scholarly journals Effects of high-fat diet intake during perinatal period on reflex-ontogeny and intestinal morphometry of rat offspring

2021 ◽  
Vol 71 (2) ◽  
pp. 138-148
Author(s):  
Jacqueline da Silva ◽  
Laércio da Luz ◽  
Luciana Silva ◽  
Angela Amancio-dos-Santos
Keyword(s):  
High Fat Diet ◽  
Somatic Growth ◽  
Relative Length ◽  
Perinatal Period ◽  
Physical Characteristics ◽  
The Body ◽  
Chow Diet ◽  
Specific Rate ◽  
Negative Consequences ◽  
High Fat

Reflex-ontogeny and intestinal morphometrics were evaluated in Wistar rats whose mothers were fed on a high-fat diet during the perinatal period. Male pups (n=52) formed four experimental groups: NN (pups from mothers with lab chow diet during gestation and lactation); NH (pups from mothers with lab chow diet during pregnancy and high-fat in lactation); HH (pups from mothers with high-fat diet during gestation and lactation); HN (pups from mothers with high-fat diet during pregnancy and lab chow in lactation). The reflex ontogeny, the maturation of physical characteristics and parameters of somatic growth were evaluated during lactation. In addition, the body mass index (BMI), the specific rate of weight gain (SRWG), the Lee index, the weight of the brain and intestinal parameters were analyzed after weaning. High-fat diet during pregnancy (HH and HN groups) delayed the maturation of reflexes and physical characteristics. The high-fat diet affected somatic growth differently, reducing somatic growth parameters in the groups NH and HH and increasing in the HN group. The highest SRWG was found in group HN. SRWG and BMI were reduced in the groups NH and HH. The relative intestinal weight was reduced in the groups NH, HH and HN. The relative length of small intestine was longer in group HN than in group NN. The total height of the mucosa and size of the villous were lower in group HH than in group NN. In conclusion, high-fat diet promoted negative consequences for the development of the nervous and enteric systems of the offspring.

scholarly journals The Effects of Triacylglycerol Structures on the Food Intake and Body Weight of Mice in a High-Fat Diet Setting

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1216-1216
Author(s):  
Xinge Hu
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
High Fat Diet ◽  
Tissue Sample ◽  
Body Weight Gain ◽  
Diet Group ◽  
The Body ◽  
Lower Percentage ◽  
Chow Diet ◽  
High Fat

Abstract Objectives The dietary fat content plays an important role in the regulation of chronic metabolic diseases such as obesity and type 2 diabetes. Here, we tested the impacts of triacylglycerol structure on the body weight gain and food intake of mice in a high-fat diet (HFD) setting. Methods Male C57/BL6J mice at 6 weeks old were fed one of the following three diets for 6 weeks, Teklad Rodent Diet chow diet (number 8640), the chow diet containing 36% (w/w) 1,2-Dipalmitoyl-3-oleoylglycerol (PPO), or the chow diet containing 36% (w/w) 1,3-Dipalmitoyl-2-oleoylglycerol (POP). Each group contained 9 mice, and their food intake and BW were measured daily. The mice were euthanized after 6 weeks (12 weeks old) for tissue sample collection. Results Both high HFD groups had significantly higher BW gain and caloric intakes than the chow diet group. Mice fed the POP diet had a lower percentage of BW gain and consumed less accumulated calories than those fed the PPO diet, as well as a significantly lower liver to BW ratio. Since week 4, the body BW rate of the POP group started to be lower than that of the PPO diet group. Conclusions TAG structures in an HFD setting affect the BW gain rate and obesity in mice. The different structures of fat added to affect the food intake and BW gain differently in an HFD setting. In the future, we would like to compare the changes of the hepatic lipogenesis enzyme in these mice. This will help us to understand how the triacylglycerol structures in the diet affect lipid metabolism in mice. Funding Sources Internal.

scholarly journals Impact of High-Fat Diet in Early-Life on Mammary Metabolic and Inflammatory Status in Later-Life in Mice

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 54-54
Author(s):  
Ying Tang ◽  
Ting-Chun Lin ◽  
Soonkyu Chung ◽  
Young-Cheul Kim ◽  
Zhenhua Liu
Keyword(s):  
Wnt Signaling ◽  
High Fat Diet ◽  
Early Life ◽  
Later Life ◽  
The Body ◽  
Chow Diet ◽  
High Fat ◽  
Inflammatory Status ◽  
Standard Chow Diet ◽  
Tnf Α

Abstract Objectives Emerging evidence indicates a potentially important role for early-life events and exposures in cancer development later in life. Moreover, accumulating evidence suggests that the incidence of cancers has reached a plateau in elders, whereas it continuously rises in young to middle adult. The present study aimed to investigate the potential impacts of high-fat diet in early-life, mimicking childhood/adolescent in humans, on mammary health in later-life of mice, equivalent to the young to middle age in human. Methods Female C57BL/8 mice (4 weeks of age) were fed a low-fat diet (LF: 10% kcal from fat) or a high-fat diet (HF: 60% kcal from fat) for 8 weeks, which is equivalent to child/adolescent age in humans. Mice in early-life groups were sacrificed after 8 weeks feeding, whereas mice in later-life groups were switched to standard chow diet (Lab Diet#5P76) and fed for additional 12 weeks before sacrifice. A panel of metabolic parameters, inflammatory cytokines, as well as gene expression related to tumorigenic Wnt-signaling were assessed by qPCR and immunoblotting analysis. Results Compared with LF group, the body weight in HF group was significantly elevated after 8-wk HF diet feeding (P < 0.05). After switching to the standard chow diet for 12 weeks, the significance remained until 24 weeks of age although with a reduced degree of magnitude (P < 0.05). For the metabolic factors, HFD reduced the expression levels of both Pparγ (P = 0.08) and adiponectin (P < 0.05) at 12 weeks and the reductions remains at 24 weeks (P < 0.01). Meanwhile, expressions of aromatase, estrogen receptor α and Tnf-α, Il-6, Il-10 as well as Cox2 among examined inflammatory mediators (Tnf-α, Il-6, Il-10, Il-2, Il-1β, Ifn-γ, Cox2) were significantly higher in HF than in LF group at 24 weeks (P < 0.05). For Wnt-signaling target genes (Cyclin D1, C-Myc, and Axin 2), a significant increase for C-Myc was observed in HF group at 12 weeks (P < 0.01). Conclusions Our results suggested that HF diet in early-life enhances adiposity and alters mammary metabolic and inflammatory status, creating a microenvironment in favor of breast tumorigenesis in later-life. Funding Sources This project was supported by USDA/Hatch (#1013548).

Effects of combined glucocorticoid/mineralocorticoid receptor modulation (CORT118335) on energy balance, adiposity, and lipid metabolism in male rats

2019 ◽  
Vol 317 (2) ◽  
pp. E337-E349
Author(s):  
Elizabeth T. Nguyen ◽  
Sarah Berman ◽  
Joshua Streicher ◽  
Christina M. Estrada ◽  
Jody L. Caldwell ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
The Body ◽  
Male Rats ◽  
Chow Diet ◽  
High Fat ◽  
Receptor Modulation

Psychological stress and excess glucocorticoids are associated with metabolic and cardiovascular diseases. Glucocorticoids act primarily through mineralocorticoid (MR) and glucocorticoid receptors (GR), and compounds modulating these receptors show promise in mitigating metabolic and cardiovascular-related phenotypes. CORT118335 (GR/MR modulator) prevents high-fat diet-induced weight gain and adiposity in mice, but the ability of this compound to reverse obesity-related symptoms is unknown. Adult male rats were subcutaneously administered CORT118335 (3, 10, or 30 mg/kg) or vehicle once daily. A 5-day treatment with CORT118335 at 30 mg/kg induced weight loss in rats fed a chow diet by decreasing food intake. However, lower doses of the compound attenuated body weight gain primarily because of decreased calorific efficiency, as there were no significant differences in food intake compared with vehicle. Notably, the body weight effects of CORT118335 persisted during a 2-wk treatment hiatus, suggesting prolonged effects of the compound. To our knowledge, we are the first to demonstrate a sustained effect of combined GR/MR modulation on body weight gain. These findings suggest that CORT118335 may have long-lasting effects, likely due to GR/MR-induced transcriptional changes. Prolonged (18 days) treatment of CORT118335 (10 mg/kg) reversed body weight gain and adiposity in animals fed a high-fat diet for 13 wk. Surprisingly, this occurred despite a worsening of the lipid profile and glucose homeostasis as well as a disrupted diurnal corticosterone rhythm, suggesting GR agonistic effects in the periphery. We conclude that species and tissue-specific targeting may result in promising leads for exploiting the metabolically beneficial aspects of GR/MR modulation.

scholarly journals High-Fat Diet Aggravates Acute Pancreatitis via TLR4-Mediated Necroptosis and Inflammation in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Yu-pu Hong ◽  
Jia Yu ◽  
Ying-ru Su ◽  
Fang-chao Mei ◽  
Man Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Pancreatitis ◽  
High Fat Diet ◽  
Sodium Taurocholate ◽  
The Body ◽  
Chow Diet ◽  
High Fat ◽  
Serum Free Fatty Acid ◽  
Tlr4 Signaling ◽  
Inflammatory Status

High-fat diet (HFD) often increases oxidative stress and enhances inflammatory status in the body. Toll-like receptor 4 (TLR4) is widely expressed in the pancreatic tissues and plays an important role in pancreatitis. This study is aimed at investigating the effect of HFD on acute pancreatitis (AP) and the role of TLR4-mediated necroptosis and inflammation in this disease. Weight-matched rats were allocated for an 8-week feeding on the standard chow diet (SCD) or HFD, and then, the AP model was induced by infusion of 5% sodium taurocholate into the biliopancreatic duct. Rats were sacrificed at an indicated time point after modeling. Additionally, inhibition of TLR4 signaling by TAK-242 in HFD rats with AP was conducted in vivo. The results showed that the levels of serum free fatty acid (FFA) in HFD rats were higher than those in SCD rats. Moreover, HFD rats were more vulnerable to AP injury than SCD rats, as indicated by more serious pathological damage and much higher pancreatic malondialdehyde (MDA) and lipid peroxidation (LPO) levels as well as lower pancreatic superoxide dismutase (SOD) activities and reduced glutathione (GSH) contents and more intense infiltration of MPO-positive neutrophils and CD68-positive macrophages. In addition, HFD markedly increased the expressions of TLR4 and necroptosis marker (RIP3) and aggravated the activation of NF-κB p65 and the expression of TNF-α in the pancreas of AP rats at indicated time points. However, TLR4 inhibition significantly attenuated the structural and functional damage of the pancreas induced by AP in HFD rats, as indicated by improvement of the above indexes. Taken together, these findings suggest that HFD exacerbated the extent and severity of AP via oxidative stress, inflammatory response, and necroptosis. Inhibition of TLR4 signaling by TAK-242 alleviated oxidative stress and decreased inflammatory reaction and necroptosis, exerting a protective effect during AP in HFD rats.

scholarly journals PEGylated Curcumin Derivative Attenuates Hepatic Steatosis via CREB/PPAR-γ/CD36 Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Yu Liu ◽  
Fei Cheng ◽  
Yuxuan Luo ◽  
Zhu Zhan ◽  
Peng Hu ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Liver Lipid ◽  
Serum Triglyceride ◽  
The Body ◽  
Chow Diet ◽  
Therapeutic Effects ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Curcumin Derivative

Curcumin has the potential to cure dyslipidemia and nonalcoholic fatty liver disease (NAFLD). However, its therapeutic effects are curbed by poor bioavailability. Our previous work has shown that modification of curcumin with polyethylene glycol (PEG) improves blood concentration and tissue distribution. This study sought to investigate the role of a novel PEGylated curcumin derivative (Curc-mPEG454) in regulating hepatic lipid metabolism and to elucidate the underlying molecular mechanism in a high-fat-diet- (HFD-) fed C57BL/6J mouse model. Mice were fed either a control chow diet (D12450B), an HFD (D12492) as the NAFLD model, or an HFD with Curc-mPEG454 administered by intraperitoneal injection at 50 mg/kg or 100 mg/kg for 16 weeks. We found that Curc-mPEG454 significantly lowered the body weight and serum triglyceride (TG) levels and reduced liver lipid accumulation in HFD-induced NAFLD mice. It was also shown that Curc-mPEG454 suppressed the HFD-induced upregulated expression of CD36 and hepatic peroxisome proliferator activated receptor-γ (PPAR-γ), a positive regulator of CD36. Moreover, Curc-mPEG454 dramatically activated cAMP response element-binding (CREB) protein, which negatively controls hepatic PPAR-γ expression. These findings suggest that Curc-mPEG454 reverses HFD-induced hepatic steatosis via the activation of CREB inhibition of the hepatic PPAR-γ/CD36 pathway, which may be an effective therapeutic for high-fat-diet-induced NAFLD.

scholarly journals Acupuncture Regulating Gut Microbiota in Abdominal Obese Rats Induced by High-Fat Diet

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Haiying Wang ◽  
Qiang Wang ◽  
Cuimei Liang ◽  
Mingxing Su ◽  
Xin Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
16S Rrna Gene Sequencing ◽  
The Body ◽  
Chow Diet ◽  
Rrna Gene ◽  
Sprague Dawley ◽  
High Fat ◽  
Obese Rats

Objective. To investigate the effects of acupuncture on metabolic health and gut microbiota dysbiosis in diet-induced abdominal obese model. Materials and Methods. Male Sprague-Dawley rats were randomly distributed into normal chow diet (NCD) group and high-fat diet (HFD) group. After 12 weeks of HFD feeding, an abdominal obese rat model was established. The abdominal obese rats were further assigned to acupuncture group (n=7) and nontreated HFD group (n=7). Acupuncture was applied to bilateral GB 26 of rats for 8 weeks. Subsequently, the body weight, waist circumference (WC), visceral fat mass, and liver weight were measured weekly in all rats. Metabolic parameters such as total cholesterol, triglyceride, alanine aminotransferase, aspartate transaminase, and blood glucose were measured by an automatic biochemical analyzer. The serum levels of insulin (INS) were determined using Rat INS ELISA Kit. Analysis of gut microbiota was carried out by 16S rRNA gene sequencing. Results. Acupuncture decreased the body weight, WC, and visceral adipose tissues of HFD-induced abdominal obese rats. In addition, insulin sensitivity, glucose homeostasis, and lipid metabolism were improved by this treatment. Furthermore, electroacupuncture effectively modified the composition of gut microbiota, mainly via decreasing Firmicutes/Bacteroidetes ratio and increasing Prevotella_9 abundance. Conclusions. Electroacupuncture can ameliorate abdominal obesity and prevent metabolic disorders in HFD-induced abdominal obese rats, via the modulation of gut microbiota.

scholarly journals Rebalancing glucolipid metabolism and gut microbiome dysbiosis by nitrate-dependent alleviation of high-fat diet-induced obesity

2020 ◽  
Vol 8 (1) ◽  
pp. e001255
Author(s):  
Linsha Ma ◽  
Liang Hu ◽  
Luyuan Jin ◽  
Jiangyi Wang ◽  
Xiangchun Li ◽  
...  
Keyword(s):  
Body Weight ◽  
Gut Microbiome ◽  
High Fat Diet ◽  
The Body ◽  
Guanosine Monophosphate ◽  
Chow Diet ◽  
High Fat ◽  
Dietary Nitrate ◽  
Group Water ◽  
Normal Water

IntroductionHigh-fat diet (HFD)-induced obesity is accompanied by compromised nitric oxide (NO) signaling and gut microbiome dysregulation. Inorganic dietary nitrate, which acts as a NO donor, exerts beneficial effects on metabolic disorders. Here, we evaluated the effects of dietary nitrate on HFD-induced obesity and provided insights into the underlying mechanism.Research design and methodsTo investigate the preventive effect of dietary nitrate on HFD-induced obesity, C57BL/6 mice were randomly assigned into four groups (n=10/group), including normal control diet group (normal water and chow diet), HFD group (normal water and HFD), HFD+NaNO3 group (water containing 2 mM NaNO3 and HFD), and HFD+NaCl group (water containing 2 mM NaCl and HFD). During the experiment, body weight was monitored and glucolipid metabolism was evaluated. The mechanism underlying the effects of nitrate on HFD-induced obesity was investigated by the following: the NO3--NO2--NO pathway; endothelial NO synthase (eNOS) and cyclic guanosine monophosphate (cGMP) levels; gut microbiota via 16SRNA analysis.ResultsDietary nitrate reduced the body weight gain and lipid accumulation in adipose and liver tissues in HFD-fed mice. Hyperlipidemia and insulin resistance caused by HFD were improved in mice supplemented with nitrate. The level of eNOS was upregulated by nitrate in the serum, liver, and inguinal adipose tissue. Nitrate, nitrite, and cGMP levels were decreased in mice fed on HFD but reversed in the HFD+NaNO3 group. Nitrate also rebalanced the colon microbiota and promoted a normal gut microbiome profile by partially attenuating the impacts of HFD. Bacteroidales S24-7, Alistipes, Lactobacillus, and Ruminococcaceae abundances were altered, and Bacteroidales S24-7 and Alistipes abundances were higher in the HFD+NaNO3 group than that in the HFD group.ConclusionsInorganic dietary nitrate alleviated HFD-induced obesity and ameliorated disrupted glucolipid metabolism via NO3--NO2--NO pathway activation and gut microbiome modulation.

scholarly journals Sitagliptin Reduces Endothelial Dysfunction and Apoptosis Induced by High-Fat Diet and Palmitate in Thoracic Aortas and Endothelial Cells via ROS-ER Stress-CHOP Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Qiongqiong Cao ◽  
Dongmei Xu ◽  
Yong Chen ◽  
Yueming Long ◽  
Fang Dai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Protein Expression ◽  
Er Stress ◽  
High Fat Diet ◽  
The Body ◽  
Ros Generation ◽  
Intragastric Administration ◽  
Chow Diet ◽  
High Fat

Macrovascular disease is tightly associated with obesity-induced metabolic syndrome. Sitagliptin (SIT), an orally stable selective inhibitor of Dipeptidyl peptidase-4 (DPP-4), has protective effects on endothelium. However, the mechanisms enabling SIT to exhibit resistance to diet-induced obesity (DIO) related with reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress in the aorta and endothelial cells have not been reported yet. Therefore, the present study was conducted to determine if SIT exerts protective role in the thoracic aortas isolated from the high-fat diet (HFD)-treated rats and palmitate (PA)-treated endothelial cells by alleviating ROS and ER stress. Male Sprague Dawley rats were randomly divided into standard chow diet (SCD), HFD and HFD plus sitagliptin administration (HFD + SIT) groups. The rats of latter two groups were given HFD fodder for 12 weeks, then the HFD + SIT rats were treated with SIT (10 mg/kg/d) by intragastric administration for another 8 weeks. The body mass, vascular tension, serum oxidative stress indices and inflammatory parameters, pathological changes, protein expression of endothelial nitric oxide synthase (eNOS), the genes associated with ER stress and apoptosis in the thoracic aorta were measured. Furthermore, cell proliferation, ROS and the protein expression associated with ER stress (especially CHOP) and apoptosis were assessed in human umbilical vein endothelial cells (HUVECs) incubated with SIT and PA. Compared to the SCD rats, the HFD rats had higher serum lipid levels, decreased vascular tension, increased inflammation, oxidative and ER stress, and apoptosis of endothelial cells. PA promoted ROS generation, ER stress and apoptosis, inhibited cell proliferation in HUVECs. SIT treatment obviously ameliorated apoptosis via alleviating ROS and ER stress in the thoracic aortas isolated from HFD-fed rats and PA-treated HUVECs. The results suggest that SIT improved endothelial function via promoting cell proliferation and alleviating ROS-ER stress-CHOP pathway both in vivo and in vitro.

Irisin induces white adipose tissue browning in mice as assessed by magnetic resonance imaging

2021 ◽  
pp. 153537022110060
Author(s):  
Yue Chen ◽  
Jie Ding ◽  
Yufei Zhao ◽  
Shenghong Ju ◽  
Hui Mao ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Adipose Tissue ◽  
Magnetic Resonance ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Chow Diet ◽  
Resonance Imaging ◽  
High Fat ◽  
White Adipocytes ◽  
Fat Fraction

This study aimed to track and evaluate the effect of low-dose irisin on the browning of white adipose tissue (WAT) in mice using magnetic resonance imaging (MRI) noninvasively in vivo. Mature white adipocytes extracted from mice were cultured, induced and characterized before being treated by irisin. The volume and fat fraction of WAT were quantified using MRI in normal chow diet and high fat mice after injection of irisin. The browning of cultured white adipocytes and WAT in mice were validated by immunohistochemistry and western blotting for uncoupling protein 1 (UCP1) and deiodinase type II (DIO2). The serum indexes were examined with high fat diet after irisin intervention. UCP1 and DIO2 in adipocytes showed increases responding to the irisin treatment. The size of white adipocytes in mice receiving irisin intervention was reduced. MRI measured volumes and fat fraction of WAT were significantly lower after Irisin treatment. Blood glucose and cholesterol levels were reduced in high fat diet mice after irisin treatment. Irisin intervention exerted browning of WAT, resulting reduction of volume and fat fraction of WAT as measured by MRI. Furthermore, it improved the condition of mice with diet-induced obesity and related metabolic disorders.

scholarly journals Partial Deficiency of Zfp217 Resists High-Fat Diet-Induced Obesity by Increasing Energy Metabolism in Mice

2021 ◽  
Vol 22 (10) ◽  
pp. 5390
Author(s):  
Qianhui Zeng ◽  
Nannan Wang ◽  
Yaru Zhang ◽  
Yuxuan Yang ◽  
Shuangshuang Li ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Chow Diet ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
Partial Deficiency

Obesity-induced adipose tissue dysfunction and disorders of glycolipid metabolism have become a worldwide research priority. Zfp217 plays a crucial role in adipogenesis of 3T3-L1 preadipocytes, but about its functions in animal models are not yet clear. To explore the role of Zfp217 in high-fat diet (HFD)-induced obese mice, global Zfp217 heterozygous knockout (Zfp217+/−) mice were constructed. Zfp217+/− mice and Zfp217+/+ mice fed a normal chow diet (NC) did not differ significantly in weight gain, percent body fat mass, glucose tolerance, or insulin sensitivity. When challenged with HFD, Zfp217+/− mice had less weight gain than Zfp217+/+ mice. Histological observations revealed that Zfp217+/− mice fed a high-fat diet had much smaller white adipocytes in inguinal white adipose tissue (iWAT). Zfp217+/− mice had improved metabolic profiles, including improved glucose tolerance, enhanced insulin sensitivity, and increased energy expenditure compared to the Zfp217+/+ mice under HFD. We found that adipogenesis-related genes were increased and metabolic thermogenesis-related genes were decreased in the iWAT of HFD-fed Zfp217+/+ mice compared to Zfp217+/− mice. In addition, adipogenesis was markedly reduced in mouse embryonic fibroblasts (MEFs) from Zfp217-deleted mice. Together, these data indicate that Zfp217 is a regulator of energy metabolism and it is likely to provide novel insight into treatment for obesity.

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