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opencc-by-4.0Sep 2021View details →

Investigating the Effect of Positional Variation on Mid-Lactation Mammary Gland Transcriptomics in Mice Fed Either a Low-Fat or High-Fat Diet

Investigating the Effect of Positional Variation on Mid-Lactation Mammary Gland Transcriptomics in Mice Fed Either a Low-Fat or High-Fat Diet.

Figure 4 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats

Figure 4. Body weight on the 120th offspring from mothers submitted the control diet or the high-fat diet. Values are presented as mean ± SEM using two-way ANOVA followed by the Bonferroni multiple-comparison test. *p<0,05; **p<0,005.

Figure 3 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats

Figure 3. Body weight on the second day life's of offspring from mothers submitted the control diet (C) or the high-fat diet (H). Values are presented as mean + SEM using Student t-test. C: n = 23; H: n = 23.

Figure 2 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats

Figure 2. Pomc (A) and npy (B) gene expression in the hypothalamus of offspring exposed or not to a control diet or high-fat diet during perinatal and/or postnatal period. Values are presented as mean ± SEM using two-way ANOVA followed by the Bonferroni multiplecomparison test. Level of significance: *p<0,05; "a": compared to CC, "b": compared to CH; "c": compared to HC; "d": compared to HH.

Figure 1. Drd1 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats

Figure 1. Drd1 (A) and drd2 (B) gene expression in the nucleus accumbens of offspring exposed or not to a control diet or high-fat diet during perinatal and/or postnatal period. Values are presented as mean ± SEM using two-way ANOVA followed by the Bonferroni multiplecomparison test. Level of significance: *p<0,05; "a": compared to CC, "b": compared to CH; "c": compared to HC; "d": compared to HH.

Figure 6 in Potential Hepatoprotective Effect of Cheatomorpha gracilis extract against High Fat Diet (HFD)-Induced Liver Damage, and its characterization by HPLC

Figure 6. Photomicrographs of hepatocytes in control and experimental treated mice. Liver tissue sections stained with oil red O (×200) (A) and scored (B) by the semi-quantitative percentage of damaged area. (Control) control mice and (AEC) treated with C. gracilis extract (250 mg/kg) alone, showed normal structure. (HFD) high fed diet treated mice, showed a significant increase of lipid content; (AEC + HFD) co-treated with high fed diet and alga extract (250 mg/kg), representative micrograph revealed significantly reduced lipid liver content. Values are expressed as the mean ± SD. **p<0.01; ***p <0.001, indicates a significant difference compared to the control group. ++ p<0.01, indicates a significant difference compared to the HFD alone group.

Figure 3 in Potential Hepatoprotective Effect of Cheatomorpha gracilis extract against High Fat Diet (HFD)-Induced Liver Damage, and its characterization by HPLC

Figure 3. Effect of ACE supplementation on plasma levels of inflammatory proteins. Data are given as mean ± SD for group of eight mice each. Values are statistically presented as follows: HFD and AEC-treated groups vs. control group: *p <0.05; **p<0.01. HFD + AEC group vs. HFD group: +p <0.05; ++p<0.01.

Figure 2 in Potential Hepatoprotective Effect of Cheatomorpha gracilis extract against High Fat Diet (HFD)-Induced Liver Damage, and its characterization by HPLC

Figure 2. Antioxidant activity of different extracts of C. gracilis. Values are mean ± SD of three experimental tests, mg GAE/g DR: mg gallic acid equivalents per g dry residue. Table 4. Effect of AEC on body weight, liver and adipose tissues relative weight of control and treated mice groups.

Figure 5 in Potential Hepatoprotective Effect of Cheatomorpha gracilis extract against High Fat Diet (HFD)-Induced Liver Damage, and its characterization by HPLC

Figure 5. Photographs of liver tissues in control and experimental treated mice. Liver tissue sections stained with hematoxylin and eosin (original magnification × 400). (A), in control mice showing normal histoarchitecture and radiating cell arrangement. (B) In mice treated with aqueous extract of C.gracilis (AEC) (250mg/kg) alone showing the normal liver structure. (C) In High fed diet (HFD) mice, representative photograph shows a significant lipid accumulation. (D) In group co-treated with HFD and AEC, was observed the reduction of fat accumulation.

Figure 1 in Potential Hepatoprotective Effect of Cheatomorpha gracilis extract against High Fat Diet (HFD)-Induced Liver Damage, and its characterization by HPLC

Figure 1. Phenolic compounds of Cheatomorpha gracilis extract by chemical High Performance Liquid Chromatography (HPLC) analysis (gallic acid, Rutin, quercetin, Apegenin, kaempferol and Naringenin).

Figure 4 in Potential Hepatoprotective Effect of Cheatomorpha gracilis extract against High Fat Diet (HFD)-Induced Liver Damage, and its characterization by HPLC

Figure 4. Effects of C.gracilis aqueous extract (AEC) on TBARS and protein carbonyls products (PCO) in HFD-treated mice. TBARS: thiobarbituric acid reactive substance. Data are presented as mean ± SD, n =8. *P≤ 0.05, **P≤ 0.01 compared with the control group. +P ≤0.05, ++P ≤0.01 as compared with HFD- treated mice.

opencc-by-4.0Jul 2022View details →

Dataset related to: Sirtuin 3 Deficiency Aggravates Kidney Disease in Response to High-Fat Diet through Lipotoxicity-Induced Mitochondrial Damage

The files contain all the dataset included in the manuscript divided by figures.   Abstract: Sirtuin 3 (SIRT3) is the primary mitochondrial deacetylase that controls the antioxidant pathway and energy metabolism. We previously found that renal Sirt3 expression and activity were reduced in mice with type 2 diabetic nephropathy associated with oxidative stress and mitochondrial abnormalities and that a specific SIRT3 activator improved renal damage. SIRT3 is modulated by diet, and to assess whether Sirt3 deficiency aggravates mitochondrial damage and accelerates kidney disease in response to nutrient overloads, wild-type (WT) and Sirt3-/- mice were fed a high-fat-diet (HFD) or standard diet for 8 months. Sirt3-/- mice on HFD exhibited earlier and more severe albuminuria compared to WT mice, accompanied by podocyte dysfunction and glomerular capillary rarefaction. Mesangial matrix expansion, tubular vacuolization and inflammation, associated with enhanced lipid accumulation, were more evident in Sirt3-/- mice. After HFD, kidneys from Sirt3-/- mice showed more oxidative stress than WT mice, mitochondria ultrastructural damage in tubular cells, and a reduction in mitochondrial mass and energy production. Our data demonstrate that Sirt3 deficiency renders mice more prone to developing oxidative stress and mitochondrial abnormalities in response to HFD, resulting in more severe kidney diseases, and this suggests that mitochondria protection may be a method to prevent HFD-induced renal injury.

opencc-by-4.0May 2020View details →

Results "Anti-obesity effects of individual or combination treatment with Spirulina platensis and green coffee bean aqueous extracts in high-fat diet-induced obese rats"

Background: Obesity, a chronic disease, is associated with serious health risks, including premature mortality. This study aimed to investigate the anti-obesity effects of individual or combination treatment with Spirulina platensis and green coffee bean aqueous extracts in high-fat diet-induced (HFD) obese rats. Methods: Rats were fed on HFD to induce obesity. Corn oil in the HFD accounted for 50.98 % of the calories. Fifty rats were divided into the following five groups (10 rats/group): control, HFD, HFD-Spirulina, HFD-coffee, HFD-Spirulina and coffee co-treatment groups. The serum levels of lipid, leptin, and insulin, as well as the hepatic mRNA levels of fatty acid synthase (FAS), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), and peroxisome proliferator-activated alpha receptor (PPARα) were estimated. Results: The Spirulina and/or green coffee bean aqueous extracts decreased the final bodyweight and liver weight, and the serum levels of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase. Additionally, the extracts decreased the serum levels of total cholesterol, triacylglycerol, low-density lipoprotein-cholesterol, leptin, and glucose, and enhanced the serum insulin level. Furthermore, the extracts enhanced the PGC-1α and PPARα mRNA levels and decreased the FAS mRNA levels. Conclusion: The individual or combination treatment with Spirulina and green coffee bean extracts decreased obesity-induced hyperlipidemia. Thus, Spirulina platensis and green coffee can be potentially used to treat obesity.

opencc-by-4.0Feb 2017View details →

Supporting data: The role of sex and body weight on the metabolic effects of high fat diet in C57BL/6N mice.

Authors: Camilla Ingvorsen*, Natasha A. Karp*, Christopher J. Lelliott * These authors contributed equally to this work This directory contains the raw data, R scripts and output files used to generate the figures and results presented in the manuscript "The role of sex and body weight in metabolic effects of high fat diet on C57BL/6N mice."

opencc-zeroJan 2024View details →

Data from: anterior pituitary transcriptomics following a high fat diet: impact of oxidative stress on cell metabolism

Anterior pituitary cells are highly active with regards to protein synthesis and secretion, processes which depend heavily on mitochondrial ATP production and functional endoplasmic reticula. It is well known that obesity adds an allostatic overload to tissues, requiring them to adapt to inflammation and oxidative stress. Therefore, we hypothesized that the pituitary is highly vulnerable to the stress of high fat diet-induced weight gain. In this study, we utilized a 10-15 week high fat diet (HFD, 60%) plus a thermoneutral housing paradigm, testing both male and female FVB.129P mice. We quantified serum hormones and cytokines, characterized the metabolic phenotype, and defined changes in the pituitary transcriptome using single-cell RNA-seq. Weight gain was significant by 3 weeks in HFD mice, and by 10 weeks all HFD groups had gained 20 g. HFD females (15 weeks) had increased energy expenditure and decreased activity. All HFD groups showed increases in serum leptin, Il-6, resistin, MCP-1, and TNFα. HFD males had increased insulin; both HFD males and females had increased TSH, and HFD females had decreased serum prolactin and growth hormone (GH) pulse amplitude. Pituitary scRNA-seq revealed modest or no changes in pituitary cell gene expression in the different cell types from HFD males after 10 or 15 weeks or HFD females after 10 weeks. However, females exposed to a HFD for 15 weeks showed significant numbers of differentially expressed genes in lactotropes and stem cells. Pathway analyses identified a reduction in pathways that supported protein translation, ribosome biogenesis, and oxidative phosphorylation, indicating mitochondrial dysfunction. Collectively, these studies reveal that pituitary cells from males are more resilient to the oxidative stress of obesity than females and identify the most vulnerable pituitary cell populations in females.

opencc-zeroApr 2022View details →

Astaxanthin from Haematococcus pluvialis prevents high-fat diet-induced hepatic steatosis and oxidative stress in mice by gut-liver axis modulating properties

Scope: Evidence is mounting that astaxanthin (ATX), a xanthophyll carotenoid, used as a nutritional supplement to prevent chronic metabolic diseases. The present study aims to identify the potential function of ATX supplementation in preventing steatohepatitis and hepatic oxidative stress in diet-induced obese mice. Methods and Results: In this study, ATX as dose of 0.25%, 0.5% and 0.75% have orally administered to mice along with a high-fat diet (HFD) to investigate the role of ATX in regulating liver lipid metabolism and gut microbiota. The study showed that ATX dose-dependently reduces body weight, lipid droplet formation, hepatic triglycerides and ameliorated hepatic steatosis and oxidative stress. 0.75% ATX altered the levels of 34 lipid metabolites related to hepatic cholesterol and fatty acid metabolism which might be associated with downregulation of lipogenesis-related genes and upregulation of bile acid biosynthesis-related genes. The result also revealed that ATX alleviates HFD-induced gut microbiota dysbiosis by significantly inhibiting the growth of obesity-related Parabacteroides and Desulfovibrio while promoting the growth of Allobaculum and Akkermansia. Conclusion: The study results suggested that dietary ATX may prevent the development of hepatic steatosis and oxidative stress with the risk of metabolic disease by gut-liver axis modulating properties.

opencc-by-4.0Dec 2021View details →

High total water loss driven by low-fat diet in desert-adapted mice

All raw data (Expedata files) and processed machine-readable csv files Availability of essential resources is one of the most important drivers of survival and to persist in changing environments, animals must either relocate or adapt in place. Testing an animal's ability to respond to alternative conditions can reveal differences in physiological responses. We used flow-through respirometry to characterize metabolic phenotypes of the desert-adapted cactus mouse (Peromyscus eremicus) under diurnally variable environmental conditions that mimic the Sonoran Desert and treated mice with two different diets: a standard diet and a low-fat diet. We found significant diet-specific differences in the rate of water loss and serum electrolyte values. Mice fed the low-fat diet lost more water relative to those eating the standard diet and patterns of de novo lipogenesis is not limited by dietary composition. Our results are consistent with the hypothesis that diet contributes to water homeostasis. Compared to other desert animals, rodents have limited capacity to dissipate heat using evaporative cooling, limiting thermoregulatory performance at higher temperatures. We predict that a mismatch in physiological requirements, the availability of different food types, and environmental conditions, could significantly impact P. eremicus survival.

opencc-zeroAug 2022View details →

Feeding foliar nano-selenium biofortified Panax notoginseng could reduce the occurrence of glycolipid metabolism disorder in mice caused by high-fat diets

Nano-selenium (nano-Se) has been extensively explored as a biostimulant for improving the quality of grain crops. However, there are few reports about the effect on the medicinal components of Chinese herbal medicine cultured with nano-Se. Here, we sprayed nano-Se during the cultivation of Panax notoginseng (SePN), and measured the changes of medicinal components compared with conventional Panax notoginseng (PN). Furthermore, we identified a more pronounced effect of SePN on reducing obesity in animals compared with PN. By measuring antioxidant capacity, histopathology, gene expression related to glycolipid metabolism, and gut microbiota composition, we propose a potential mechanism for SePN to improve animal health. Compared with the control groups, foliar spraying of nano-Se increased saponins content (Rb2, Rb3, Rc, F2, Rb2, and Rf) in the roots of Panax notoginseng, and the content of Rb2 increased by 3.9 times in particular. Interestingly, animal studies indicated that taking selenium-rich Panax notoginseng (SePN) can further ameliorate liver antioxidation (SOD, MDA, and GSH) and enzyme activities involved in glycolipid metabolism (ATGL and PFK). It also relieved inflammation and regulated the expression of genes (MCAD, PPAR-α, and PCSK9) related to fatty acid oxidation. The abundance ratio of Firmicutes/Bacteroides and beneficial bacteria abundance (Bifidobacterium, Butyricimonas, and Parasutterella) in gut microbiota were improved relative to the control. In summary, the application of nano-Se on PN may effectively raise the content of Panax notoginseng saponins (PNS) and immensely lower the risk of metabolic disorders of glycolipids.

opencc-zeroOct 2022View details →

Gut microbiome analysis of high fat diet- and control-fed on PXR-KO mice

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease due to the current epidemics of obesity and diabetes. The pregnane X receptor (PXR) is a xenobiotic-sensing nuclear receptor known for trans-activating liver genes involved in drug metabolism and transport, and more recently implicated in energy metabolism. The gut microbiota can modulate the host xenobiotic biotransformation and contribute to the development of obesity. While the male sex confers a higher risk for NAFLD than women before menopause, the mechanism remains unknown. We hypothesized that the presence of PXR promotes obesity by modifying the gut-liver axis in a sex-specific manner. Male and female C57BL/6 (wild-type/WT) and PXR-knockout (PXR-KO) mice were fed control or high fat diet (HFD) for 16-weeks. Serum parameters, liver histopathology, transcriptomic profiling, 16S-rDNA sequencing, and bile acid (BA) metabolomics were performed. PXR enhanced HFD-induced weight gain, hepatic steatosis and inflammation especially in males, accompanied by PXR-dependent up-regulation in hepatic genes involved in microbial response, inflammation, oxidative stress, and cancer; PXR-dependent increase in intestinal Firmicutes/Bacteroides ratio (hallmark of obesity) and the pro-inflammatory Lactobacillus, as well as a decrease in the anti-obese Allobaculum and the anti-inflammatory Bifidobacterum, with a PXR-dependent reduction of beneficial BAs in liver. The resistance to NAFLD in females may be explained by PXR-dependent decrease in pro-inflammatory bacteria (Ruminococcus gnavus and Peptococcaceae). In conclusion, PXR exacerbates hepatic steatosis and inflammation accompanied by obesity- and inflammation-prone gut microbiome signature, suggesting that gut microbiome may contribute to PXR-mediated exacerbation of NAFLD.

Table 2 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats

Table 2. Relative food intake of the high-fat diet and control diet during the food preference study in offspring exposed or not a control diet or high-fat diet during perinatal and/or postnatal period.<table><tbody><tr><th></th><th>High-fat diet (g/100 g body weight)</th><th></th></tr></tbody><tbody><tr><th></th><td>102º day</td><td>110º day</td><td>116º day</td></tr><tr><th>CC</th><td>12.6 ± 0.6</td><td>11.3 ± 0.2</td><td>11.1 ± 0.7</td></tr><tr><th>CH</th><td>12.8 ± 0.6</td><td>12.4 ± 0.3</td><td>11.4 ± 0.4</td></tr><tr><th>HC</th><td>16.7 ± 1.1 a.b*</td><td>13.7 ± 0.9</td><td>10.0 ± 0.5</td></tr><tr><th>HH</th><td>15.3 ± 0.7 a.b*</td><td>11.7 ± 0.9</td><td>10.7 ± 0.5</td></tr><tr><th></th><td>Control diet (g/100 g body weight)</td><td></td></tr><tr><th></th><td>102º day</td><td>110º day</td><td>116º day</td></tr><tr><th>CC</th><td>1.4 ± 0.2</td><td>1.1 ± 0.1</td><td>1.1 ± 0.3</td></tr><tr><th>CH</th><td>2.1 ± 0.2</td><td>1.5 ± 0.3</td><td>0.9 ± 0.1</td></tr><tr><th>HC</th><td>1.8 ± 0.2</td><td>1.0 ± 0.3</td><td>1.0 ± 0.3</td></tr><tr><th>HH</th><td>1.9 ± 0.2</td><td>1.1 ± 0.2</td><td>0.7 ± 0.1</td></tr></tbody></table>Values are presented as mean + SEM using two-way ANOVA followed by the Bonferroni multiple-comparison test. *p<0,005; “a”: compared to CC, “b”: compared to CH; “c”: compared to HC; “d”: compared to HH.