Similar Datasets
Project description:The diet induced obesity (DIO) mouse model has been widely used for obesity studies. Comparing to the composition of nutrients in the diet, the effects of storage conditions for high fat diet (HFD) on metabolic homeostasis have not been systemically investigated. In the current study, we tested the effects of HFD stored in different conditions and found the mice fed by HFD stored in the fridge (HFDfri) gained less weight than freezer (HFDfre). Further analysis revealed the changes of the relative abundance of medium chain triglyceride (MCT) in the HFDfri, which has much lower intestinal absorption rates, contributed to the body weight differences. In contrast, advanced liver damages and elevation of unfolded protein responses (UPR) was observed in the mice fed by the HFDfri. Depletion of UPR regulated gene Nnmt alleviated liver damages via inhibition of integrated stress response (ISR). Our study provided the initial evidence that HFD storage conditions have great impacts on both body weight changes and liver damages in the DIO model.
2022-12-31 | GSE203039 | GEO
Project description:The diet induced obesity (DIO) mouse model has been widely used for obesity studies. Comparing to the composition of nutrients in the diet, the effects of storage conditions for high fat diet (HFD) on metabolic homeostasis have not been systemically investigated. In the current study, we tested the effects of HFD stored in different conditions and found the mice fed by HFD stored in the fridge (HFDfri) gained less weight than freezer (HFDfre). Further analysis revealed the changes of the relative abundance of medium chain triglyceride (MCT) in the HFDfri, which has much lower intestinal absorption rates, contributed to the body weight differences. In contrast, advanced liver damages and elevation of unfolded protein responses (UPR) was observed in the mice fed by the HFDfri. Depletion of UPR regulated gene Nnmt alleviated liver damages via inhibition of integrated stress response (ISR). Our study provided the initial evidence that HFD storage conditions have great impacts on both body weight changes and liver damages in the DIO model.
2022-12-31 | GSE203038 | GEO
Project description:The storage conditions of high fat diet are the key factors for diet induced obesity and liver damage.
| PRJNA838220 | ENA
Project description:The storage conditions of high fat diet are the key factors for diet induced obesity and liver damage [HFDfre vs. HFDfri]
| PRJNA838224 | ENA
Project description:The storage conditions of high fat diet are the key factors for diet induced obesity and liver damage [WT vs. Nnmt KO]
| PRJNA838225 | ENA
Project description:ObjectiveMurine-specific muricholic acids (MCAs) are reported to protect against obesity and associated metabolic disorders. However, the response of mice with genetic depletion of MCA to an obesogenic diet has not been evaluated. We used Cyp2c-deficient (Cyp2c-/-) mice, which lack MCAs and thus have a human-like bile acid (BA) profile, to directly investigate the potential role of MCAs in diet-induced obesity.MethodsMale and female Cyp2c-/- mice and wild-type (WT) littermate controls were fed a standard chow diet or a high-fat diet (HFD) for 18 weeks. We measured BA composition from a pool of liver, gallbladder, and intestine, as well as weekly body weight, food intake, lean and fat mass, systemic glucose homeostasis, energy expenditure, intestinal lipid absorption, fecal lipid, and energy content.ResultsCyp2c-deficiency depleted MCAs and caused other changes in BA composition, namely a decrease in the ratio of 12α-hydroxylated (12α-OH) BAs to non-12α-OH BAs, without altering the total BA levels. While WT male mice became obese after HFD feeding, Cyp2c-/- male mice were protected from obesity and associated metabolic dysfunctions. Cyp2c-/- male mice also showed reduced intestinal lipid absorption and increased lipid excretion, which was reversed by oral gavage with the 12α-OH BA and taurocholic acid (TCA). Cyp2c-/- mice also showed increased liver damage, which appeared stronger in females.ConclusionsMCA does not protect against diet-induced obesity but may protect against liver injury. Reduced lipid absorption in Cyp2c-deficient male mice is potentially due to a reduced ratio of 12α-OH/non-12α-OH BAs.
| S-EPMC8449133 | biostudies-literature
Project description:ObjectiveCelastrol was recently identified as a potential novel treatment for obesity. However, the effect of Celastrol on nonalcoholic fatty liver disease (NAFLD) remains elusive. The aim of this study is to evaluate the role of Celastrol in NAFLD.MethodsFunctional studies were performed using wild-type C57BL/6J (WT) mice and liver specific Sirt1-deficient (LKO) mice. The molecular mechanism was explored in primary mouse liver and primary hepatocytes.ResultsWhen WT mice receiving a high-fat diet (HFD) were treated with Celastrol, reductions in body weight, subcutaneous and visceral fat content, and liver lipid droplet formation were observed, along with reduced hepatic intracellular triglyceride and serum triglyceride, free fatty acid, and ALT concentrations. Furthermore, Celastrol decreased hepatic sterol regulatory element binding protein 1c (Srebp-1c) expression, enhanced the phosphorylation of hepatic AMP-activated protein kinase α (AMPKα), and increased the expression of hepatic serine-threonine liver kinase B1 (LKB1). Additionally, Celastrol treatment improved glucose tolerance and insulin sensitivity in WT mice fed the HFD. Celastrol administration also improved the anti-inflammatory and anti-oxidative status by inhibiting nuclear factor kappa B (NFκB) activity and the mRNA levels of proinflammatory cytokines and increasing mitochondrial DNA copy number and anti-oxidative stress genes expression in WT mice liver, in vivo and in vitro. Moreover, Celastrol induced hepatic Sirt1 expression in WT mice, in vivo and in vitro. These Celastrol-mediated protective effects in WT mice fed a HFD were abolished in LKO mice fed a HFD. It was more interesting that Celastrol aggravated HFD-induced liver damage in LKO mice fed a HFD by inhibiting the phosphorylation of AMPKα and boosting the translocation of NFκB into the nucleus, thereby resulting in the increase of Srebp-1c expression and the mRNA levels of liver proinflammatory cytokines.ConclusionsCelastrol ameliorates NAFLD by decreasing lipid synthesis and improving the anti-oxidative and anti-inflammatory status. And Sirt1 has an important role in Celastrol-ameliorating liver metabolic damage caused by HFD.
| S-EPMC5220393 | biostudies-literature
Project description:Obesity is a multifactorial health problem resulting from genetic, environmental, and behavioral factors. A particularly interesting aspect of obesity is the differences observed in response to the same high-fat diet (HFD). In this study, we performed lipidomic profiling on livers from HFD-fed C57BL/6J mice using ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry. Mice were divided into three groups: normal diet (ND), HFD-obesity prone (HFD-OP), and HFD-obesity resistant (HFD-OR). Principal components analyses showed a difference between the HFD-OP and HFD-OR groups. Individuals in the HFD-OR group were closer to those in the ND group compared with those in the HFD-OP group. In particular, phosphocholine (PC) and triglyceride (TG) levels differed significantly depending on the length of the acyl chain and degree of unsaturation, respectively. PC species were either positively or negatively correlated with concentrations of glucose, insulin, leptin, and hepatic cholesterol according to the length of the acyl chain. Decreased expression of the scavenger receptor B1 and ATP-binding cassette A1 in HFD-OP mice indicated that the acyl chain length of PC species may be related to high-density lipoprotein cholesterol metabolism. This study demonstrates that lipidomic profiling is an effective approach to analyzing global lipid alterations as they pertain to obesity.
| S-EPMC4655311 | biostudies-literature
Project description:Elafin is an antimicrobial and anti-inflammatory protein. We hypothesize that elafin expression correlates with diabetes. Among non-diabetic and prediabetic groups, men have significantly higher serum elafin levels than women. Men with type 2 diabetes mellitus (T2DM) have significantly lower serum elafin levels than men without T2DM. Serum elafin levels are inversely correlated with fasting blood glucose and hemoglobin A1c levels in men with T2DM, but not women with T2DM. Lentiviral elafin overexpression inhibited obesity, hyperglycemia, and liver steatosis in high-fat diet (HFD)-treated male mice. Elafin-overexpressing HFD-treated male mice had increased serum leptin levels, and serum exosomal miR181b-5p and miR219-5p expression. Transplantation of splenocytes and serum exosomes from elafin-overexpressing HFD-treated donor mice reduced food consumption and fat mass, and increased adipose tissue leptin mRNA expression in HFD-treated recipient mice. Elafin improved leptin sensitivity via reduced interferon-gamma expression and induced adipose leptin expression via increased miR181b-5p and miR219-5p expression. Subcutaneous and oral administration of modified elafin inhibited obesity, hyperglycemia, and liver steatosis in the HFD-treated mice. Circulating elafin levels are associated with hyperglycemia in men with T2DM. Elafin, via immune-derived miRNAs and cytokine, activates leptin sensitivity and expression that subsequently inhibit food consumption, obesity, hyperglycemia, and liver steatosis in HFD-treated male mice.
| S-EPMC7393145 | biostudies-literature
Project description:Analysis of GPR120 which play roles for the fatty acid sensor in adipose tissue. Results provide insight into the transcriptional effects caused by the loss of the GPR120 proteins and provide further insight into their functions. GPR120 KO mice and the corresponding wild-type with normal diet(ND) or high fat diet(HFD), were subjected to Affymetrix Mus musculus microarrays. Epididymal adipose tissue and liver were analyzed in triplicates.
2012-02-22 | E-GEOD-32095 | biostudies-arrayexpress