scholarly journals The effect of dietary guar gum on the activities of some key enzymes of carbohydrate and lipid metabolism in mouse liver

1985 ◽  
Vol 53 (2) ◽  
pp. 215-222 ◽  
Author(s):  
John C. Stanley ◽  
Eric A. Newsholme
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Malate Dehydrogenase ◽  
Food Consumption ◽  
Guar Gum ◽  
Body Weight Gain ◽  
Dry Weight ◽  
Weight Basis ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
High Sucrose

1. The effects of a 100 g/kg substitution of guar gum on the body-weight gain, food consumption and faecal dry weight of mice fed on a high-sucrose diet and on the activities of hepatic glucose-6-phosphate dehydrogenase (EC 1. 1. 1. 49), 6-phosphogluconate dehydrogenase (EC 1. I. 1. 44), malate dehydrogenase (oxaloacetate- decarboxylating) (NADP+) (EC I. 1. 1. 40), ATP-citrate (pro-3S)-lyase (EC 4. I.3.8), 6-phosphofructokinase (EC 2.7. 1. 11), pyruvate kinase (EC 2. 7. 1. 40)and fructose-1, Qbisphosphatase (EC 3. 1. 3. 11) were studied.2. Guar gum had no effect on body-weight gain or food consumption but increased faecal dry weight.3. Guar gum increasedtheactivitiesofglucose-6-phosphatedehydrogenase, malatedehydrogenase(oxaloacetate- decarboxylating) (NADP+) and 6-phosphofructokinase expressed on a wet-liver-weight basis.4. Guar gum increased the activities of glucose-6-phosphate dehydrogenase, malate dehydrogenase (oxaloacetate- decarboxylating)(NADP+), ATP-citrate (pro-3S)-lyase and 6-phosphofructokinase expressed on a liver-protein basis.5. Guar gum increased the activities of glucose-6-phosphate dehydrogenase and malate dehydrogenase (oxaloacetate-decarboxylating)(NADP+) expressed on a body-weight basis.6. These results suggest that guar gum increases the flux through some pathways of hepatic lipogenesis when mice are fed on high-sucrose diets.

scholarly journals The effect of dietary bagasse on the activities of some key enzymes of carbohydrate and lipid metabolism in mouse liver

1985 ◽  
Vol 54 (2) ◽  
pp. 415-420 ◽  
Author(s):  
John C. Stanley ◽  
Eric A. Newsholme
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Consumption ◽  
Body Weight Gain ◽  
Dry Weight ◽  
Weight Basis ◽  
The Body ◽  
Phosphogluconate Dehydrogenase ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
High Sucrose

1. The effects of a 100 g/kg diet substitution of bagasse on the body-weight gain, food consumption and faecal dry weight of mice given a high-sucrose diet and on the activities of hepatic glucose-6-phosphate dehydrogenase (EC 1. 1. 1. 49), 6-phosphogluconate dehydrogenase (EC I. I. I. 44), malate dehydrogenase (oxaloacetatedecarboxylating) (NADP+) (EC I. I. I. 40), ATP-citrate (pro-3S) lyase (EC 4. 1. 3.8), 6-phosphofructokinase (EC 2. 7. 1. II), pyruvate kinase (EC 2.7. 1. 40) and fructose-1,6-bisphosphatase (EC 3. 1. 3. II) were studied.2. Bagasse had no effect on body-weight gain, food consumption or faecal dry weight.3. Bagasse decreased the activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and phosphofructokinase expressed on a wet weight basis and on a protein basis.4. Bagasse decreased the activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydro-genase expressed on a body-weight basis.5. These results suggest that bagasse decreases the flux through some pathways of hepatic lipogenesis when mice are given high-sucrose diets.

scholarly journals Absence of effects of dietary wheat bran on the activities of some key enzymes of carbohydrate and lipid metabolism in mouse liver and adipose tissue

1986 ◽  
Vol 55 (2) ◽  
pp. 287-294 ◽  
Author(s):  
John C. Stanley ◽  
Jacqueline A. Lambadrios ◽  
Eric A. Newsholme
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Wheat Bran ◽  
Body Weight Gain ◽  
Dry Weight ◽  
Phosphogluconate Dehydrogenase ◽  
Carbohydrate And Lipid Metabolism ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
High Sucrose

1. The effects of a 100 g/kg dietary substitution of wheat bran on the body-weight gain, food consumption and faecal dry weight of mice given a high-sucrose diet and on the activities of some key enzymes of carbohydrate and lipid metabolism in liver and adipose tissue were studied.2. Wheat bran had no effect on body-weight gain, food consumption or faecal dry weight.3. Wheat bran had no effect on the activities of hepatic glucose-6-phosphate dehydrogenase (EC 1.1.1.49), 6-phosphogluconate dehydrogenase (EC 1. 1.1.44), malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+) (EC 1. 1. 1.40), ATP-citrate (pro-3S)-lyase (EC 4.1.3.8), pyruvate kinase (EC 2.7.1.40) and fructose-1, 6-bisphosphatase (EC 3.1.3.11). The activity of hepatic 6-phosphofructokinase (EC 2.7.1.11) increased but only when expressed on a body-weight basis.4. Wheat bran had no effect on the activities of adipose tissue glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+), (ATP-citrate igro-3S)-lyase, hexokinase (EC 2. 7. 1. 1), 6-phosphofructokinase and pyruvate kinase.5. These results suggest that unlike guar gum and bagasse, wheat bran does not change the flux through some pathways of lipogenesis in liver and adipose tissue when mice are given high-sucrose diets.

scholarly journals Synergistic Effects of DHA and Sucrose on Body Weight Gain in PUFA-Deficient Elovl2 -/- Mice

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 852
Author(s):  
Pauter ◽  
Fischer ◽  
Bengtsson ◽  
Asadi ◽  
Talamonti ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Synergistic Effects ◽  
Plasma Lipoproteins ◽  
Sucrose Content ◽  
Omega 3 ◽  
High Sucrose

The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) is implicated in theregulation of both lipid and carbohydrate metabolism. Thus, we questioned whether dietary DHAand low or high content of sucrose impact on metabolism in mice deficient for elongation of verylong-chain fatty acids 2 (ELOVL2), an enzyme involved in the endogenous DHA synthesis. Wefound that Elovl2 -/- mice fed a high-sucrose DHA-enriched diet followed by the high sucrose, highfat challenge significantly increased body weight. This diet affected the triglyceride rich lipoproteinfraction of plasma lipoproteins and changed the expression of several genes involved in lipidmetabolism in a white adipose tissue. Our findings suggest that lipogenesis in mammals issynergistically influenced by DHA dietary and sucrose content.

The effect of diet on some parameters measured in toxicological studies in the rat

1980 ◽  
Vol 14 (3) ◽  
pp. 253-261 ◽  
Author(s):  
M. J. L. Clapp
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Consumption ◽  
Dietary Protein ◽  
Body Weight Gain ◽  
Alanine Transaminase ◽  
Haematological Parameters ◽  
Transaminase Activity ◽  
Histological Studies ◽  
Toxicological Studies

The bodyweight, food consumption and various biochemical and haematological parameters were measured in, and breeding and histological studies made of, groups of rats fed 6 different diets. All diets acceptably supported reproduction. 1 diet restricted body weight gain by 30%, and increased plasma alanine transaminase activity. Nephrocalcinosis was seen in females fed diets with a calcium: phosphorous ratio of <1. Levels of dietary protein were positively correlated with the incidence of renal pelvic dilatation in offspring at 7 weeks of age.

Tamarind Seed Polysaccharide

2013 ◽  
Vol 32 (3) ◽  
pp. 198-208 ◽  
Author(s):  
James T. Heimbach ◽  
Hiroshi Egawa ◽  
Palma Ann Marone ◽  
Mark R. Bauter ◽  
Elke Kennepohl
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Consumption ◽  
Body Weight Gain ◽  
Clinical Chemistry ◽  
Clinical Signs ◽  
Female Rats ◽  
Feed Consumption ◽  
Test Substance ◽  
Tamarind Seed

Forty male and 40 female Crl:SD® CD® IGS rats were fed diets containing 0, 40 000, 80 000, or 120 000 ppm tamarind seed polysaccharide (equivalent to 3450.8, 6738.9, or 10 597.1 mg/kg bw/day and 3602.1, 7190.1, or 10 690.7 mg/kg bw/day for males and females, respectively) for 28 days. Animals were observed for adverse clinical signs, body weight, feed consumption, hematology and clinical chemistry parameters, urinalysis values were recorded, and at the end of the study the rats underwent a full necropsy. Functional Observational Battery (FOB) and Motor Activity (MA) tests were performed on all animals. There were no mortalities, no clinical or ophthalmologic signs, body weight, body weight gain, food consumption and food efficiency, FOB or MA findings associated with the administration of tamarind seed polysaccharide. Initial statistically significant decreases in body weight gain and food consumption resolved after the first week and were considered the result of reduced palatability. There were no adverse changes in hematology, coagulation, clinical chemistry or urinalysis parameters in male or female rats considered the result of test substance administration. At necropsy, there were no macroscopic, histopathological findings, estrus cycle, or organ weight changes deemed related to administration of the test substance. Under the conditions of this study and based on the toxicological endpoints evaluated, the no-observed-adverse-effect level (NOAEL) for tamarind seed polysaccharide in the diet was the highest concentration tested of 120 000 ppm (equivalent to 10 597 mg/kg bw/day and 10 691 mg/kg bw/day for male and female rats, respectively).

The pathogenic effects of Eimeria praecox and E. acervulina in the chicken

Parasitology ◽  
1968 ◽  
Vol 58 (3) ◽  
pp. 691-700 ◽  
Author(s):  
P. L. Long
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Weight Gain ◽  
Food Consumption ◽  
Intestinal Permeability ◽  
Technical Assistance ◽  
Body Weight Gain ◽  
Eimeria Acervulina ◽  
No Weight Loss ◽  
Pathogenic Effects

Eimeria praecox produced less effect on body-weight gain and food consumption than E. acervulina. No deaths occurred and no weight loss followed infection with doses of oocysts up to 10. However, there was a depression of body-weight gain in birds infected with both species and changes in the permeability of the intestine were noted from as early as 3½ h after infection. This suggests that increased intestinal permeability is not the major factor in the greater pathogenicity of E. acervulina compared with E. praecox. Eimeria acervulina produced considerably greater effects on the host as evidenced by mortality, body weight gain and food consumption.I wish to thank Mr B. J. Millard and Mr M. Shirley for technical assistance and Dr B. M. Freeman for help with the statistics in Table 2.

scholarly journals Social Isolation Affects the Development of Obesity and Type 2 Diabetes in Mice

Endocrinology ◽  
2007 ◽  
Vol 148 (10) ◽  
pp. 4658-4666 ◽  
Author(s):  
Katsunori Nonogaki ◽  
Kana Nozue ◽  
Yoshitomo Oka
Keyword(s):  
Type 2 Diabetes ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Social Isolation ◽  
Food Consumption ◽  
Leptin Receptor ◽  
Body Weight Gain ◽  
Kkay Mice

Social isolation is associated with increased risks of mortality and morbidity. In this study, we show that chronic individual housing accelerated body weight gain and adiposity in KK mice but not C57BL6J mice, and fully developed diabetes in KKAy mice. Individually housed KK and KKAy mice increased body weight gain over the initial 2 wk without increased daily average food consumption compared with group-housed animals. The individually housed KK and KKAy mice then gradually increased food consumption for the next 1 wk. The chronic social isolation-induced obesity (SIO) was associated with hyperleptinemia and lower plasma corticosterone and active ghrelin levels but not hyperinsulinemia. Elevated plasma leptin in the SIO suppressed expression of 5-HT2C receptor in white adipose tissue. The SIO was also associated with decreased expression of β3-adrenergic receptors in white adipose tissue and hypothalamic leptin receptor, which might be secondary to the enhanced adiposity. Interestingly, social isolation acutely reduced food consumption and body weight gain compared with group-housed obese db/db mice with leptin receptor deficiency. Social isolation-induced hyperglycemia in KKAy mice was associated with increased expression of hepatic gluconeogenetic genes independent of insulin. These findings suggest that social isolation promotes obesity due to primary decreased energy expenditure and secondary increased food consumption, which are independent of the disturbed leptin signaling, in KK mice, and develops into insulin-independent diabetes associated with increased expression of hepatic gluconeogenetic genes in KKAy mice. Thus, social isolation can be included in the environmental factors that contribute to the development of obesity and type 2 diabetes.

scholarly journals Targeted leptin receptor blockade: role of ventral tegmental area and nucleus of the solitary tract leptin receptors in body weight homeostasis

2014 ◽  
Vol 222 (1) ◽  
pp. 27-41 ◽  
Author(s):  
M Matheny ◽  
K Y E Strehler ◽  
M King ◽  
N Tümer ◽  
P J Scarpace
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Ventral Tegmental Area ◽  
Food Consumption ◽  
Leptin Receptor ◽  
Body Weight Gain ◽  
Solitary Tract ◽  
Leptin Receptors ◽  
Ventral Tegmental

The present investigation examined whether leptin stimulation of ventral tegmental area (VTA) or nucleus of the solitary tract (NTS) has a role in body weight homeostasis independent of the medial basal hypothalamus (MBH). To this end, recombinant adeno-associated viral techniques were employed to target leptin overexpression or overexpression of a dominant negative leptin mutant (leptin antagonist). Leptin antagonist overexpression in MBH or VTA increased food intake and body weight to similar extents over 14 days in rats. Simultaneous overexpression of leptin in VTA with antagonist in MBH resulted in food intake and body weight gain that were less than with control treatment but greater than with leptin alone in VTA. Notably, leptin overexpression in VTA increased P-STAT3 in MBH along with VTA, and leptin antagonist overexpression in the VTA partially attenuated P-STAT3 levels in MBH. Interestingly, leptin antagonist overexpression elevated body weight gain, but leptin overexpression in the NTS failed to modulate either food intake or body weight despite increased P-STAT3. These data suggest that leptin function in the VTA participates in the chronic regulation of food consumption and body weight in response to stimulation or blockade of VTA leptin receptors. Moreover, one component of VTA-leptin action appears to be independent of the MBH, and another component appears to be related to leptin receptor-mediated P-STAT3 activation in the MBH. Finally, leptin receptors in the NTS are necessary for normal energy homeostasis, but mostly they appear to have a permissive role. Direct leptin activation of NTS slightly increases UCP1 levels, but has little effect on food consumption or body weight.

scholarly journals Polymannuronic acid ameliorated obesity and inflammation associated with a high-fat and high-sucrose diet by modulating the gut microbiome in a murine model

2017 ◽  
Vol 117 (9) ◽  
pp. 1332-1342 ◽  
Author(s):  
Fang Liu ◽  
Xiong Wang ◽  
Hongjie Shi ◽  
Yuming Wang ◽  
Changhu Xue ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Gut Microbiome ◽  
Body Weight Gain ◽  
High Fat ◽  
Microbial Composition ◽  
The Metabolic Syndrome ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
High Sucrose

AbstractPolymannuronic acid (PM), one of numerous alginates isolated from brown seaweeds, is known to possess antioxidant activities. In this study, we examined its potential role in reducing body weight gain and attenuating inflammation induced by a high-fat and high-sucrose diet (HFD) as well as its effect on modulating the gut microbiome in mice. A 30-d PM treatment significantly reduced the diet-induced body weight gain and blood TAG levels (P<0·05) and improved glucose tolerance in male C57BL/6J mice. PM decreased lipopolysaccharides in blood and ameliorated local inflammation in the colon and the epididymal adipose tissue. Compared with low-fat and low-sucrose diet (LFD), HFD significantly reduced the mean number of species-level operational taxonomic units (OTU) per sample as well as species richness (P<0·05) but did not appear to affect other microbial diversity indices. Moreover, compared with LFD, HFD altered the abundance of approximately 23 % of the OTU detected (log10 linear discriminant analysis (LDA) score>2·0). PM also had a profound impact on the microbial composition in the gut microbiome and resulted in a distinct microbiome structure. For example, PM significantly increased the abundance of a probiotic bacterium, Lactobacillus reuteri (log10 LDA score>2·0). Together, our results suggest that PM may exert its immunoregulatory effects by enhancing proliferation of several species with probiotic activities while repressing the abundance of the microbial taxa that harbor potential pathogens. Our findings should facilitate mechanistic studies on PM as a potential bioactive compound to alleviate obesity and the metabolic syndrome.

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