The Thiamine Requirement of Pigs as Related to the Fat Content of the Diet

1944 ◽  
Vol 27 (3) ◽  
pp. 253-262
Author(s):  
N. R. Ellis ◽  
L. L. Madsen
Keyword(s):  
Body Temperature ◽  
High Fat Diet ◽  
General Health ◽  
Maximum Rate ◽  
Good Health ◽  
High Fat ◽  
Low Fat ◽  
Young Pigs ◽  
Medium Level ◽  
High Level

Summary The thiamine requirements of young pigs have been studied on three diets containing approximately 2, 11, and 28% of fat. As indicated by failure in appetite and cessation of growth, the animals on the low level of fat showed evidence of thiamine depletion on the average in 25 days, those on the medium level in 28 days, and on the high level in 33 days. Lack of thiamine resulted in marked weakening of the heart, decrease in body temperature, emaciation, and other changes. When thiamine was fed to pigs depleted of their stores of this substance, the response in appetite, growth, and general health was usually prompt and striking. Intermediate levels of thiamine produced the greatest response in the pigs fed the high-fat diet, followed in order by those on the intermediate and the low-fat. It was found that the level of thiamine required to produce a maximum rate of growth and otherwise maintain the pigs in good health fell within the range of 125 to 141 μg. per 100 gm. of carbohydrate and protein. These levels of thiamine, however, were insufficient to promote the storage of normal amounts in the meat tissue such as is found in commercial pork cuts.

scholarly journals Berberine elevates cardiolipin in heart of offspring from mouse dams with high fat diet-induced gestational diabetes mellitus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Laura K. Cole ◽  
Genevieve C. Sparagna ◽  
Marilyne Vandel ◽  
Bo Xiang ◽  
Vernon W. Dolinsky ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Mitochondrial Function ◽  
High Fat Diet ◽  
Fatty Acid Uptake ◽  
Isoquinoline Alkaloid ◽  
Acid Uptake ◽  
High Fat ◽  
Low Fat

AbstractBerberine (BBR) is an isoquinoline alkaloid from plants known to improve cardiac mitochondrial function in gestational diabetes mellitus (GDM) offspring but the mechanism is poorly understood. We examined the role of the mitochondrial phospholipid cardiolipin (CL) in mediating this cardiac improvement. C57BL/6 female mice were fed either a Lean-inducing low-fat diet or a GDM-inducing high-fat diet for 6 weeks prior to breeding. Lean and GDM-exposed male offspring were randomly assigned a low-fat, high-fat, or high-fat diet containing BBR at weaning for 12 weeks. The content of CL was elevated in the heart of GDM offspring fed a high fat diet containing BBR. The increase in total cardiac CL was due to significant increases in the most abundant and functionally important CL species, tetralinoleoyl-CL and this correlated with an increase in the expression of the CL remodeling enzyme tafazzin. Additionally, BBR treatment increased expression of cardiac enzymes involved in fatty acid uptake and oxidation and electron transport chain subunits in high fat diet fed GDM offspring. Thus, dietary BBR protection from cardiac dysfunction in GDM exposed offspring involves improvement in mitochondrial function mediated through increased synthesis of CL.

P063 A COMPREHENSIVE, MULTIOMIC DIET INTERVENTION STUDY COMPARING A LOW FAT, HIGH FIBER DIET TO AN IDEALIZED STANDARD AMERICAN DIET IN ULCERATIVE COLITIS PATIENTS

2020 ◽  
Vol 26 (Supplement_1) ◽  
pp. S8-S9
Author(s):  
Julia Fritsch ◽  
Alejandra Quintero ◽  
Judith Pignac-Kobinger ◽  
Luis Garces ◽  
Ana Santander ◽  
...  
Keyword(s):  
Quality Of Life ◽  
High Fat Diet ◽  
High Fat ◽  
Dietary Interventions ◽  
Low Fat ◽  
High Fiber ◽  
Fiber Diet ◽  
Omega 6 ◽  
High Fiber Diet

Abstract Background and Aims There is a lack of evidence-based dietary interventions in ulcerative colitis (UC) management. A diet high in fat and animal meat has been linked to an increased risk of UC. The aim of our study was to use a multilayered, multi-omic approach to comprehensively characterize the effect of a low fat, high fiber diet or a high fat diet in UC patients. Methods We enrolled patients with UC who were in remission or had mild disease with a flare within the last 18 months. We used a cross-over design in which patients received two dietary interventions: a low fat diet (LFD), containing 10% total calories from fat with an omega 6 to 3 ratio of below 3:1, and an idealized standard American diet (SAD), containing 35–40% total calories from fat with an omega 6 to 3 ratio of 20–30:1. Each diet was four weeks long with a two-week wash-out in between. The diet was catered and delivered to patients’ homes. Clinical symptoms, quality of life, and biochemical data were collected. Stool was collected for microbiome and metabolomic analyses. The primary endpoint was to determine adherence to a specified diet using catered meals; the secondary endpoint was to determine the clinical and subclinical effects of a low fat, high fiber diet or high fat diet in UC. Results Baseline diets varied widely but were generally lower in fiber as well as fruits and vegetables and higher in saturated fat than either of the study diets. There was a high rate of adherence to catered meals (SAD=86.68%, LFD=84.8%) with a 96.8% and 94.33% adherence to fat for SAD and LFD respectively. Patients that started in remission remained in remission (partial Mayo and sIBDQ). Following a LFD, patients saw a 20% improvement in their quality of life as measured by sIBDQ compared to their baseline. The effect of diet intervention on microbial diversity was reflected in the beta diversity with a significant increase in Faecalibacterium prausnitzii after LFD. CRP, sIBDQ, IL-6, and IL1β had a significant effect on overall gut microbiota composition as measured by Bray Curtis beta diversity (PERMANOVA)(P<0.007, P<0.001, P<0.021, P<0.048 respectively). The top taxa that contributes the most to this microbial variation from these clinical parameters was Faecalibacterium prausnitzii. Patients following a SAD had an increase in lauric acid, myristic acid, and N-oleoyl-L-phenylalanine with an increase in omega-6 metabolism pathways. Patients following a LFD had higher glycine, alanine, and phenyllactic acid with omega 3 metabolism pathways increased after LFD. Conclusions A low fat, high fiber diet is well tolerated and did not increase biochemical markers of inflammation. Catered meals and collection of microbiome, metabolome and biochemical data may allow early stratification of diet responders.

scholarly journals Antiobesity and Hypolipidemic Activity of Moringa oleifera Leaves against High Fat Diet-Induced Obesity in Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Souravh Bais ◽  
Guru Sewak Singh ◽  
Ramica Sharma
Keyword(s):  
Body Weight ◽  
Body Temperature ◽  
Total Cholesterol ◽  
High Fat Diet ◽  
Moringa Oleifera ◽  
Chronic Administration ◽  
The Body ◽  
Atherogenic Index ◽  
High Fat ◽  
Diet Induced Obesity

In the present study, the methanolic extract of Moringa oleifera leaves (MEMOL) was evaluated for antiobesity activity in rats. The antiobesity potential of MEMOL was studied against high fat diet-induced obesity (HFD) in rats. In this study, chronic administration of HFD in rats produced hypercholesterolemia (116.2 ± 0.27 mg/dL), which led to an increase in the body weight (225 gr), total cholesterol, triglycerides (263.0 ± 4.69 mg/dL), and attenuation in the levels of HDL (34.51 ± 2.20 mg/dL) as well as changes in body temperature of animals. Treatment of obese rats with MEMOL for 49 days resulted in a significant (P<0.001) change in body weight, total cholesterol, triglycerides, and LDL level along with a significant (P<0.001) increase in body temperature as compared to the HFD-induced obesity. MEMOL treated rats also showed a significant decrease in the level of liver biomarkers, organ weight, and blood glucose level. Further, rats treated with MEMOL (200 mg and 400 mg/kg) show reduced atherogenic index (1.7 ± 0.6 and 0.87 ± 0.76). The results indicate that the rats treated with Moringa oleifera (MO) have significantly attenuated the body weight without any change in the feed intake and also elicited significant thermogenic effect and to act as hypolipidemic and thermogenic property in obesity related disorders.

Abstract 480: Exacerbation of Arterial Stiffness in Obese Adiponectin Deficient Mice

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Megha Murali ◽  
Carla Taylor ◽  
Peter Zahradka ◽  
Jeffrey Wigle
Keyword(s):  
Arterial Stiffness ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
High Fat Diet ◽  
Pulse Wave ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
High Fat Diets ◽  
Fat Diets

Background and Objective: Arterial stiffness is recognized as being an independent predictor of incipient vascular disease associated with obesity and metabolic syndrome. In obese subjects, the decrease in the plasma level of adiponectin, an anti-diabetic and anti-atherogenic adipokine, is well known. Hence the aim of our study was to examine the effect of loss of adiponectin on the development of arterial stiffness in response to a high fat diet. Methods and Results: Male 8-week old adiponectin knockout (APN KO) and C57BL/6 (control) mice were fed a high fat diet (60% Calories from fat) for 12 weeks to induce obesity and insulin resistance (n=10/group). APN KO and C57BL/6 mice were fed a low fat diet (10% Calories from fat) and used as lean controls (n=10/group). After 12 weeks on the high fat diet, the APN KO mice weighed significantly more than the C57BL/6 mice (45.1±1.3 g vs 40.1±1.1 g, p=0.0008) but there was no difference in the final weights between genotypes fed the low fat diet. APN KO mice on both high and low fat diets for 12 weeks developed insulin resistance as measured by oral glucose tolerance test (Area under curve (AUC) mmol/L х min = 437±70 and 438±57) as compared to the C57BL/6 mice fed low or high fat diets (AUC mmol/L х min = 251±27 and 245±43). Arterial stiffness was determined by Doppler pulse wave velocity analysis of the femoral artery. Pulse wave velocity was increased in APN KO mice fed a high fat diet relative to those fed the low fat diet (12.56±0.78 cm/s vs 9.47±0.95 cm/s, p=0.0035; n=8-10). Pulse wave velocity was not different between C57BL/6 control mice on the low or high fat diets (10.63±0.73 cm/s and 10.86±0.50 cm/s), thus revealing that only mice deficient in adiponectin developed arterial stiffness in response to high fat diet. Conclusions: Potentiation of the vascular stiffness in diet-induced obese APN KO mice indicates that adiponectin has a role in modulating vascular structure and the APN KO mouse models the vascular changes that occur in human obesity and metabolic disorders. Morphometric analysis of the aortic tissues for vessel thickness and expression of extracellular proteins will further validate the potential role of adiponectin on the maintenance of arterial elasticity in addition to its known effect on eNOS mediated vasoprotection.

scholarly journals Influence of gender on OVA-induced airway inflammation in C57/B6J mice on a high-fat diet

2018 ◽  
Vol 16 ◽  
pp. 205873921876094 ◽  
Author(s):  
Gang Yu ◽  
Lili Zhu ◽  
Haiyan Li ◽  
Youyou Shao ◽  
Lei Chong ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Inflammatory Cells ◽  
Normal Weight ◽  
Male Mice ◽  
High Fat ◽  
Low Fat ◽  
Control Male ◽  
Low Fat Diet ◽  
Asthma Group

Overweight/obesity has been suggested as a risk factor for asthma development, and prospective studies have confirmed that high body weight precedes asthma symptoms. However, the nature of the association between overweight/obese status and asthma remains unclear. Animal models of obesity-related asthma are very useful for understanding disease pathophysiology. Although C57/B6J mice are the most widely used animal model for researching obesity-related asthma, gender differences are not always taken into consideration. Therefore, to explore the effect of gender on the development of obesity-related asthma, both female and male C57/B6J mice were used in this study. The mice were fed with a high-fat diet or a low-fat diet as control. Body weight, body length, liver weight, and Lee’s Index were used to evaluate obesity status, and lung histology, lung inflammatory cells infiltration, and inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were examined for asthma evaluation. We found that the mean body weight of male mice on a high-fat diet gradually increased and was significantly higher than control male mice on a low-fat diet ( P < 0.01), while no significant differences were found between female mice at the end of 12 weeks of feeding. Furthermore, the obese asthma group female and male mice exhibited significantly high inflammatory cells infiltration than normal weight or obese female and male mice ( P < 0.01). However, the obese asthma group presented higher Neu infiltration, Th1 cytokine, and interferon gamma (IFNγ) concentrations in BALF than the asthma group in both the genders ( P < 0.01). In conclusion, both female and male mice are suitable for the obesity-related asthma model, although male mice might be more stable. Besides, obesity-related asthma is not Th2 type asthma.

Experimental obesity and osteoarthritis

1960 ◽  
Vol 198 (4) ◽  
pp. 765-770 ◽  
Author(s):  
Leon Sokoloff ◽  
Olaf Mickelsen ◽  
Emanuel Silverstein ◽  
George E. Jay ◽  
Richard S. Yamamoto
Keyword(s):  
Weight Gain ◽  
Dietary Restriction ◽  
High Fat Diet ◽  
Deleterious Effect ◽  
Degenerative Joint Disease ◽  
Fat Content ◽  
Joint Disease ◽  
High Fat ◽  
Low Fat ◽  
Hybrid Mice

Experimental obesity was produced in DBA/2JN, STR/N and C57L/HeN mice as well as in Osborne-Mendel rats by several dietary regimens. One of these, containing 60% vegetable fat, increased the amount of degenerative joint disease in the rats and in two strains of mice. No increase of osteoarthritis occurred as a result of a 37.4% fat content in the diet, or from obesity produced by Ingle's diet, which has a relatively low-fat content. The mechanism by which the high-fat diet increased the joint disease is unknown, because neither obesity nor a high-fat diet alone had a deleterious effect on the articulations of the mice. Obese hybrid mice derived from a spontaneously obese and arthritis-prone strain (STR/1N) were resistant to articular degeneration. Dietary restriction of weight gain in the STR/1N mice failed to decrease the osteoarthritis in them.

scholarly journals SERUM LIPID PROFILE;

2008 ◽  
Vol 15 (04) ◽  
pp. 500-507
Author(s):  
MUHAMMAD ANWAR BURIRO ◽  
MUHAMMAD TAYYAB
Keyword(s):  
Sunflower Oil ◽  
High Fat Diet ◽  
Serum Lipid ◽  
Nigella Sativa ◽  
Albino Rats ◽  
High Fat ◽  
Low Fat ◽  
Control Groups ◽  
Low Fat Diet ◽  
Lipid Fractions

Objective: To determine the effects of Nigella sativa and sunflower oil diet intake on serum lipid profile in albino rats. Material& Methods: Eighty four albino rats with equal number of males and females were selected for the study, they were divided into six differentgroups, Control groups1,111,V,were given low fat diet(3%),high fat diet(20%), high fat diet supplemented with bile salt (1% colic acid) andantithyroid drug (0.5% propylthiouracil). The Experimental groups were given the above diets with supplemented Nigella sativa. Low fat dietincreased all the lipid fractions significantly when given at12 and 24 weeks duration as compared to 0 week. Results: The high fat diet whengiven at different intervals decreased all lipid fractions significantly as compared to baseline level. The high fat diet with propylthiouracil andbile salt also increased all the lipid fractions and the increase was more as compared to previous groups. The supplements of Nigella sativain the groups decreased all the lipid fractions significantly as compared to the control groups except HDL-c, which was significantly increasedin all the experimental groups as compared to control groups. Conclusion: On the basis of these findings conclusions are made, that Nigellasativa has got TG,TC, and LDL-c lowering and HDL-c raising effects.3% sunflower oil low fat diet has got TG,TC,HDL-c, and LDL-c raisingeffects.20% sunflower oil high fat diet has got TG,TC,HDL-c and LDL-c lowering effects. Both Nigella sativa and sunflower oil have got lowatherogenic index (TC/HDL) and may be recommended in hyperlipidaemic patients or normal individuals.

Abstract P430: VSMCs Increase Glutamine Utilization For Energy Metabolism During Obesity

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Krystal M Roggerson ◽  
Sharon Francis
Keyword(s):  
Oxygen Consumption ◽  
Energy Metabolism ◽  
High Fat Diet ◽  
Vascular Remodeling ◽  
Energy Demand ◽  
Critical Role ◽  
Fold Increase ◽  
Metabolic Reprogramming ◽  
High Fat ◽  
Low Fat

Obesity increases the risk of developing cardiovascular disease through vascular remodeling though the underlying mechanisms are not entirely understood. However, metabolic fuel partitioning and mitochondrial flexibility during energy metabolism may play a critical role. We demonstrated serum and glucocorticoid-inducible kinase 1 (SGK-1) is up-regulated in the vasculature of diet-induced obese mice and that SGK-1 deletion is protective against obesity-induced vascular remodeling by metabolically reprogramming vascular smooth muscle cell (VSMC) energy metabolism towards oxidative phosphorylation (OXPHOS) and away from glycolysis. Mitochondrial substrate availability and utilization of the primary metabolic fuels glucose, long chain fatty acids (LCFAs) and glutamine can drive metabolic reprogramming. Therefore, alterations in fuel utilization may contribute to vascular remodeling during obesity. The purpose of this study was to examine SGK-1’s role in 1) fuel dependency: a cell’s reliance for a specific fuel and 2) fuel capacity: a cell’s ability to oxidize a specific fuel to meet cellular energy demand under low-fat and high-fat diet-induced obesity. Using the MitoXpress Oxygen Consumption assay which measures OXPHOS, primary VSMCs isolated from wildtype (WT) and SMC-specific SGK-1 knockout (smSGK-1 KO) mice fed a 10% kcal low-fat or 45% kcal high-fat diet for eight weeks were seeded in a 96-well plate at a density of 6x10 4 cells/well in culture medium. To assess fuel dependency, cells were treated with fuel pathway inhibitors UK5099, Etomoxir or BPTES to block glucose, LCFA or glutamine oxidation, respectively. To measure fuel capacity, VSMCs were treated with a combination of two pathway inhibitors simultaneously. Next, samples were overlaid with a fluorescent extracellular oxygen consumption reagent, sealed with high-sensitivity mineral oil, then signals were read at 1.5-minute intervals for 2 hours at Ex/Em= 380/650 nm. Our results show WT VSMCs are exclusively glucose-dependent for OXPHOS regardless of dietary conditions. However, SGK-1 deletion induces a dependency for all three fuels for OXPHOS in VSMCs under low- and high-fat conditions. Even though WT and smSGK-1 KO VSMCs preferentially oxidized glucose for OXPHOS under low-fat conditions; SGK-1 deletion resulted in a 2.2-fold increase in glutamine capacity. Alternatively, WT VSMCs exposed to obesogenic conditions preferentially oxidized glutamine whereas SGK-1 deletion induced a nearly equal partitioning of all three fuels during obesity suggesting elevated mitochondrial flexibility. Overall, this study suggests SGK-1 increases glucose dependency for energy metabolism under physiological and obesogenic conditions. Also, increased glutamine utilization for OXPHOS during obesity may be an underlying cause of VSMC dysfunction and subsequent vascular impairment.

scholarly journals High-fat and low-fat (behavioural) phenotypes: biology or environment?

1999 ◽  
Vol 58 (4) ◽  
pp. 773-777 ◽  
Author(s):  
John E. Blundell ◽  
John Cooling
Keyword(s):  
Risk Factors ◽  
Body Weight ◽  
Risk Factor ◽  
Weight Gain ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Positive Energy ◽  
High Fat ◽  
Low Fat ◽  
Conceptual Tool

It is now widely accepted that obesity develops by way of genetic mechanisms conferring specific dispositions which interact with strong environmental pressures. It is also accepted that certain dispositions constitute metabolic risk factors for weight gain. It is less well accepted that certain patterns of behaviour (arising from biological demands or environmental influences) put individuals at risk of developing a positive energy balance and weight gain (behavioural risk factors). Relevant patterns of behaviour include long-lasting habits for selecting and eating particular types of foods. Such habits define two distinct groups characterized as high-fat (HF) and low-fat (LF) phenotypes. These habits are important because of the attention given to dietary macronutrients in body-weight gain and the worldwide epidemic of obesity. Considerable evidence indicates that the total amount of dietary fat consumed remains the most potent food-related risk factor for weight gain. However, although habitual intake of a high-fat diet is a behavioural risk factor for obesity, it does not constitute a biological inevitability. A habitual low-fat diet does seem to protect against the development of obesity, but a high-fat diet does not guarantee that an individual will be obese. Although obesity is much more prevalent among HF than LF, some HF are lean with BMI well within the normal range. The concept of 'different routes to obesity' through a variety of nutritional scenarios can be envisaged, with predisposed individuals varying in their susceptibility to different dietary inputs. In a particular subgroup of individuals (young adult males) HF and LF displayed quite different profiles of appetite control, response to nutrient challenges and physiological measures, including BMR, RQ, heart rate, plasma leptin levels and thermogenic responses to fat and carbohydrate meals. These striking differences suggest that HF and LF can be used as a conceptual tool to investigate the relationship between biology and the environment (diet) in the control of body weight.

Whole body insulin sensitivity in Osborne-Mendel and S 5B/Pl rats eating a low- or high-fat diet

1992 ◽  
Vol 263 (4) ◽  
pp. R785-R789 ◽  
Author(s):  
T. A. Buchanan ◽  
J. S. Fisler ◽  
S. Underberger ◽  
G. F. Sipos ◽  
G. A. Bray
Keyword(s):  
Insulin Sensitivity ◽  
High Fat Diet ◽  
Whole Body ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
High Fat Diets ◽  
Glucose Clearance ◽  
Fat Diets ◽  
Fat Feeding

To determine whether whole body insulin sensitivity differs between a rat strain that does not (S 5B/Pl) and a strain that does [Osborne-Mendel (OM)] become obese when eating a high-fat diet, we performed euglycemic clamp studies in animals from each strain during low- and high-fat feeding. Clamps were performed after 2 days ("initial clamp") and 9 days ("final clamp") on each diet. Plasma glucose and insulin levels during the final 60 min of initial and final clamps were similar in S 5B/Pl and OM rats regardless of diet. Insulin sensitivity, measured as the glucose clearance rate during the final 60 min of the clamp, averaged 35 +/- 3 ml.kg-1.min-1 in S 5B/Pl rats after 2 days on a low-fat diet. This did not change significantly during an additional 7 days on the low-fat diet. The high-fat diet was associated with a 13% reduction in insulin sensitivity after 2 days and a 30% reduction after 9 days in S 5B/Pl rats. OM rats exhibited similar patterns of insulin sensitivity during low- and high-fat diets, albeit at lower insulin sensitivity overall (P < 0.0005 vs. S 5B/Pl). Mean glucose clearance after 2 days on the low-fat diet was 27 +/- 2 mg.kg-1.min-1 and did not change significantly during seven more days of low-fat feeding. The high-fat diet was associated with a 19% reduction in glucose clearance after 2 days and a 38% reduction after 9 days in OM rats. The magnitude of reduction in insulin sensitivity during high-fat diets did not differ significantly between strains.(ABSTRACT TRUNCATED AT 250 WORDS)

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