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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.

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.

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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-4.0May 2020View details →

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-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.

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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.

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Table 1 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 1. Experimental design. The rats were fed commercial standard diet for rodents control diet or high-fat diet during pregnancy, lactation and post-weaning (up to 100 days of life).During the feeding period, rats consumed both diets (control diet and high-fat diet). The numbers in parentheses indicate the animals number in each nutritional group.<table><tbody><tr><th>Experimental Design</th></tr></tbody><tbody><tr><th>Genitors (n)</th><td>Gestation and lactation</td><td>Offspring during lactation (n)</td><td>Offspring (n)</td><td>Post-weaning (21-100° life’s day)</td><td>Food preference (102-116º life’s day)</td></tr><tr><th></th><td></td><td></td><td>CC (12)</td><td>Control diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr><tr><th>GC (5)</th><td>Control diet</td><td>C (23)</td><td>CH (11)</td><td>High-fat diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr><tr><th></th><td></td><td></td><td>HC (11)</td><td>Control diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr><tr><th>GH (5)</th><td>High-fat diet</td><td>H (23)</td><td>HH (12)</td><td>High-fat diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr></tbody></table>

opencc-zeroJan 2023View details →

Data of multiple different high-fat diets

Background and Objectives: The spectrum of non-alcoholic fatty liver disease (NAFLD), known as non-alcoholic steatohepatitis (NASH), can lead to advanced liver disease. It is known that a variety of diets play a significant role in the development of NAFLD/NASH. The goal of this study is to determine the most appropriate composition of diet to induce NASH in an animal model. Methods: This research used Rattus norvegicus strain Wistar (n=27), which were divided into four groups and given each diet for 12 weeks: normal diet (ND, n=7), high-fat diet (HFD, n=6), Western diet (WD, n=7), high-fat-high-fructose diet (HFHFD, n=7). Subjects were documented for body weight. Blood samples were taken for biochemical analysis: low-density lipoprotein (LDL), triglyceride, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), hepatic lipase, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and lipopolysaccharide (LPS). Feces were taken for short-chain fatty acid (SCFA) analysis. Liver histology was analyzed using NAS (NAFLD activity score). The comparison test was carried out using the one-way ANOVA or Kruskal–Wallis test. Results: The highest mean of body weight was in the WD group (346.14 g). Liver enzymes, LDL, triglyceride, propionic acid, and acetic acid in each group were not significantly different. TNF-α, IL-6, and hepatic lipase were significant (p = 0.000; p = 0.000; p = 0.004) and the highest was in the HFD group. Butyrate level was significant (p = 0.021) and the least was in the HFHFD group (4.77 mMol/g). Only WD and HFHFD had an NAS ≥ 5 (14% and 14%). The highest percentage of borderline NAS was found in WD (57%). Conclusions: The HFD group induced significant liver inflammation but did not produce NASH histologically, whereas the WD and HFHFD groups had the potential to develop NASH because the diets affected metabolic and inflammatory parameters as well as liver histology.