glucose load, on plasma glucose levels remain inconclusive. The aim of this study, therefore, was to repeat and extend these previous studies by examining the plasma glucose response during a 75 g oral glucose tolerance test (OGTT) with the addition of different doses of fructose. MethodsHealthy adults (n = 13) received an OGTT without addition of fructose and OGTTs with addition of different doses of fructose (1, 2, 5, 7.5 and 15 g) in a random order, on six separate occasions. Plasma glucose levels were measured every 15 min for 120 min during the study. FindingsThe plasma glucose incremental area under the curve (iAUC) of the OGTT without addition of fructose was not significantly different from any OGTT with fructose (p ≥ 0.2 for all fructose doses). Similar results were observed when these data were clustered with data from a similar, previous study (pooled mean difference: 10.6; 95%CI: 45.0; 23.8 for plasma glucose iAUC of the OGTT without addition of fructose versus an OGTT with 5 g fructose; fixed-effect meta-analysis, n = 38). Of interest, serum fructose increased from 4.8 μmol/L (interquartile range: 4.1–5.9) at baseline to 5.3 μmol/L (interquartile range: 4.8–7.5) at T = 60 min during an OGTT without addition of fructose (p = 0.002). ConclusionLow doses of fructose added to an OGTT do not affect plasma glucose levels in healthy adults. The role of endogenous fructose production, as a potential explanation of these null-findings, deserves further investigation.

Behavioral responses to sweet compounds via T1R2-independent pathways in chickens

Elucidating the taste sensing systems in chickens will enhance our understanding of poultry nutrition and improve the feeding strategies used in poultry farming. It is known that chickens lack the sweet taste receptor subunit, taste receptor type 1 member 2 (T1R2), in their genome. Thus, the present study investigated T1R2-independent sweet-sensing pathways in chickens. RT-PCR analysis revealed that glucose transporters known to play an important role in T1R2-independent sweet sensing in mammals—namely sodium-glucose cotransporter 1 (SGLT1) and ATP-gated K+ channel subunits—are expressed in the palate, the main taste organ in chickens. In behavioral tests, chickens slightly preferred glucose, galactose, sucrose, maltose, lactose, and stevioside, while high doses of sucrose and fructose were rejected. Chickens did not show any preference for noncaloric sweeteners or sugar alcohol, such as acesulfame K, aspartame, saccharin, sucralose, or sorbitol. The preference for galactose was inhibited by an inhibitor of SGLT1 in a dose-dependent manner. In addition, we found that glucagon-like peptide 1 (GLP-1) and mRNA of the GLP-1 receptor, which are involved specifically in sweet transmission in mice, are also present in the oral tissues of chickens. The present results imply that chickens can sense various sweet compounds via T1R2-independent pathways in oral tissues.

Transient increase in plasma urate induced by a single oral dose of fructose in rats

Transient increase in plasma urate induced by a single oral dose of fructose in rats

Fructose intolerance is not associated with malabsorption in patients with functional gastrointestinal disorders.

Symptoms following fructose ingestion, or fructose intolerance, are common in patients with functional gastrointestinal disorders (FGID) and are generally attributed to intestinal malabsorption. The relationships between absorption, symptoms, and intestinal gas production following fructose ingestion were studied in patients with FGID. Thirty FGID patients ingested a single dose of fructose 35g or water in a randomized, double-blind, crossover study. Blood and breath gas samples were collected, and gastrointestinal symptoms rated. Plasma fructose metabolites and short-chain fatty acids were quantified by targeted liquid chromatography-tandem mass spectrometry. Patients were classified as fructose intolerant or tolerant based on symptoms following fructose ingestion. The median (IQR) areas under the curve of fructose plasma concentrations within the first 2h (AUC0-2h ) after fructose ingestion were similar for patients with and without fructose intolerance (578 (70)µM·h vs. 564 (240)µM·h, respectively, p=0.39), as well as for the main fructose metabolites. There were no statistically significant correlations between the AUC0-2h of fructose or its metabolites concentrations and the AUCs of symptoms, breath hydrogen, and breath methane. However, the AUCs of symptoms correlated significantly and positively with the AUC0-2h of hydrogen and methane breath concentrations (r=0.73, r=0.62, respectively), and the AUCs of hydrogen and methane concentrations were greater in the fructose-intolerant than in the fructose-tolerant patients after fructose ingestion (p≤0.02). Fructose intolerance in FGID is not related to post-ingestion plasma concentrations of fructose and its metabolites. Factors other than malabsorption, such as altered gut microbiota or sensory function, may be important mechanisms.

Effect of a moderate dose of fructose in solid foods on TAG, glucose and uric acid before and after a 1-month moderate sugar-feeding period.

There are few data on the effects on TAG, glucose and uric acid of chronic consumption of a moderate dose of fructose in solid foods. Twenty-eight participants with prediabetes and/or obesity and overweight commenced the study (BMI 32·3 kg/m2, age 44·7 years, fasting glucose 5·3 (sd 0·89) mmol/l and 2-h glucose 6·6 (sd 1·8) mmol/l). Twenty-four men and women who completed the study consumed, in random order, two acute test meals of muffins sweetened with either fructose or sucrose. This was followed by 4-week chronic consumption of 42 g/d of either fructose or sucrose in low-fat muffins after which the two meal tests were repeated. The sugar type in the chronic feeding period was also randomised. Fasting TAG increased after chronic consumption of fructose by 0·31 (sd 0·37) mmol/l compared with sucrose in those participants with impaired fasting glucose (IFG)/impaired glucose tolerance (IGT) (P = 0·004). Total cholesterol (0·33 mmol/l), LDL-cholesterol (0·24 mmol/l) and HDL-cholesterol (0·08 mmol/l) increased significantly over the 1- month feeding period with no differences between muffin types. Fasting glucose was not different after 1 month of muffin consumption. Uric acid response was not different between the two sugar types either baseline or 1 month, and there were no differences between baseline and 1 month. The increase in fasting TAG in participants with IFG/IGT suggests the need for caution in people at increased risk of type 2 diabetes.

High-Fructose Diet Increases Inflammatory Cytokines and Alters Gut Microbiota Composition in Rats.

High-fructose diet induced changes in gut microbiota structure and function, which have been linked to inflammatory response. However, the effect of small or appropriate doses of fructose on gut microbiota and inflammatory cytokines is not fully understood. Hence, the abundance changes of gut microbiota in fructose-treated Sprague-Dawley rats were analyzed by 16S rRNA sequencing. The effects of fructose diet on metabolic disorders were evaluated by blood biochemical parameter test, histological analysis, short-chain fatty acid (SCFA) analysis, ELISA analysis, and Western blot. Rats were intragastrically administered with pure fructose at the dose of 0 (Con), 2.6 (Fru-L), 5.3 (Fru-M), and 10.5 g/kg/day (Fru-H) for 20 weeks. The results showed that there were 36.5% increase of uric acid level in the Fru-H group when compared with the Con group. The serum proinflammatory cytokines (IL-6, TNF-α, and MIP-2) were significantly increased (P < 0.05), and the anti-inflammatory cytokine IL-10 was significantly decreased (P < 0.05) with fructose treatment. A higher fructose intake induced lipid accumulation in the liver and inflammatory cell infiltration in the pancreas and colon and increased the abundances of Lachnospira, Parasutterella, Marvinbryantia, and Blantia in colonic contents. Fructose intake increased the expressions of lipid accumulation proteins including perilipin-1, ADRP, and Tip-47 in the colon. Moreover, the higher level intake of fructose impaired intestinal barrier function due to the decrease of the expression of tight junction proteins (ZO-1 and occludin). In summary, there were no negative effects on body weight, fasting blood glucose, gut microbiota, and SCFAs in colonic contents of rats when fructose intake is in small or appropriate doses. High intake of fructose can increase uric acid, proinflammatory cytokines, intestinal permeability, and lipid accumulation in the liver and induce inflammatory response in the pancreas and colon.

Investigation of a Pharmacological Approach for Reduction of Renal Uptake of Radiolabeled ADAPT Scaffold Protein.

Albumin binding domain-Derived Affinity ProTeins (ADAPTs) are small (5 kDa) engineered scaffold proteins that are promising targeting agents for radionuclide-based imaging. A recent clinical study has demonstrated that radiolabeled ADAPTs can efficiently visualize human epidermal growth factor receptor 2 (HER2) expression in breast cancer using SPECT imaging. However, the use of ADAPTs directly labeled with radiometals for targeted radionuclide therapy is limited by their high reabsorption and prolonged retention of activity in kidneys. In this study, we investigated whether a co-injection of lysine or gelofusin, commonly used for reduction of renal uptake of radiolabeled peptides in clinics, would reduce the renal uptake of [99mTc]Tc(CO)3-ADAPT6 in NMRI mice. In order to better understand the mechanism behind the reabsorption of [99mTc]Tc(CO)3-ADAPT6, we included several compounds that act on various parts of the reabsorption system in kidneys. Administration of gelofusine, lysine, probenecid, furosemide, mannitol, or colchicine did not change the uptake of [99mTc]Tc(CO)3-ADAPT6 in kidneys. Sodium maleate reduced the uptake of [99mTc]Tc(CO)3-ADAPT6 to ca. 25% of the uptake in the control, a high dose of fructose (50 mmol/kg) reduced the uptake by ca. two-fold. However, a lower dose (20 mmol/kg) had no effect. These results indicate that common clinical strategies are not effective for reduction of kidney uptake of [99mTc]Tc(CO)3-ADAPT6 and that other strategies for reduction of activity uptake or retention in kidneys should be investigated for ADAPT6.

Surprising findings in a 'well-understood' nutrient-assimilation pathway.

A study published in this issue of Nature Metabolism adds to the emerging evidence that the small intestine is an initial site of dietary fructose metabolism, especially at low fructose doses, thus decreasing exposure of the liver and the colonic microbiome to intact fructose.

Cholesterotropic and cuprotropic chemicals.

A dozen or so chemicals modify both cholesterol and copper metabolism. Ascorbic acid and cadmium, etc., inhibit copper metabolism and raise cholesterol. Calcium and clofibrate, etc., enhance copper and lower cholesterol. Perhaps the doses of dietary cholesterol and fructose in this experiment were too severe to permit fenofibrate to lower cholesterol in a manner similar to clofibrate. © 2020 Society of Chemical Industry.

Cholesterotropic and cuprotropic chemicals.

A dozen or so chemicals modify both cholesterol and copper metabolism. Ascorbic acid and cadmium, etc., inhibit copper metabolism and raise cholesterol. Calcium and clofibrate, etc., enhance copper and lower cholesterol. Perhaps the doses of dietary cholesterol and fructose in this experiment were too severe to permit fenofibrate to lower cholesterol in a manner similar to clofibrate. © 2020 Society of Chemical Industry.

Dietary copper‐fructose interactions alter gut microbiome in a sex‐differential manner likely contributes to the sex differences in the metabolic phenotype

ObjectiveInadequate copper intake and increased fructose consumption represent two important nutritional problems in the US. Dietary copper‐fructose interactions alter gut microbial activity and contribute to the development of metabolic phenotype. The aim of this study is to determine whether dietary copper‐fructose interactions alter gut microbiome in a sex‐differential manner, which may contribute to the sex differences in the metabolic phenotype.MethodsMale and female weanling Sprague‐Dawley (SD) rats were fed (ad lib) with a modified AIN‐93G purified rodent diet with defined copper content in the form of cupric carbonate for 8 weeks. The copper content is 6mg/kg and 1.6mg/kg in adequate copper diet (CuA) and marginal copper deficient diet (CuM), respectively. Animals had free access to either deionized water or deionized water containing 10% fructose (w/v) as the only drink during the experiment. Body weight gain, plasma ALT, AST and liver histology were evaluated. Fecal and cecal microbiome were analyzed by 16S rDNA sequencing. Fecal and cecal Short chain fatty acids were analyzed by GC‐MS.ResultsRats fed with CuA or CuM with or without fructose (CuAF or CuMF) did not gain body weight in both male and female. No obvious liver injury was observed in both male and female rats in terms of plasma ALT and AST. A few of female rats developed very mild steatosis, whereas no obvious steatosis was observed in male rats fed with CuAF or CuMF. 16S rDNA sequencing analysis of fecal and cecal DNA showed that Firmicutes was significantly decreased, whereas Bacteroidetes and Proteobacteria were significantly increased in CuAF and CuMF fed female rats compared to controls, suggesting gut microbiota dysbiosis. The significant alterations of gut microbiota composition in phylum level in female rats attribute to the effect of dietary fructose as shown by two‐way ANOVA. However, this effect was not obvious in male rats. In parallel, fecal and cecal short chain fatty acid, butyrate was significantly decreased in female rats fed with CuMF and to a less extent in male rats compared to controls. This effect was due to dietary factors of both copper and fructose in female rats, and copper in male rats.ConclusionFemale rats exhibit more sensitivity to dietary copper and fructose‐induced metabolic phenotypes and gut microbiota dysbiosis compared to male rats. The metabolic phenotypes are closely associated with the alterations of gut microbiome. These results are different with previous reports, likely due to the factors, such as the dose of copper and fructose as well as species and location.Support or Funding InformationThis study was supported in part by NIH Grants U01AA021901, U01AA022489, R01AA023681, P20GM113226, P50AA024337 and the Jewish Heritage Fund for Excellence Pilot Grant Program at the University of Louisville School of Medicine. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health (C.J.M.); the Veterans Administration (C.J.M.); and the Uof L Clinical and Translational Pilot Program (C.J.M.).

Effect of fructose and its epimers on postprandial carbohydrate metabolism: A systematic review and meta-analysis.

To synthesize the evidence of the effect of small doses (≤30-g/meal) of fructose and its epimers (allulose, tagatose, and sorbose) on the postprandial glucose and insulin response to carbohydrate-containing meals. MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched through to April 9, 2019. We included randomized (RCTs) and non-randomized acute, single-meal, controlled feeding trials that added ≤30-g of fructose or its epimers either prior to or with a carbohydrate-containing meal compared with the same meal alone. Outcomes included the incremental area under the curve (iAUC) for glucose and insulin, the Matsuda Insulin Sensitivity Index, and the Early Insulin Secretion Index. Data were expressed as ratio of means (RoM) with 95% CIs and pooled using the inverse variance method. The overall certainty of the evidence was evaluated using GRADE. Forty trial comparisons (n=400) were included (none for sorbose). Allulose significantly reduced the postprandial iAUC glucose response by 10% (0.90 [0.84 to 0.96], P<0.01). Tagatose significantly reduced the postprandial iAUC insulin response by 25% (0.75 [0.62 to 0.91], P<0.01) and showed a non-significant 3% reduction in the postprandial iAUC glucose response (0.97 [0.94 to 1.00], P=0.07). There was no effect of fructose on any outcome. The certainty of the evidence was graded as low to moderate for fructose, moderate for allulose, and low for tagatose. Small doses of allulose and tagatose, but not fructose, lead to modest improvements on postprandial glucose and insulin regulation. There is a need for long-term RCTs to confirm the sustainability of these improvements.

Metabolic effects of a prolonged, very-high-dose dietary fructose challenge in healthy subjects

Increased fructose intake has been associated with metabolic consequences such as impaired hepatic lipid metabolism and development of nonalcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the role of fructose in glucose and lipid metabolism in the liver, heart, skeletal muscle, and adipose tissue. Ten healthy subjects (age: 28±19 y; BMI: 22.2±0.7 kg/m2) underwent comprehensive metabolic phenotyping prior to and 8 wk following a high-fructose diet (150 g daily). Eleven patients with NAFLD (age: 39.4±3.95 y; BMI: 28.4±1.25) were characterized as "positive controls." Insulin sensitivity was analyzed by a 2-step hyperinsulinemic euglycemic clamp, and postprandial interorgan crosstalk of lipid and glucose metabolism was evaluated, by determining postprandial hepatic and intra-myocellular lipid and glycogen accumulation, employing magnetic resonance spectroscopy (MRS) at 7 T. Myocardial lipid content and myocardial function were assessed by 1H MRS imaging and MRI at 3 T. High fructose intake resulted in lower intake of other dietary sugars and did not increase total daily energy intake. Ectopic lipid deposition and postprandial glycogen storage in the liver and skeletal muscle were not altered. Postprandial changes in hepatic lipids were measured [Δhepatocellular lipid (HCL)_healthy_baseline: -15.9±10.7 compared with ± ΔHCL_healthy_follow-up: -6.9±4.6; P=0.17] and hepatic glycogen (Δglycogen_baseline: 64.4±14.1 compared with Δglycogen_follow-up: 51.1±9.8; P=0.42). Myocardial function and myocardial mass remained stable. As expected, impaired hepatic glycogen storage and increased ectopic lipid storage in the liver and skeletal muscle were observed in insulin-resistant patients with NAFLD. Ingestion of a high dose of fructose for 8 wk was not associated with relevant metabolic consequences in the presence of a stable energy intake, slightly lower body weight, and potentially incomplete absorption of the orally administered fructose load. This indicated that young, metabolically healthy subjects can at least temporarily compensate for increased fructose intake. This trial was registered at www.clinicaltrials.gov as NCT02075164.

Fructose consumption during pregnancy and lactation causes DNA damage and biochemical changes in female mice.

The consumption of fructose during pregnancy can cause hyperglycaemia and may stimulate production of reactive oxygen species; however, there are only a few studies reporting whether fructose consumption during pregnancy causes DNA damage. Therefore, the aim of this study was to evaluate the effects of fructose consumption on genetic and biochemical parameters in Swiss mice treated during pregnancy and lactation. For this, 15 couples of 60-day-old Swiss mice were divided into three groups of five couples: negative control (water) and two fructose groups (fructose dose of 10%/l and 20%/l). During this period, we evaluated food consumption, energy efficiency and body weight. Samples of blood were collected from the females before copulation, after the 15th day of conception and on the 21st day after the lactation period, for the glycaemic and lipid profiles as well as comet assay and micronucleus (MN) test. Comet assay and MN test evaluate DNA damage and clastogenicity, respectively. In the gestation and lactation period, the two fructose doses tested showed DNA damage as observed in the comet assay, which is associated with an increase in dietary intake, body weight, lipid profile and fasting glycaemia in females. Thus, it can be suggested that the high consumption of fructose during these periods is harmful for pregnancy and lactation.

The effects of prenatal dexamethasone exposure and fructose challenge on pituitary-adrenocortical activity and anxiety-like behavior in female offspring

Prenatal glucocorticoid overexposure could largely influence pituitary-adrenal activity and anxiety-like behavior in offspring. Our aim was to study the possible potentiating effect of moderate dose of fructose – common ingredient of today’s diet – on prenatal glucocorticoid treatment-induced hypothalamo-pituitary-adrenal (HPA) axis changes. Pregnant female rats were treated with multiple dexamethasone (Dx) doses (3 x 0.5 mg/kg/b.m. Dx; 16th-18th gestational day). Half of female offspring from control and Dx treated dams were supplemented with 10% fructose solution, from weaning till adulthood. Immunohistochemistry, unbiased stereological evaluation and hormonal analysis are used to provide the morpho-functional state of pituitary and adrenal gland. Anxiety-like behavior was assessed using the light/dark box test and the elevated plus maze test. Prenatally Dx exposed females, with or without fructose consumption, had markedly reduced adrenocortical volume (p < 0.05) comparing to controls. Increased basal plasma ACTH level in these females (p < 0.05) maintained corticosterone concentration at control level produced by smaller adrenal glands. In parallel, anxiety-like behavior was shown by both tests used. In conclusion, prenatal Dx exposure cause negative psychophysiological outcome reflected in increased HPA axis activity and anxiety behavior in female offspring, while moderately increased fructose consumption failed to evoke any alteration or to potentiate effects of prenatal Dx exposure.

The effect of fructose supplementation on feed intake, nutrient digestibility and digesta retention time in Reeves’s muntjac (Muntiacus reevesi)

The aim of the study was to determine the effect of fructose supplementation in the diet on feed intake, nutrient digestibility and digesta retention time in Reeves's muntjac (Muntiacus reevesi), a browsing cervid. In Experiment 1, six adult males of Reeves's muntjac were used in a replicated 3×3 Latin square design and fed a diet consisting of dehydrated chopped lucerne (ad libitum), high-fibre pellet (120g/day) and wheat bran (30g/day) without (F0) or with addition of 12 and 24g fructose/day (F12 and F24, respectively). In Experiment 2, the same six adult muntjacs were used in crossover design and fed F0 or F12. Doses of supplemental fructose were set to increase intake of water-soluble carbohydrates (WSC; ≈40g/day; ≈8% of WSC in consumed dry matter [DM]) by 25 and 50% relative to F0. Feed intake was controlled daily (Experiment 1 and 2) and total tract digestibility and digesta retention time were determined (Experiment 2). In Experiment 1, DM intake of chopped dehydrated lucerne decreased with fructose supplementation (F0 vs. F12 and F24; p=.01) but was not different between F12 and F24 (p=.76). Total DM intake was also not different between treatments (p≥.13). In Experiment 2, DM intake of lucerne, total DM intake and nutrient digestibility was not affected by fructosesupplementation (p≥.17), but mean retention time of long particles in the whole GIT tended to be longer for F12 compared to F0 (p=.09). Under conditions of the current study, additional fructose intake (resulting in a range of WSC content in consumed DM from 8.6% to 13%) had only minor impact on feed intake and investigated functions of the gastrointestinal tract of Reeves's muntjac.

EXPERIMENTAL MODELING OF DIABETES TYPE 2

The search of means of the diabetes mellitus therapy is one of the urgent medical andsocial problems nowadays, taking into consideration spreading of this disease in theworld and severity of its complications.Objective - to reproduce diabetes mellitus type 2 in rats by means of a combination of ahigh-fat diet with low doses of streptozotocin and fructose intake.Material and methods. Diabetes mellitus type 2 was modeled by administeringstreptozotocin at a dose of 30 mg / kg intraperitoneally, keeping rats on a high-fat diet with free access to a solution of fructose at a concentration of 200 g / l. during 30 days.A control group of rats of the corresponding sex and age was injected intraperitoneallywith citrate buffer with a previous keeping on a standard diet with free access to water.Results. As a result of the experiment, changes of the main indices of carbohydrate andlipid metabolism, the development of glucose tolerance state in rats with streptozotocinadministration were determined, and morphological changes in the tissues of thepancreas were revealed.Conclusion. The results obtained allow to assert that the streptozotocin-induced modelof diabetes mellitus in combination with a high-fat diet and fructose is adequate andclose to type 2 diabetes in a human being and can be used in studies on animals.