scholarly journals Variability in metabolic rate, feed intake and fatness among selection and inbred lines of mice

1997 ◽  
Vol 70 (3) ◽  
pp. 225-235 ◽  
Author(s):  
D. E. MOODY ◽  
D. POMP ◽  
M. K. NIELSEN

Mouse populations differing in metabolic rate have been developed through selection for high (MH) and low (ML) heat loss (HLOSS), along with randomly selected controls (MC). Objectives of this study were to (a) compare MH, ML and MC lines for HLOSS and correlated traits of feed intake, body composition and organ weights; (b) compare three widely used inbred mouse lines with MH, ML and MC for the same traits; and (c) investigate potential genotype by diet interaction resulting from feeding diets differing in fat percentage. Heat loss (kcal/day) of MH and ML mice differed by 37% of the mean and remained significant (33%) when HLOSS was expressed on a fat-free mass basis. MH mice consumed more energy than ML with a greater difference in mice fed high-fat compared with standard diets (27% vs 13·9%). Despite greater energy consumption, MH mice were leaner than ML with a difference in total body fat percentage of 40%. The greatest difference in HLOSS between selection and inbred lines was between MH and C57BL/6J (BL), which differed by 26·3%. MH and BL mice also differed in energy intake (15·5%). Body composition of BL mice was similar to MH when fed a standard diet, but similar to ML when fed a high-fat diet. Crosses between MH and ML or between MH and BL would be useful to investigate the genetic regulation of, and identify quantitative trait loci influencing HLOSS, energy intake and body composition. Feeding of a high-fat diet may allow diet-specific loci influencing body composition to be identified in MH and BL lines.

Author(s):  
Haley A. Hallowell ◽  
Keah V. Higgins ◽  
Morgan Roberts ◽  
Robert M. Johnson ◽  
Jenna Bayne ◽  
...  

Due to its immunomodulatory potential, the intestinal microbiota has been implicated as a contributing factor in the development of the meta-inflammatory state that drives obesity-associated insulin resistance and type 2 diabetes. A better understanding of this link would facilitate the development of targeted treatments and therapies to treat the metabolic complications of obesity. To this end, we validated and utilized a novel swine model of obesity, the Mangalica pig, to characterize changes in the gut microbiota during the development of an obese phenotype, and in response to dietary differences. In the first study, we characterized the metabolic phenotype and gut microbiota in lean and obese adult Mangalica pigs. Obese or lean groups were created by allowing either ad libitum (obese) or restricted (lean) access to a standard diet for 54 weeks. Mature obese pigs were significantly heavier and exhibited 170% greater subcutaneous adipose tissue mass, with no differences in muscle mass compared to their lean counterparts. Obese pigs displayed impaired glucose tolerance and hyperinsulinemia following oral glucose challenge, indicating that a metabolic phenotype also manifested with changes in body composition. Consistent with observations in human obesity, the gut microbiota of obese pigs displayed altered bacterial composition. In the second study, we characterized the longitudinal changes in the gut microbiota in response to diet and aging in growing Mangalica pigs that were either limit fed a standard diet, allowed ad libitum access to a standard diet, or allowed ad libitum access to a high fat-supplemented diet over an 18-week period. As expected, weight gain was highest in pigs fed the high fat diet compared to ad libitum and limit fed groups. Furthermore, the ad libitum and high fat groups displayed significantly greater adiposity consistent with the development of obesity relative to the limit fed pigs. The intestinal microbiota was generally resilient to differences in dietary intake (limit fed vs ad libitum), though changes in the microbiota of pigs fed the high fat diet mirrored changes observed in mature obese pigs during the first study. This is consistent with the link observed between the microbiota and adiposity. In contrast to intestinal bacterial populations, bacteriophage populations within the gut microbiota responded rapidly to differences in diet, with significant compositional changes in bacteriophage genera observed between the dietary treatment groups as pigs aged. These studies are the first to describe the development of the intestinal microbiota in the Mangalica pig, and are the first to provide evidence that changes in body composition and dietary conditions are associated with changes in the microbiome of this novel porcine model of obesity.


2020 ◽  
Vol 17 (2) ◽  
pp. 192
Author(s):  
RONALDO LAU ◽  
SULISTIANA PRABOWO ◽  
RIAMI RIAMI

<p align="justify"><strong>ABSTRACT</strong><strong></strong></p><p align="justify"><strong>Background</strong>: High fat diet increase the absorption of lipid in the intestinum, that can lead to increase LDL cholesterol level in the blood. Sea grapes extract (<em>Caulerpa racemosa</em>) contains antioxidant polyphenolic group that can reduce MTP and ACAT-2 in the body that can decrease LDL cholesterol level in the blood.The purpose of this study is to know the effect of sea grapes extract  on decreasing LDL cholesterol of white male Wistar rats (<em>Rattus norvegicus</em>) fed with high fat diet.</p><p align="justify"><strong>Method</strong>:  24 white male Wistar rats, that divided into 3 groups: 1) group of rats fed with standard diet for 28 days; 2) group of rats fed with high fat diet for 28 days; 3) group of rats fed with high fat diet for 28 days and given 10 gram/kg body weight/day of sea grapes extract on 15<sup>th</sup>-28<sup>th</sup> days. Then the blood LDL cholesterol level measured on the 29<sup>th</sup> day.</p><p align="justify"><strong>Result :</strong> One-Way ANOVA Test showed there was significant difference (p=0.004) of LDL level between the group of rats fed with standard diet (12.37 mg/dl) compared to group of rats fed with high fat diet (17.87 mg/dl). There was significant difference (p=0.001) of LDL level between the group of rats fed with high fat diet (17.87 mg/dl) compared to group of rats fed with high fat diet and sea grapes extract (10.12 mg/dl).</p><p align="justify"><strong>Conclusion: </strong>high fat diet significantly increase blood LDL cholesterol level and sea grapes extract (<em>Caulerpa racemosa</em>) significantly decrease blood LDL cholesterol level.</p><p align="justify"> </p><p align="justify"><strong>Keywords :</strong>Sea grapes extract, LDL cholesterol, high fat diet</p>


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Maki Murakoshi ◽  
Tomohito Gohda ◽  
Eri Adachi ◽  
Saki Ichikawa ◽  
Shinji Hagiwara ◽  
...  

AbstractProgranulin (PGRN) has been reported to bind tumor necrosis factor (TNF) receptor and to inhibit TNFα signaling. We evaluated the effect of augmentation of TNFα signaling by PGRN deficiency on the progression of kidney injury. Eight-week-old PGRN knockout (KO) and wild-type (WT) mice were fed a standard diet or high-fat diet (HFD) for 12 weeks. Albuminuria, markers of tubular damage, and renal mRNA levels of inflammatory cytokines were higher in HFD-fed KO (KO-HFD) mice than in HFD-fed WT (WT-HFD) mice. Body weight, vacuolization in proximal tubules, and systemic and adipose tissue inflammatory markers were lower in the KO-HFD mice than in the WT-HFD mice. The renal megalin expression was lower in the KO mice than in the WT mice regardless of the diet type. The megalin expression was also reduced in mouse proximal tubule epithelial cells stimulated with TNFα and in those with PGRN knockdown by small interfering RNA in vitro. PGRN deficiency was associated with both exacerbated renal inflammation and decreased systemic inflammation, including that in the adipose tissue of mice with HFD-induced obesity. Improved tubular vacuolization in the KO-HFD mice might partially be explained by the decreased expression of megalin in proximal tubules.


2004 ◽  
Vol 287 (1) ◽  
pp. R147-R156 ◽  
Author(s):  
Assim Alfadda ◽  
Rosangela A. DosSantos ◽  
Zaruhi Stepanyan ◽  
Husnia Marrif ◽  
J. Enrique Silva

To define the role of mitochondrial glycerol-3-phosphate dehydrogenase (mGPD; EC 1.1.99.5 ) in energy balance and intermediary metabolism, we studied transgenic mice not expressing mGPD (mGPD−/−). These mice had ≈14% lower blood glucose; ≈50% higher serum glycerol; ≈80% higher serum triglycerides; and at thermoneutrality, their energy expenditure (Qo2) was 15% lower than in wild-type (WT) mice. Glycerol-3-phosphate levels and lactate-to-pyruvate ratios were threefold elevated in muscle, but not in liver, of mGPD−/− mice. WT and mGPD−/− mice were then challenged with a high-fat diet, fasting, or food restriction. The high-fat diet caused more weight gain and adiposity in mGPD−/− than in WT female mice, without the genotype differentially affecting Qo2 or energy intake. After a 30-h fast, WT female lost 60% more weight than mGPD−/− mice but these latter became more hypothermic. When energy intake was restricted to 50–70% of the ad libitum intake for 10 days, mGPD−/− female mice lost less weight than WT controls, but they had lower Qo2 and body temperature. WT and mGPD−/− male mice did not differ significantly in their responses to these challenges. These results show that the lack of mGPD causes significant alterations of intermediary metabolism, which are more pronounced in muscle than liver and lead to a thrifty phenotype that is more marked in females than males. Lower T4-to-T3 conversion in mGPD−/− females and a greater reliance of normal females on mGPD to respond to high-fat diets make the lack of the enzyme more consequential in the female gender.


2021 ◽  
pp. 1-14
Author(s):  
Jian Bao ◽  
Zheng Liang ◽  
Xiaokang Gong ◽  
Jing Yu ◽  
Yifan Xiao ◽  
...  

Background: Alzheimer’s disease (AD) is the most common form of dementia in older adults and extracellular accumulation of amyloid-β (Aβ) is one of the two characterized pathologies of AD. Obesity is significantly associated with AD developing factors. Several studies have reported that high fat diet (HFD) influenced Aβ accumulation and cognitive performance during AD pathology. However, the underlying neurobiological mechanisms have not yet been elucidated. Objective: The objective of this study was to explore the underlying neurobiological mechanisms of HFD influenced Aβ accumulation and cognitive performance during AD pathology. Methods: 2.5-month-old male APP/PS1 mice were randomly separated into two groups: 1) the normal diet (ND) group, fed a standard diet (10 kcal%fat); and 2) the HFD group, fed a high fat diet (40 kcal%fat, D12492; Research Diets). After 4 months of HFD or ND feeding, mice in the two groups were subjected for further ethological, morphological, and biochemical analyses. Results: A long-term HFD diet significantly increased perirenal fat and impaired dendritic integrity and aggravated neurodegeneration, and augmented learning and memory deficits in APP/PS1 mice. Furthermore, the HFD increased beta amyloid cleaving enzyme 1 (BACE1) dephosphorylation and SUMOylation, resulting in enhanced enzyme activity and stability, which exacerbated the deposition of amyloid plaques. Conclusion: Our study demonstrates that long-term HFD consumption aggravates amyloid-β accumulation and cognitive impairments, and that modifiable lifestyle factors, such as obesity, can induce BACE1 post-modifications which may contribute to AD pathogenesis.


Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Darren Mehay ◽  
Sarah Bingaman ◽  
Yuval Silberman ◽  
Amy Arnold

Angiotensin (Ang)-(1-7) is a protective hormone of the renin-angiotensin system that improves insulin sensitivity, glucose tolerance, and energy balance in obese rodents. Our recent findings suggest that Ang-(1-7) activates mas receptors (MasR) in the arcuate nucleus of the hypothalamus (ARC), a brain region critical to control of energy balance and glucose homeostasis, to induce these positive metabolic effects. The distribution of MasR in the ARC and their role in metabolic regulation, however, is unknown. We hypothesized: (1) MasR are expressed in the ARC; and (2) deletion of ARC MasR leads to worsened metabolic outcomes following high fat diet (HFD). To test this, male and female C57Bl/6J mice were fed a 60% HFD or matched control diet ad libitum for 12 weeks. RNAscope in situ hybridization was performed on coronal ARC sections in rostral-middle-caudal regions to determine percentage of MasR positive neurons (n=5/group). In a second experiment, we assessed body composition and insulin and glucose tolerance in transgenic mice with deletion of MasR in ARC neurons (MasR-flox with AAV5-hsyn-GFP-Cre). RNAscope revealed a wide distribution on MasR-positive cells throughout the rostral to caudal extent of the ARC. The average percentage of MasR positive neurons was increased in females versus males, with HFD tending to increase MasR expression in both sexes (control diet male: 11±2; control diet female: 17±3; HFD male: 15±5; HFD female: 24±2; p sex : 0.030; p diet : 0.066; p int : 0.615; two-way ANOVA). Deletion of MasR in ARC neurons worsened insulin sensitivity in HFD but not control diet females (area under the curve for change in glucose from baseline: -1989±1359 HFD control virus vs. 2530±1762 HFD Cre virus; p=0.016), while fasting glucose, glucose tolerance, and body composition did not change. There was no effect of ARC MasR deletion on metabolic outcomes in control diet or HFD male mice. These findings suggest females have more MasR positive neurons in the ARC compared to males, which may be a sex-specific protective mechanism for glucose homeostasis. While further studies are needed to explore the role of ARC MasR in metabolic regulation, these findings support targeting Ang-(1-7) as an innovative strategy in obesity.


2021 ◽  
Vol 33 (12) ◽  
pp. 713
Author(s):  
Rodrigo L. Furtado ◽  
Jonathan Elias R. Martins ◽  
Maria Alice F. Oliveira ◽  
Denise D. Guerreiro ◽  
Naiza A. R. de Sá ◽  
...  

This study demonstrates the effect of a single high-intensity interval training (HIIT) session on the redox status of rat ovaries with excess adiposity. Forty Wistar female rats (mean (±s.e.m.) weight 94.40 ± 13.40 g) were divided into two groups and fed either a standard diet (SD) or a high-fat diet (HFD) for 62 days. At the end of this period, the rats were subjected to a single HIIT session and were killed 24 h after exercise. Both groups subjected to exercise (SDex and HFDex) generated a significantly higher antioxidant environment by presenting a higher thiol content, which represents a lower oxidation rate of GSH than their respective controls (SD and HFD). The percentage of morphologically normal primary follicles decreased, whereas that of antral follicles increased, in the SDex group. In addition, the HFD group had a higher percentage of degenerated antral follicles than the SD and SDex groups. Cells immunoreactive for α-smooth muscle actin were seen in the cortical stroma and thecal layer enclosing late secondary and tertiary follicles in all groups. Moreover, heme oxygenase and cytochrome P450 family 19 subfamily A member 1 (Cyp19A1) labelling was seen in all antral follicles. Progesterone concentrations were significantly higher in the HFDex than SDex group. In conclusion, this study indicates that a single session of HIIT may result in an improvement in ovary redox status because of metabolic muscle activity by inducing physiological adaptation after exercise in a paracrine manner.


2019 ◽  
Vol 122 (03) ◽  
pp. 241-251
Author(s):  
Siti N. Wulan ◽  
Freek G. Bouwman ◽  
Klaas R. Westerterp ◽  
Edwin C. M. Mariman ◽  
Guy Plasqui

AbstractFor the same BMI, South Asians have a higher body fat percentage than Caucasians. There might be differences in the fatty acid (FA) handling in adipose tissue when both ethnicities are exposed to high-fat overfeeding. The objective of the present study was to investigate the molecular adaptation in relation to FA metabolism in response to overfeeding with a high-fat diet (OHFD) in South Asian and Caucasian men. Ten South Asian men (BMI 18–29 kg/m2) and ten Caucasian men (BMI 22–33 kg/m2), matched for body fat percentage, aged 20–40 years were included. A weight-maintenance diet (30 % fat, 55 % carbohydrate and 15 % protein) was given for 3 d followed by 3 d of overfeeding (150 % energy requirement) with a high-fat diet (60 % fat, 25 % carbohydrate and 15 % protein) while staying in a respiration chamber. Before and after overfeeding, abdominal subcutaneous fat biopsies were taken. Proteins were isolated, analysed and quantified for short-chain 3-hydroxyacyl-CoA dehydrogenase (HADH), carnitine palmitoyl-transferase 1α (CPT1a), adipose TAG lipase, perilipin A (PLINA), perilipin B, lipoprotein lipase and fatty acid binding protein 4 using Western blotting. OHFD decreased the HADH level (P &lt; 0·05) in Caucasians more than in Asians (P &lt; 0·05), but the baseline and after intervention HADH level was relatively higher in Caucasians. The level of CPT1a decreased in South Asians and increased in Caucasians (P &lt; 0·05). PLINA did not change with diet but the level was higher in South Asians (P &lt; 0·05). The observed differences in HADH and PLINA levels as well as in CPT1a response may be important for differences in the long-term regulation of energy (fat) metabolism in these populations.


Author(s):  
Ana Lemus-Conejo ◽  
Elena Grao-Cruces ◽  
Rocio Toscano ◽  
Lourdes M Varela ◽  
Carmen Claro ◽  
...  

Bioactive peptides are related to the prevention and treatment of many diseases. GPETAFLR is an octapeptide which was isolated from lupine (Lupinus angustifolius L.) and showed anti-inflammatory properties. The aim of this study was to evaluate the potential activity of GPETAFLR to prevent non-alcoholic fatty liver disease (NAFLD) in high-fat diet (HFD)-induced obese mice. C57BL/6J mice were fed a standard diet or an HFD. Two of the groups fed the HFD diet were treated with GPETAFLR in their drinking water at 0,5 mg/kg/d or 1 mg/kg/d. To determine the ability of GPETAFLR to improve the onset and progression of NAFLD, histological studies, hepatic enzyme profile, inflammatory cytokine and lipid metabolism-related genes and proteins were analyzed. Our results suggest that HFD-induced inflammatory metabolic disorders were alleviated by treatment with GPETAFLR. In conclusion, dietary lupine consumption could repair HFD-induced hepatic damage, possibly via modifications in the liver&rsquo;s lipid signalling pathways.


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