Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA139895 | ENA |
REPOSITORIES: ENA
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Project description:Assembly of HSPGs in the liver is defective in diabetes mellitus. A major consequence is impaired clearance of post-prandial lipoproteins, which ordinarily depends on the binding of these particles to hepatic HSPGs. Impaired clearance leads to prolonged exposure of the arterial wall to these harmful lipoproteins. We pin-pointed suppression of NDST-1 in livers of type 1 diabetic rats as at least a partial explanation for defective HSPG assembly. Dr. Williams' lab examined glycan-related gene expression in the livers of three groups of mice: wild-type, ad-lib-fed type 2 diabetic mice (db/db), and calorically restricted db/db mice (caloric restriction was shown several years ago to correct their clearance of atherogenic post-prandial lipoproteins). The results will indicate the molecular basis for defective HSPG assembly in type 2 diabetes, which is a question of considerable medical importance. RNA preparations from mice livers (wild-type, ad-lib-fed type 2 diabetic mice, and calorically restricted mice) were sent to Microarray Core (E). The RNA was amplified, labeled, and hybridized to GLYCO_v3 microarrays.
2011-04-29 | E-GEOD-28938 | biostudies-arrayexpress
Project description:Purpose: RNAseq analyses were conducted to screen for the genes undergoing transcriptional changes either in the liver of high-fat-diet (HFD)-induced obese mice or in the liver of Lepr-deficient db/db mice compared to the livers of the respective control mice Methods: C57BL/6 wild-type male mice were fed on high-fat diet (HFD) or a low-fat diet (NCD) for 18 weeks starting from 6 weeks of age, and the livers were collected at 24 weeks of age at ad libitum-fed condition.Misty/misty or db/db were sacrificed at ad libitum-fed condition at 10weeks and the liver was collected. Results: 2079 genes and 1085 genes were identified in high-fat-diet fed mice and db/db mice, respectively.
2022-01-06 | GSE188344 | GEO
Project description:Caloric Restriction in Leptin Deficiency Worsens Myocardial Steatosis: Failure to Upregulate PPAR gamma and Thermogenic Glyecrolipid/Fatty Acid Cycling Growing evidence supports an anti-lipotoxic role for leptin in preventing inappropriate peripheral tissue lipid deposition. Obese, leptin deficient ob/ob mice develop left ventricular (LV) hypertrophy and myocardial steatosis with increased apoptosis and decreased longevity. Here we investigated the cardiac effects of caloric restriction in leptin deficiency. Echocardiography was performed on C57Bl/6 wild-type mice (WT) and 7-month-old ob/ob mice fed ad lib, leptin-repleted (LR-ob/ob), or calorie-restricted (CR-ob/ob) for four weeks. Ventricular tissue was examined by electron microscopy (EM), mitochondrial coupling assay, and microarray expression profiling. LR and CR-ob/ob mice showed decreased body weight, heart weight, and LV wall thickness compared to ad lib ob/ob mice. LV fractional shortening was decreased in ad lib ob/ob mice, but restored to WT levels in LR and CR groups. However, EM revealed severe cardiac steatosis in the CR-ob/ob group compared to only moderate steatosis in ad lib ob/ob . Despite marked cardiac steatosis, CR (like LR) restored mitochondrial coupling to WT levels. CR up-regulated genes associated with oxidative stress and cell death, changes suggestive of cardiac lipotoxicity. LR, but not CR was shown to induce core genes involved in glycerolipid/free fatty acid cycling, a highly thermogenic pathway that can reduce intracellular lipid stores. LR, but not CR up-regulated and restored PGC1 and PPARto wild type levels; CR paradoxically further suppressed cardiac PPAR. Thus, leptin is essential in protecting the heart from lipotoxicity, and the inability to up-regulate the thermogenic glycerolipid/free fatty acid cycling pathway may impair the response of leptin deficient animals to the lipotoxic stress of calorie restriction. 6 month aged ob/ob mice were either leptin repleted with osmotic mini-pumps, calorie restricted to match the caloric intake of the leptin repleted mice, or fed ad lib for one month. 6-8 month C57Bl/6J mice were aged to serve as controls.
2011-04-29 | E-GEOD-16790 | biostudies-arrayexpress
Project description:To determine hepatic gene expression changes in fasted state, we employed the microarray analysis. We collected the livers from 8-weeks-old male WT and CREBH KO mice in both fasted and fed ad lib states.
2020-01-11 | GSE143420 | GEO
Project description:Caloric Restriction in Leptin Deficiency Worsens Myocardial Steatosis: Failure to Upregulate PPAR gamma and Thermogenic Glyecrolipid/Fatty Acid Cycling Growing evidence supports an anti-lipotoxic role for leptin in preventing inappropriate peripheral tissue lipid deposition. Obese, leptin deficient ob/ob mice develop left ventricular (LV) hypertrophy and myocardial steatosis with increased apoptosis and decreased longevity. Here we investigated the cardiac effects of caloric restriction in leptin deficiency. Echocardiography was performed on C57Bl/6 wild-type mice (WT) and 7-month-old ob/ob mice fed ad lib, leptin-repleted (LR-ob/ob), or calorie-restricted (CR-ob/ob) for four weeks. Ventricular tissue was examined by electron microscopy (EM), mitochondrial coupling assay, and microarray expression profiling. LR and CR-ob/ob mice showed decreased body weight, heart weight, and LV wall thickness compared to ad lib ob/ob mice. LV fractional shortening was decreased in ad lib ob/ob mice, but restored to WT levels in LR and CR groups. However, EM revealed severe cardiac steatosis in the CR-ob/ob group compared to only moderate steatosis in ad lib ob/ob . Despite marked cardiac steatosis, CR (like LR) restored mitochondrial coupling to WT levels. CR up-regulated genes associated with oxidative stress and cell death, changes suggestive of cardiac lipotoxicity. LR, but not CR was shown to induce core genes involved in glycerolipid/free fatty acid cycling, a highly thermogenic pathway that can reduce intracellular lipid stores. LR, but not CR up-regulated and restored PGC1-alpha and PPAR-alpha to wild type levels; CR paradoxically further suppressed cardiac PPAR-alpha. Thus, leptin is essential in protecting the heart from lipotoxicity, and the inability to up-regulate the thermogenic glycerolipid/free fatty acid cycling pathway may impair the response of leptin deficient animals to the lipotoxic stress of calorie restriction.
2011-04-29 | GSE16790 | GEO
Project description:Multi-omics integration analysis of rumen microorganisms isolated from cows fed either an ad lib or restricted diet, and comparing this with methane emission rates for the cows.
2023-07-20 | PXD040349 | Pride
Project description:C57BL/6J mice were from The Jackson Laboratory (Maine, USA) and were housed/caged and fed a standard chow diet until 6 weeks of age whereupon they were placed in one of 4 different dietary regimens for a period of 3 weeks prior to mating. Mice were housed under pathogen-free conditions of 21± 1°C, 40 to 60% humidity, and a 12 h-12 h light/dark cycle. The 4 diet regimens used in this study were: [1] ad lib Standard Chow (Control diet) with ad lib drinking water. [2] Ad lib Standard Chow, with ad lib drinking water containing 0.64 mg/ml (97 mg/Kg body weight) monosodium glutamate (MSG diet). [3] Ad lib Test Diet Purina 5001 with 20% 55-HFCS (5B4K, Purina, USA), and ad lib drinking water (HFCS diet). [4] Ad lib Purina 5001 with 20% 55-HFCS, and ad lib drinking water containing 0.64 mg/ml (97 mg/K body weight) monosodium glutamate (HFCS+MSG diet). See Table 1 for diet composition. Following mating, the 4 groups of dams were maintained on their respective diets throughout the gestation and nursing period. Male offspring used in these experiments were weighed, then weaned onto the same diets and maintained in this regimen until they reached either 16 or 32 weeks of age. Total RNA was prepared from the liver and visceral white adipose tissue (WAT) taken from 16-week-old mice in the 4 different diet groups using Qiagen RNeasy Kit (Qiagen USA) according to the manufacturers instructions and stored at -80 o C.<br>
2009-10-01 | E-MEXP-1909 | biostudies-arrayexpress
Project description:To identify putative lncRNA changes in the livers of db/db mice and C57 mice, we isolated the liver tissues and carried out a microarray analysis. Here, we found significant changes of lncRNAs in the livers of db/db mice. Among them, abnormal expression of ultraconserved elements was noticed.
2017-12-14 | GSE107396 | GEO
Project description:The type 2 diabetes medication, rosiglitazone, has come under scrutiny for possibly increasing the risk of cardiac disease and death. To investigate the effects of rosiglitazone on the diabetic heart, we performed cardiac transcriptional profiling of a murine model of type 2 diabetes, the C57BL/KLS-leprdb/leprdb (db/db) mouse. We compared cardiac gene expression profiles from three groups: untreated db/db mice (db-c), db/db mice after rosiglitazone treatment (db-t), and non-diabetic db/+ mice.
2012-03-29 | GSE36875 | GEO
Project description:Expression data from livers of ad libitum and calorie-restricted mice
| PRJNA362285 | ENA