scholarly journals Growth and Progression of TRAMP Prostate Tumors in Relationship to Diet and Obesity

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Melissa J. L. Bonorden ◽  
Michael E. Grossmann ◽  
Sarah A. Ewing ◽  
Olga P. Rogozina ◽  
Amitabha Ray ◽  
...  

To clarify effects of diet and body weight on prostate cancer development, three studies were undertaken using the TRAMP mouse model of this disease. In the first experiment, obesity was induced by injection of gold thioglucose (GTG). Age of prostate tumor detection (~33 wk) and death (~43 wk) was not significantly different among the groups. In the second study, TRAMP-C2 cells were injected into syngeneic C57BL6 mice and tumor progression was evaluated in mice fed either high-fat or low-fat diets. The high fat fed mice had larger tumors than did the low-fat fed mice. In the third study, tumor development was followed in TRAMP mice fed a high fat diet from 6 weeks of age. There were no significant effects of body weight status or diet on tumor development among the groups. When the tumors were examined for the neuroendocrine marker synaptophysin, there was no correlation with either body weight or diet. However, there was a significant correlation of the expression of synaptophysin with earlier age to tumor detection and death. In summary, TRAMP-C2 cells grew faster when the mice were fed a high-fat diet. Further synaptophysin may be a marker of poor prognosis independent of weight and diet.

2018 ◽  
Vol 16 ◽  
pp. 205873921876094 ◽  
Author(s):  
Gang Yu ◽  
Lili Zhu ◽  
Haiyan Li ◽  
Youyou Shao ◽  
Lei Chong ◽  
...  

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.


1999 ◽  
Vol 58 (4) ◽  
pp. 773-777 ◽  
Author(s):  
John E. Blundell ◽  
John Cooling

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.


RSC Advances ◽  
2017 ◽  
Vol 7 (86) ◽  
pp. 54717-54725 ◽  
Author(s):  
Yuliang Cheng ◽  
Jie Zhang ◽  
Kaiyun Luo ◽  
Genyi Zhang

The changes of body weight (A) and food intake (B) of mice fed on different diets of low-fat (LF), high-fat (HF), HF + grain form β-glucan (HFGF), and HF + extracted β-glucan (HFEX).


2020 ◽  
Vol 48 (11) ◽  
pp. 030006052096401
Author(s):  
Wang Shuo ◽  
Haicong Li ◽  
Nishijo Muneko ◽  
Nishino Yoshikazu ◽  
Nobuo Kato ◽  
...  

Objective Regulator of calcineurin 1 (RCAN1) controls plasticity of the nervous system and depressive conditions by regulating brain-derived neurotropic factor (BDNF) and plays a crucial role in neural and cardiac pathways. The apolipoprotein E gene ( ApoE) is a robust risk factor for progression of Alzheimer’s disease. A fatty diet is considered detrimental for metabolic disorders, such as obesity and cardiovascular diseases. Methods We examined the neuronal and cardiac protective roles of RCAN1 in ApoE−/− mice that were fed a high- or low-fat diet with and without voluntary movement for 3 months. Organ weights, laboratory data, histology, RNA expression, and behavior were examined. Results A high-fat diet with exercise improved depressive function, as examined by the forced swimming test, and RCAN1 mRNA expression was induced in the hippocampus. A low-fat diet with exercise resulted in a reduced body weight, higher heart weight/body weight ratio, and lower circulating triglyceride levels compared with a low-fat diet without exercise. RCAN1 mRNA expression was increased in cardiomyocytes in ApoE−/− mice. Conclusions The combination of a high-fat diet and exercise might reduce depressive function, whereas a low-fat diet with exercise leads to cardioprotection. Induction of RCAN1 expression might affect neuroplasticity and cardiac function.


1988 ◽  
Vol 255 (6) ◽  
pp. R974-R981 ◽  
Author(s):  
K. Arase ◽  
J. S. Fisler ◽  
N. S. Shargill ◽  
D. A. York ◽  
G. A. Bray

We examined the effect of dietary fat on the response to 3-hydroxybutyrate (3-OHB) and insulin infused chronically into the third ventricle in three strains of rats with differing susceptibility to obesity induced by a high-fat diet: Osborne-Mendel rats are most susceptible; Sprague-Dawley-rats are intermediate; and S 5B/Pl rats are most resistant. Ten days after implantation of cannulas into the third ventricle, rats were fed either a low-fat diet or a high-fat diet for 14 days. On day 7, osmotic minipumps were attached to the ventricular cannulas. 3-OHB infusions (3.6 mumol/24 h) reduced food intake and body weight in Sprague-Dawley and Osborne-Mendel rats eating either diet. The dietary fat-resistant S 5B/Pl rats did not respond to the intracerebroventricular infusion of 3-OHB. The infusion of insulin (10 mU/24 h) lowered food intake and body weight in animals eating the low-fat (high-carbohydrate) diet but not in animals eating the high-fat diet. Diet profoundly affects the response to intracerebroventricular infusions of insulin but is without effect on the response to 3-OHB.


2009 ◽  
Vol 296 (4) ◽  
pp. E898-E903 ◽  
Author(s):  
Gabriel Paulino ◽  
Claire Barbier de la Serre ◽  
Trina A. Knotts ◽  
Pieter J. Oort ◽  
John W. Newman ◽  
...  

The vagal afferent pathway is important in short-term regulation of food intake, and decreased activation of this neural pathway with long-term ingestion of a high-fat diet may contribute to hyperphagic weight gain. We tested the hypothesis that expression of genes encoding receptors for orexigenic factors in vagal afferent neurons are increased by long-term ingestion of a high-fat diet, thus supporting orexigenic signals from the gut. Obesity-prone (DIO-P) rats fed a high-fat diet showed increased body weight and hyperleptinemia compared with low-fat diet-fed controls and high-fat diet-induced obesity-resistant (DIO-R) rats. Expression of the type I cannabinoid receptor and growth hormone secretagogue receptor 1a in the nodose ganglia was increased in DIO-P compared with low-fat diet-fed controls or DIO-R rats. Shifts in the balance between orexigenic and anorexigenic signals within the vagal afferent pathway may influence food intake and body weight gain induced by high fat diets.


2017 ◽  
Author(s):  
Matthew John Dalby

This research investigated the role of the intestinal microbiota in shaping host food intake and body weight through immunomodulation, the impact of refined and unrefined diets, and though fermentable fibre induced gastrointestinal hormone secretion. Gut-derived lipopolysaccharide activating TLR4 has been proposed to contribute to obesity. To investigate this, TLR4-/- or CD14-/- mice and C57BL/6J controls were fed a high-fat or low-fat diet. Neither TLR4-/- or CD14-/- were protected against high-fat diet-induced obesity. High-fat diet increased hypothalamic expression of SerpinA3N and SOCS3 regardless of genotype; however, inflammatory gene expression was not increased. To investigate the use of chow control diets in obesity-associated microbiota changes, C57BL/6J mice were fed a chow diet, refined high-fat, or low-fat diet. Both high-fat and low-fat refined diets resulted in similar dramatic alterations in the composition of the intestinal microbiota at the phylum, family, and species level compared to chow, while only high-fat diet feeding resulted in obesity and glucose intolerance. The roles of colonic GLP-1 and PYY in mediating fermentable fibre in reducing food intake and body fat were investigated using GLP-1R-/- and PYY-/- mice fed a high-fat diet supplemented with inulin or cellulose. Inulin supplementation reduced body fat and food intake in C57BL/6J control mice while GLP-1R-/- and PYY-/- mice showed an attenuated response to dietary inulin. In summary, this research questions the role of TLR4 and LPS in diet-induced obesity. These results demonstrate the importance of the control diet used in studies of obesity in mice and indicate that many of the obesity-associated changes in the gut microbiota are due to comparing refined high-fat diets with chow diets. These results also provide evidence for an essential role for both GLP-1 and PYY in mediating the food intake and bodyweight-reducing effects of fermentable fibre.


2018 ◽  
Vol 239 (1) ◽  
pp. 93-105 ◽  
Author(s):  
Maitrayee Sahu ◽  
Prashanth Anamthathmakula ◽  
Abhiram Sahu

Pharmacological studies have suggested hypothalamic phosphodiesterase-3B to mediate leptin and insulin action in regulation of energy homeostasis. Whereas Pde3b-null mice show altered energy homeostasis, it is unknown whether this is due to ablation of Pde3b in the hypothalamus. Thus, to address the functional significance of hypothalamic phosphodiesterase-3B, we used Pde3b flox/flox and Nkx2.1-Cre mice to generate Pde3b Nkx2.1KD mice that showed 50% reduction of phosphodiesterase-3B in the hypothalamus. To determine the effect of partial ablation of phosphodiesterase-3B in the hypothalamus on energy and glucose homeostasis, males and females were subjected to either a low- or high-fat diet for 19–21 weeks. Only female but not male Pde3b Nkx2.1KD mice on the low-fat diet showed increased body weight from 13 weeks onward with increased food intake, decreased fat pad weights and hypoleptinemia. Glucose tolerance was improved in high-fat diet-fed male Pde3b Nkx2.1KD mice in association with decreased phosphoenolpyruvate carboxykinase-1 and glucose-6-phosphatase mRNA levels in the liver. Also, insulin sensitivity was increased in male Pde3b Nkx2.1KD mice on the low-fat diet. Changes in body weight or in glucose homeostasis were not associated with any alteration in hypothalamic proopiomelanocortin, neuropepide Y and agouti-related peptide mRNA levels. These results suggest that partial loss of phosphodiesterase-3B in the hypothalamus produces a sex-specific response in body weight and glucose homeostasis, and support a role, at least in part, for hypothalamic phosphodiesterase-3B in regulation of energy and glucose homeostasis in mice.


Nutrients ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 963 ◽  
Author(s):  
Ming-Hua Sung ◽  
Fang-Hsuean Liao ◽  
Yi-Wen Chien

Medium-chain triglycerides (MCTs) are distinguished from other triglycerides in that each fat molecule consists of 6 to 12 carbons in length. MCTs and long-chain triglycerides (LCTs) are absorbed and utilized in different ways. The aim of this study was to assess the effects of replacing soybean oil with MCT oil, in a low- or high-fat diet, on lipid metabolism in rats with streptozotocin-induced type 2 diabetes mellitus (T2DM). There were, thirty-two T2DM Sprague-Dawley rats divided into low-fat-soybean oil (LS), low-fat-MCT oil (LM), high-fat-soybean oil (HS), and high-fat-MCT oil (HM) groups. After 8 weeks, blood sugar, serum lipids, liver lipids, and enzyme activities related to lipid metabolism were measured. Under a high-fat diet condition, replacement of soybean oil with MCT oil lowered serum low-density lipoprotein cholesterol (LDL-C), non-esterified fatty acids, and liver total cholesterol; whilst it increased serum high-density lipoprotein cholesterol (HDL-C) and the HDL-C/LDL-C ratio. A low-fat diet with MCT oil resulted in lower body weight and reproductive white adipose tissues compared to the HS groups, and higher hepatic acyl-CoA oxidase activities (the key enzyme in the peroxisomal beta-oxidation) compared to the LS group in T2DM rats. In conclusion, MCTs showed more protective effects on cardiovascular health in T2DM rats fed a high-fat diet, by improving serum lipid profiles and reducing hepatic total cholesterol.


1975 ◽  
Vol 34 (1) ◽  
pp. 15-24 ◽  
Author(s):  
J. D. Wood ◽  
J. T. Reid

1. An experiment was done with rats (body-weight 160 g) to study the effects on fat metabolism and body composition of low (10 g/kg)- or high (140 g/kg)-fat diets fed as one meal for one 4 h period/d (meal-feeders) or as six spaced meals/d (nibblers). The daily energy intake/unit metabolic body-weight (body-weight0.73) was the same for all four groups, and this level of intake was about 80% of that consumed by rats allowed unrestricted access to the low-fat diet. The experimental period was 76 d.2. Rats given the high-fat diet deposited more body fat/d and, as a result, grew faster and were energetically more efficient than rats given the low-fat diet. The high-fat diet depressed de novo lipogenesis from glucose in epididymal and perirenal fat pads, whose fatty acid composition resembled that of the diet.3. For both diets meal-feeders had greater stomach plus small intestine weights than nibblers and had higher plasma free fatty acid levels, when they were killed 15 h after their last meal.4. Meal-feeders given the low-fat diet had the greatest rate of lipogenesis for fat pads.5. Meal-feeders given the high-fat diet deposited less of the main dietary fatty acids in their fat pads.6. There was no evidence that meal-feeders eating a high-fat diet adapt their metabolism so completely that they become more efficient utilizers than those nibbling this diet. Meal-feeders eating the low-fat diet became no fatter than nibblers of this diet, possibly because they were eating less than their daily ad lib. intake.


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