Metabolic Parameters In Mice Research Articles

Metabolic effects in mice of cream processing: Direct ultra-high-temperature process lowers high-fat-induced adipose tissue inflammation

Although UHT heat treatment is being optimized to improve the stability and functional properties of dairy products, its metabolic effects remain scarcely known. As such, we studied the effect of the type of UHT process on lipid metabolism, intestinal barrier, and inflammation in mice. Nine-week-old male C57Bl/6J mice were fed a diet composed of nonlipidic powder mixed with different UHT dairy creams (final: 13% milkfat) for 1 or 4 wk. All creams contained 0.02% of thickener (carrageenan) and were treated via either (1) classical indirect heating process (Th), (2) indirect process at higher temperature (Th+), or (3) direct process by steam injection (ThD). Plasma, epididymal adipose tissue (EAT), and intestine were analyzed. Multivariate principal component analyses were used to identify differential effects of processes. Th+ differed by a globally higher liver damage score compared with that of the other creams. After 4 wk, the duodenal expression of lipid absorption genes fatty acid binding protein 4 (Fatp4) and microsomal triglycerides transfer protein (Mttp) was lower in the Th+ versus Th group. Expression in the colon of tight junction protein zonula occludens 1 (Zo1) and of some endoplasmic reticulum stress markers was lower in both Th+ and ThD versus the Th group. In EAT, ThD had lower gene expression of several inflammatory markers after 4 wk. Some differential effects may be related to heat-induced physicochemical changes of creams. The type of cream UHT process differentially affected metabolic parameters in mice after a 4-wk fat-rich diet, partly due to cream structure. Altogether, direct steam injection process induced the lowest early markers of high-fat-induced metabolic inflammation in EAT.

Nox4 genetic inhibition in experimental hypertension and metabolic syndrome

Metabolic syndrome is a combination of symptoms including obesity, dyslipidaemia, glucose intolerance and hypertension. Oxidative stress appears to be a pathophysiological factor that links these signs and encourages progression towards heart failure and diabetes. Nox4 is a hydrogen peroxide nicotinamide adenine dinucleotide phosphate(NADPH) oxidase isoform -found in various cardiovascular cells and tissues, but also in tissues such as the liver- which is involved in glucose and lipid homeostasis. To test whether inhibition of the Nox4 enzyme could improve blood pressure and metabolic parameters in mice receiving either angiotensinII or a high-fat diet. Systolic and diastolic arterial pressures, pulse rate and heart rate were obtained in 24male mice (12wild-type [WT] and 12Nox4-/-) before and during 14days of angiotensinII infusion. After angiotensinII infusion, cardiac histological remodeling was assessed. Weight and biochemical parameters were measured in 18male and 18female mice (nine WT and nine Nox4-/- per gender) after 10weeks on a standard chow diet, then 15weeks on a high-fat diet. Glucose tolerance and insulin sensitivity were tested at age 25weeks. Knock-out animals did not demonstrate a baseline blood pressure phenotype, but blocking Nox4 protected against angiotensinII-mediated arterial and pulse pressure increases. No protection against angiotensinII-induced cardiac fibrosis was observed. From a metabolic point of view, Nox4 inhibition reduced plasma triglycerides in male and female mice under a chow diet. However, Nox4 deletion did not affect the metabolic profile under a high-fat diet in males or females, but increased glucose intolerance in females. Our data identify Nox4 as a key source of radical oxygen species involved in hypertension and some metabolic problems.

3,5‐diiodothyronine (3,5‐T2) reduces blood glucose independently of insulin sensitization in obese mice

Thyroid hormones regulate metabolic response. While triiodothyronine (T3) is usually considered to be the active form of thyroid hormone, one form of diiodothyronine (3,5-T2) exerts T3-like effects on energy consumption and lipid metabolism. 3,5-T2 also improves glucose tolerance in rats and 3,5-T2 levels correlate with fasting glucose in humans. Presently, however, little is known about mechanisms of 3,5-T2 effects on glucose metabolism. Here, we set out to compare effects of T3, 3,5-T2 and another form of T2 (3,3-T2) in a mouse model of diet-induced obesity and determined effects of T3 and 3,5-T2 on markers of classical insulin sensitization to understand how diiodothyronines influence blood glucose. Cell- and protein-based assays of thyroid hormone action. Assays of metabolic parameters in mice. Analysis of transcript and protein levels in different tissues by qRT-PCR and Western blot. T3 and 3,5-T2 both reduce body weight, adiposity and body temperature despite increased food intake. 3,3'-T2 lacks these effects. T3 and 3,5-T2 reduce blood glucose levels, whereas 3,3'-T2 worsens glucose tolerance. Neither T3 nor 3,5-T2 affects markers of insulin sensitization in skeletal muscle or white adipose tissue (WAT), but both reduce hepatic GLUT2 glucose transporter levels and glucose output. T3 and 3,5-T2 also induce expression of mitochondrial uncoupling proteins (UCPs) 3 and 1 in skeletal muscle and WAT respectively. 3,5-T2 influences glucose metabolism in a manner that is distinct from insulin sensitization and involves reductions in hepatic glucose output and changes in energy utilization.

β-Lapachone Prevents Diet-Induced Obesity by Increasing Energy Expenditure and Stimulating the Browning of White Adipose Tissue via Downregulation of miR-382 Expression.

There has been great interest in the browning of fat for the treatment of obesity. Although β-lapachone (BLC) has potential therapeutic effects on obesity, the fat-browning effect and thermogenic capacity of BLC on obesity have never been demonstrated. Here, we showed that BLC stimulated the browning of white adipose tissue (WAT), increased the expression of brown adipocyte-specific genes (e.g., uncoupling protein 1 [UCP1]), decreased body weight gain, and ameliorated metabolic parameters in mice fed a high-fat diet. Consistently, BLC-treated mice showed significantly higher energy expenditure compared with control mice. In vitro, BLC increased the expression of brown adipocyte-specific genes in stromal vascular fraction-differentiated adipocytes. BLC also controlled the expression of miR-382, which led to the upregulation of its direct target, Dio2. Upregulation of miR-382 markedly inhibited the differentiation of adipocytes into beige adipocytes, whereas BLC recovered beige adipocyte differentiation and increased the expression of Dio2 and UCP1. Our findings suggest that the BLC-mediated increase in the browning of WAT and the thermogenic capacity of BAT significantly results in increases in energy expenditure. Browning of WAT by BLC was partially controlled via the regulation of miR-382 targeting Dio2 and may lead to the prevention of diet-induced obesity.

Nicotinamide N-methyltransferase regulates hepatic nutrient metabolism through Sirt1 protein stabilization.

Nicotinamide N-methyltransferase (Nnmt) methylates nicotinamide, a form of vitamin B3, to produce N1-methylnicotinamide (MNAM). Nnmt is an emerging metabolic regulator in adipocytes but its role in the liver, a tissue with the strongest Nnmt expression, is not known. In spite of its overall high expression, here we find that hepatic expression of Nnmt is highly variable and correlates with multiple metabolic parameters in mice and in humans. Further, we find that suppression of hepatic Nnmt expression in vivo alters glucose and cholesterol metabolism and that the metabolic effects of Nnmt in the liver are mediated by its product MNAM. Supplementation of high fat diet with MNAM decreases serum and liver cholesterol and liver triglycerides levels in mice. Mechanistically, increasing Nnmt expression or MNAM levels stabilizes sirtuin 1 protein, an effect, which is required for their metabolic benefits. In summary, we describe a novel regulatory pathway for vitamin B3 that could provide a new opportunity for metabolic disease therapy.

Improvement of Metabolic Parameters in Mice Supplemented with Vitamin D throughout Life

Rationale Metabolic endotoxemia contributes to chronic inflammation and adiposity, which may result in diabetes progression. We showed that healthy mice receiving low vs high vitamin D (25 vs 5000 IU/kg diet) from conception increased serum LPS at adulthood. This study determined if lifelong exposure to similar vitamin D levels in utero up to 6 months of age protects against adverse metabolic effects of a high fat diet. Methods Three-week old C57BL/6J dams were fed a modified AIN93G diet with high (H) or low (L) vitamin D during pregnancy and lactation until postnatal day (PND) 15, when a high fat diet (44% fat, 36% carbohydrates) was fed. On PND 21, male pups remained on their respective diets (LL or HH), or were switched (LH or HL). At 6 months, serum LPS, glucose and insulin concentrations were determined (ELISA) following an oral glucose tolerance test, and organs were weighed. Results High vitamin D resulted in lower pup weights at weaning (LD: 9.54 ± 0.16 vs. HD: 9.03 ± 0.15; p=0.02) but not at 6 months, lower epididymal fat weight (LL: 37.0 ± 1.62; LH: 34.1 ± 1.79; HL: 37.4 ± 2.27; HH: 29.7 ± 1.80; pup diet: 0.006), lower serum LPS (LL: 4.77 ± 0.41; LH: 4.08 ± 0.32; HL: 4.35 ± 0.35; HH: 2.56 ± 0.34; dam diet: 0.011; pup diet: 0.002), lower fasting glucose (LL: 13.1 ± 0.65 vs. HH: 10.7 ± 0.44; p<0.039), and similar glucose tolerance and insulin resistance. Conclusion Reduced fat accumulation due to high vitamin D post-weaning and lower systemic LPS concentrations with lifelong exposure may contribute to lower fasting glucose levels; a risk factor for diabetes. Funded by Banting and Best Diabetes Centre Novo Nordisk Studentship, Centrum Foundation Research Innovation Fund, Department of Nutritional Sciences, U of T

Effect of high sugar intake on glucose transporter and weight regulating hormones in mice and humans.

ObjectiveSugar consumption has increased dramatically over the last decades in Western societies. Especially the intake of sugar-sweetened beverages seems to be a major risk for the development of obesity. Thus, we compared liquid versus solid high-sugar diets with regard to dietary intake, intestinal uptake and metabolic parameters in mice and partly in humans.MethodsFive iso-caloric diets, enriched with liquid (in water 30% vol/vol) or solid (in diet 65% g/g) fructose or sucrose or a control diet were fed for eight weeks to C57bl/6 mice. Sugar, liquid and caloric intake, small intestinal sugar transporters (GLUT2/5) and weight regulating hormone mRNA expression, as well as hepatic fat accumulation were measured. In obese versus lean humans that underwent either bariatric surgery or small bowel resection, we analyzed small intestinal GLUT2, GLUT5, and cholecystokinin expression.ResultsIn mice, the liquid high-sucrose diet caused an enhancement of total caloric intake compared to the solid high-sucrose diet and the control diet. In addition, the liquid high-sucrose diet increased expression of GLUT2, GLUT5, and cholecystokinin expression in the ileum (P<0.001). Enhanced liver triglyceride accumulation was observed in mice being fed the liquid high-sucrose or -fructose, and the solid high-sucrose diet compared to controls. In obese, GLUT2 and GLUT5 mRNA expression was enhanced in comparison to lean individuals.ConclusionsWe show that the form of sugar intake (liquid versus solid) is presumably more important than the type of sugar, with regard to feeding behavior, intestinal sugar uptake and liver fat accumulation in mice. Interestingly, in obese individuals, an intestinal sugar transporter modulation also occurred when compared to lean individuals.

Oilseeds ameliorate metabolic parameters in male mice, while contained lignans inhibit 3T3-L1 adipocyte differentiation in vitro

The focus was directed to the study of two of the most lignan-rich food sources: sesame and flaxseeds. Recent epidemiological and experimental evidences suggesting that these foods may improve metabolic functions underlying metabolic syndrome (MetS). To characterize the effect of these oilseeds on metabolic functions, we conducted an experimental study aimed at preventing adiposity and metabolic imbalance in a mouse model of high-fat diet (HFD)-induced MetS. Statistical analysis was performed by two-way analysis of variance test followed by post hoc Bonferroni analysis. We studied the effect of the oilseeds sesame and flaxseed on metabolic parameters in mice on a HFD. When the HFD was integrated with 20% of sesame or flaxseed flours, the mice showed a decrease in body fat, already at day 15, from time 0. The size of the adipocytes was smaller in epididymal fat, liver steatosis was inhibited, and insulin sensitivity was higher in mice on the supplemented diets. The supplemented diets also resulted in a significant increase in the serum levels of the lignan metabolites enterodiol and enterolactone compared with the controls. The expression of genes associated with the inflammatory response, glucose metabolism, adipose metabolism and nuclear receptor were altered by the oilseed-supplemented diets. Some of the most abundant lignans in these oilseeds were studied in 3T3-L1 preadipocyte cells and were effective in inhibiting adipocyte differentiation at the minimal dose of 1 nM. The consumption of sesame and flaxseed may be beneficial to decrease metabolic parameters that are generally altered in MetS.

Efficacy Comparison of Korean Ginseng and American Ginseng on Body Temperature and Metabolic Parameters

Ginseng has beneficial effects in cancer, diabetes and aging. There are two main varieties of ginseng: Panax ginseng (Korean ginseng) and Panax quinquefolius (American ginseng). There are anecdotal reports that American ginseng helps reduce body temperature, whereas Korean ginseng improves blood circulation and increases body temperature; however, their respective effects on body temperature and metabolic parameters have not been studied. We investigated body temperature and metabolic parameters in mice using a metabolic cage. After administering ginseng extracts acutely (single dose of 1000 mg/kg) or chronically (200 mg/kg/day for four weeks), core body temperature, food intake, oxygen consumption and activity were measured, as well as serum levels of pyrogen-related factors and mRNA expression of metabolic genes. Acute treatment with American ginseng reduced body temperature compared with PBS-treated mice during the night; however, there was no significant effect of ginseng treatment on body temperature after four weeks of treatment. VO 2, VCO 2, food intake, activity and energy expenditure were unchanged after both acute and chronic ginseng treatment compared with PBS treatment. In acutely treated mice, serum thyroxin levels were reduced by red and American ginseng, and the serum prostaglandin E2 level was reduced by American ginseng. In chronically treated mice, red and white ginseng reduced thyroxin levels. We conclude that Korean ginseng does not stimulate metabolism in mice, whereas a high dose of American ginseng may reduce night-time body temperature and pyrogen-related factors.

Deletion of prolyl carboxypeptidase attenuates the metabolic effects of diet-induced obesity

α-Melanocyte-stimulating hormone (α-MSH) is a critical regulator of energy metabolism. Prolyl carboxypeptidase (PRCP) is an enzyme responsible for its degradation and inactivation. PRCP-null mice (PRCP(gt/gt)) showed elevated levels of brain α-MSH, reduced food intake, and a leaner phenotype compared with wild-type controls. In addition, they were protected against diet-induced obesity. Here, we show that PRCP(gt/gt) animals have improved metabolic parameters compared with wild-type controls under a standard chow diet (SD) as well as on a high-fat diet (HFD). Similarly to when they are exposed to SD, PRCP(gt/gt) mice exposed to HFD for 13 wk showed a leaner phenotype due to decreased fat mass, increased energy expenditure, and locomotor activity. They also showed improved insulin sensitivity and glucose tolerance compared with WT controls and a significant reduction in fasting glucose levels. These improvements occured before changes in body weight and composition were evident, suggesting that the beneficial effect of PRCP ablation is independent of the adiposity levels. In support of a reduced gluconeogenesis, liver PEPCK and G-6-Pase mRNA levels were reduced significantly in PRCP(gt/gt) compared with WT mice. A significant decrease in liver weight and hepatic triglycerides were also observed in PRCP(gt/gt) compared with WT mice. Altogether, our data suggest that PRCP is an important regulator of energy and glucose homeostasis since its deletion significantly improves metabolic parameters in mice exposed to both SD and HFD.

The Effects of C75, an Inhibitor of Fatty Acid Synthase, on Sleep and Metabolism in Mice

Sleep is greatly affected by changes in metabolic state. A possible mechanism where energy-sensing and sleep-regulatory functions overlap is related to lipid metabolism. Fatty acid synthase (FAS) plays a central role in lipid metabolism as a key enzyme in the formation of long-chain fatty acids. We studied the effects of systemic administration of C75, an inhibitor of FAS, on sleep, behavioral activity and metabolic parameters in mice. Since the effects of C75 on feeding and metabolism are the opposite of ghrelin's and C75 suppresses ghrelin production, we also tested the role of ghrelin signaling in the actions of C75 by using ghrelin receptor knockout (KO) mice. After a transient increase in wakefulness, C75 elicited dose-dependent and long lasting inhibition of REMS, motor activity and feeding. Simultaneously, C75 significantly attenuated slow-wave activity of the electroencephalogram. Energy expenditure, body temperature and respiratory exchange ratio were suppressed. The diurnal rhythm of feeding was completely abolished by C75. There was significant correlation between the anorectic effects, the decrease in motor activity and the diminished energy expenditure after C75 injection. We found no significant difference between wild-type and ghrelin receptor KO mice in their sleep and metabolic responses to C75. The effects of C75 resemble to what was previously reported in association with visceral illness. Our findings suggest that sleep and metabolic effects of C75 in mice are independent of the ghrelin system and may be due to its aversive actions in mice.

Inhibition of soluble epoxide hydrolase reduces food intake and increases metabolic rate in obese mice

Background and aimsThis study evaluated the responses to soluble epoxide hydrolase (s-EH) inhibition, an essential enzyme in the metabolism of arachidonic acid, on food intake, body weight and metabolic parameters in mice fed a high fat-high fructose diet (HFD) for 10 weeks. Methods and resultsAfter 5 weeks of HFD, mice were divided into two groups: 1) s-EH inhibitor (AR9281, 200mg/kg/day by gavage twice daily), and 2) vehicle (0.3ml per gavage). Food intake, body weight, oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory quotient (RQ), and motor activity were measured weekly for more 5 weeks. HFD increased body weight (37±1 vs. 26±1g), and plasma of glucose (316±8 vs. 188±27mg/dl), insulin (62.1±8.1 vs. 15.5±5.0μU/ml), and leptin levels (39.4±3.6 vs. 7.5±0.1ng/ml) while reducing VO2, VCO2 and motor activity. s-EH inhibition for 5 weeks decreased caloric intake by ∼32% and increased VO2 by ∼17% (42.8±1.4 vs. 50.2±1.5ml/kg/min) leading to significant weight loss. Inhibition of s-EHi also caused significant reductions in plasma leptin levels and visceral fat content. Uncoupling protein 1 (UCP1) content in brown adipose tissue was also elevated by ∼50% during s-EH inhibition compared to vehicle treatment. ConclusionThese results suggest that s-EH inhibition with AR9281 promotes weight loss by reducing appetite and increasing metabolic rate, and that increased UCP1 content may contribute to the increase in energy expenditure.

Inhibition of soluble epoxide hydrolase reduces food intake and increases metabolic rate in mice fed high fat‐high fructose diet

This study evaluated the responses to soluble epoxide hydrolase (s‐EH) inhibition on food intake, body weigh and metabolic parameters in mice fed a high fat‐high fructose diet (HFD) for 10 weeks. After 5 weeks of HFD, mice were divided into two groups: 1) s‐EH inhibitor (AR1153, 200 mg/kg/day), and 2) vehicle (0.3 ml) were administered orally. Food intake, body weight, oxygen consumption (VO2), carbon dioxide production (CO2), respiratory quotient (RQ), and motor activity were measured weekly. HFD increased body weight (37¡Ó1 vs 26¡Ó1 g), glucose (316¡Ó8 vs 188¡Ó27 mg/dl), insulin (62.1¡Ó8.1 vs 15.5¡Ó5.0 ƒÝU/ml), and leptin levels (39.4¡Ó3.6 vs 7.5¡Ó0.1 ng/ml) and reduced VO2, CO2 and motor activity. s‐EH inhibition for 5 weeks decreased caloric intake by ~32% and increased VO2 by ~17% compared to week 5 of HFD leading to significant weight loss. No significant changes in VO2 or body weight were observed in vehicle‐treated group. AR1153 or vehicle caused similar reductions on glucose and insulin levels, whereas leptin levels and visceral fat were reduced only in AR1153‐treated group. Uncoupling protein 1 (UCP1) content in brown adipose tissue was also elevated by ~50% during s‐EH inhibition compared to vehicle treatment. These results suggest that s‐EH inhibition promotes weight loss by reducing appetite and increasing metabolic rate, and that increased UCP1 content may have contributed to the increase in energy expenditure

Dietary Krill Oil Supplementation Reduces Hepatic Steatosis, Glycemia, and Hypercholesterolemia in High-Fat-Fed Mice

Krill oil (KO) is rich in n-3 fatty acids that are present in phospholipids rather than in triglycerides. In the present study, we investigated the effects of dietary KO on cardiometabolic risk factors in male C57BL/6 mice fed a high-fat diet. Mice (n = 6-10 per group) were fed for 8 weeks either: (1) a nonpurified chow diet (N); (2) a high-fat semipurified diet containing 21 wt % buttermilk + 0.15 wt % cholesterol (HF); (3) HF supplemented with 1.25 wt % KO (HFKO1.25); (4) HF with 2.5 wt % KO (HFKO2.5); or (5) HF with 5 wt % KO (HFKO5.0). Dietary KO supplementation caused a significant reduction in liver wt (i.e., hepatomegaly) and total liver fat (i.e., hepatic steatosis), due to a dose-dependent reduction in hepatic triglyceride (mean +/- SEM: 35 +/- 6, 47 +/- 4, and 51 +/- 5% for HFKO1.25, -2.5, and -5.0 vs HF, respectively, P < 0.001) and cholesterol (55 +/- 5, 66 +/- 3, and 71 +/- 3%, P < 0.001). Serum cholesterol levels were reduced by 20 +/- 3, 29 +/- 4, and 29 +/- 5%, and blood glucose was reduced by 36 +/- 5, 34 +/- 6, and 42 +/- 6%, respectively. Serum adiponectin was increased in KO-fed animals (HF vs HFKO5.0: 5.0 +/- 0.2 vs 7.5 +/- 0.6 microg/mL, P < 0.01). These results demonstrate that dietary KO is effective in improving metabolic parameters in mice fed a high-fat diet, suggesting that KO may be of therapeutic value in patients with the metabolic syndrome and/or nonalcoholic fatty liver disease.

Dietary phospholipid-rich dairy milk extract reduces hepatomegaly, hepatic steatosis and hyperlipidemia in mice fed a high-fat diet

Recent studies have suggested that milk and certain dairy food components have the potential to protect against cardiovascular disease. In order to determine whether the addition of milk-derived phospholipids to the diet results in an improvement in metabolic and cardiovascular risk factors, we studied four groups (n=10) of C57BL/6 mice that were fed: (1) a normal non-purified diet (N); (2) the normal non-purified diet supplemented with phospholipid-rich dairy milk extract (PLRDME, 2.5% by wt) (NPL); (3) a high-fat semi-purified diet (HF) containing 21% butterfat+0.15% cholesterol by wt; or (4) HF supplemented with 2.5% by wt PLRDME (HFPL). Dietary PLRDME supplementation did not have a significant effect on metabolic parameters in mice fed the N diet. In contrast, in high-fat fed mice, PLRDME caused a significant decrease in: (a) liver wt (1.57±0.06g vs. 1.20±0.04g, P<0.001), (b) total liver lipid (255±22mg vs. 127±13mg, P<0.001, (c) liver triglyceride (TG) and total cholesterol (TC) 236±25μmol/g vs. 130±8μmol/g (P<0.01), 40±7μmol/g vs. 21±2μmol/g (P<0.05), respectively); and serum lipids (TG: 1.4±0.1mmol/L vs. 1.1±0.1mmol/L, P=0.01; TC: 4.6±0.2mmol/L vs. 3.6±0.2mmol/L, P<0.001; and PL: 3.3±0.1mmol/L vs. 2.6±0.1mmol/L, P<0.01). These data indicate that dietary PLRDME has a beneficial effect on hepatomegaly, hepatic steatosis and elevated serum lipid levels in mice fed a high-fat diet, providing evidence that PLRDME might be of therapeutic value in human subjects as a hepatoprotective or cardioprotective nutraceutical.

Effects of short-term mild calorie restriction diet and renutrition with ruminant milks on leptin levels and other metabolic parameters in mice

Objective The adaptation of an organism to a calorie-restricted diet is characterized by metabolic, endocrine, and immunologic changes. The objective of this study was to determine, in a mouse model, the changes in serum leptin levels in response to short-term mild calorie-restricted and renutrition diets using different ruminant milks. Methods Weaned Swiss albino mice were fed with a mild calorie-restricted diet for 12 d, after which they were renourished with cow, goat, sheep, or buffalo milk for 7 d. Body, thymus, and spleen weights and biochemical, hematologic, and endocrine parameters were evaluated. Results The mild calorie restriction did not significantly modify insulin and leptin levels. The renutrition diets increased insulin levels, being significant ( P < 0.05) only when buffalo and sheep milks were used. Leptin concentrations increased in the control ad libitum (AD) group during the assayed period. After the administration of cow and goat milks, lower leptin levels were observed compared with the control AD group. All repletion diets significantly increased body, thymus, and spleen weights; however, spleen weight did not reach the values observed in the control AD group. Serum glucose and triacylglycerol levels increased after feeding with the renutrition diets. However, serum cholesterol did not increase after the renutrition period. We observed a significant decrease ( P < 0.05) in the leukocyte counts in calorie-restricted mice in comparison with AD mice; after the renutrition period, the leukocyte count did not reach the values for the AD mice. Conclusion This study suggests that a short-term change in diet with a relatively low body weight loss does not significantly affect leptin concentrations in our mouse model. However, the assayed milks could be effectively used as alternative milk sources for weight gain and for the improvement of other metabolic parameters.

Abstracts for Oral Presentation

Abstracts for Oral Presentation