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[PMID]:29367486
[Au] Autor:Miyazawa N; Yoshimoto H; Kurihara S; Hamaya T; Eguchi F
[Ad] Endereço:Faculty of Regional Environment Science, Tokyo University of Agriculture.
[Ti] Título:Improvement of Diet-induced Obesity by Ingestion of Mushroom Chitosan Prepared from Flammulina velutipes.
[So] Source:J Oleo Sci;67(2):245-254, 2018 Feb 01.
[Is] ISSN:1347-3352
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The anti-obesity effects of mushroom chitosan prepared from Flammulina velutipes were investigated using an animal model with diet-induced obesity. In this study, 5-week-old imprinting control region (ICR) mice were divided into six groups of 10 mice each and fed different diets based on the MF powdered diet (standard diet) for 6 weeks: standard diet control group, high-fat diet control group (induced dietary obesity) consisting of the standard diet and 20% lard, and mushroom chitosan groups consisting of the high-fat diet with mushroom chitosan added at 100, 500, 1,000, and 2,000 mg/kg body weight. On the final day of the experiment, mean body weight was 39.1 g in the high-fat control group and 36.3 g in the 2,000 mg/kg mushroom chitosan group, compared to 35.8 g in the standard diet control group. In the mushroom chitosan groups, a dose-dependent suppression of weight gain and marked improvements in serum triglycerides, total cholesterol, LDL-cholesterol, and HDL-cholesterol were found. The mushroom chitosan groups showed fewer and smaller fat deposits in liver cells than the high-fat diet control group, and liver weight was significantly reduced. Glutamic oxaloacetic transaminase (GOT) and glutamate pyruvic transaminase (GPT), which are indices of the hepatic function, all showed dose-dependent improvement with mushroom chitosan administration. These results suggested that mushroom chitosan acts to suppress enlargement of the liver from fat deposition resulting from a high-fat diet and to restore hepatic function. The lipid content of feces showed a marked increase correlated with the mushroom chitosan dose. These findings suggest the potential use of mushroom chitosan as a functional food ingredient that contributes to the prevention or improvement of dietary obesity by inhibiting digestion and absorption of fats in the digestive tract and simultaneously promotes lipolysis in adipocytes.
[Mh] Termos MeSH primário: Quitosana/administração & dosagem
Quitosana/isolamento & purificação
Dieta Hiperlipídica/efeitos adversos
Flammulina/química
Obesidade/prevenção & controle
Fitoterapia
[Mh] Termos MeSH secundário: Adipócitos/metabolismo
Administração Oral
Animais
Fármacos Antiobesidade
Quitosana/farmacologia
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Lipólise/efeitos dos fármacos
Masculino
Camundongos Endogâmicos ICR
Hepatopatia Gordurosa não Alcoólica/prevenção & controle
Obesidade/etiologia
Obesidade/metabolismo
Ganho de Peso/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Obesity Agents); 9012-76-4 (Chitosan)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.5650/jos.ess17159


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[PMID]:27770485
[Au] Autor:da Silva Teixeira S; Filgueira C; Sieglaff DH; Benod C; Villagomez R; Minze LJ; Zhang A; Webb P; Nunes MT
[Ad] Endereço:Departamento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
[Ti] Título:3,5-diiodothyronine (3,5-T2) reduces blood glucose independently of insulin sensitization in obese mice.
[So] Source:Acta Physiol (Oxf);220(2):238-250, 2017 Jun.
[Is] ISSN:1748-1716
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: Thyroid hormones regulate metabolic response. While triiodothyronine (T3) is usually considered to be the active form of thyroid hormone, one form of diiodothyronine (3,5-T2) exerts T3-like effects on energy consumption and lipid metabolism. 3,5-T2 also improves glucose tolerance in rats and 3,5-T2 levels correlate with fasting glucose in humans. Presently, however, little is known about mechanisms of 3,5-T2 effects on glucose metabolism. Here, we set out to compare effects of T3, 3,5-T2 and another form of T2 (3,3-T2) in a mouse model of diet-induced obesity and determined effects of T3 and 3,5-T2 on markers of classical insulin sensitization to understand how diiodothyronines influence blood glucose. METHODS: Cell- and protein-based assays of thyroid hormone action. Assays of metabolic parameters in mice. Analysis of transcript and protein levels in different tissues by qRT-PCR and Western blot. RESULTS: T3 and 3,5-T2 both reduce body weight, adiposity and body temperature despite increased food intake. 3,3'-T2 lacks these effects. T3 and 3,5-T2 reduce blood glucose levels, whereas 3,3'-T2 worsens glucose tolerance. Neither T3 nor 3,5-T2 affects markers of insulin sensitization in skeletal muscle or white adipose tissue (WAT), but both reduce hepatic GLUT2 glucose transporter levels and glucose output. T3 and 3,5-T2 also induce expression of mitochondrial uncoupling proteins (UCPs) 3 and 1 in skeletal muscle and WAT respectively. CONCLUSIONS: 3,5-T2 influences glucose metabolism in a manner that is distinct from insulin sensitization and involves reductions in hepatic glucose output and changes in energy utilization.
[Mh] Termos MeSH primário: Glicemia/efeitos dos fármacos
Di-Iodotironinas/farmacologia
Resistência à Insulina
[Mh] Termos MeSH secundário: Animais
Dieta Hiperlipídica
Metabolismo Energético/efeitos dos fármacos
Células Hep G2
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Obesidade
Tri-Iodotironina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Diiodothyronines); 06LU7C9H1V (Triiodothyronine); 534-51-0 (3,5-diiodothyronine); 70-40-6 (3,3'-diiodothyronine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1111/apha.12821


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[PMID]:28456841
[Au] Autor:Blanco-Gandía MC; Aracil-Fernández A; Montagud-Romero S; Aguilar MA; Manzanares J; Miñarro J; Rodríguez-Arias M
[Ad] Endereço:Departamento de Psicobiología, Facultad de Psicología, Unidad de Investigación Psicobiología de las Drogodependencias, , Universitat de València, Avda. Blasco Ibáñez, 21, 46010, Valencia, Spain.
[Ti] Título:Changes in gene expression and sensitivity of cocaine reward produced by a continuous fat diet.
[So] Source:Psychopharmacology (Berl);234(15):2337-2352, 2017 Aug.
[Is] ISSN:1432-2072
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Preclinical studies report that free access to a high-fat diet (HFD) alters the response to psychostimulants. OBJECTIVES: The aim of the present study was to examine how HFD exposure during adolescence modifies cocaine effects. Gene expression of CB1 and mu-opioid receptors (MOr) in the nucleus accumbens (N Acc) and prefrontal cortex (PFC) and ghrelin receptor (GHSR) in the ventral tegmental area (VTA) were assessed. METHODS: Mice were allowed continuous access to fat from PND 29, and the locomotor (10 mg/kg) and reinforcing effects of cocaine (1 and 6 mg/kg) on conditioned place preference (CPP) were evaluated on PND 69. Another group of mice was exposed to a standard diet until the day of post-conditioning, on which free access to the HFD began. RESULTS: HFD induced an increase of MOr gene expression in the N Acc, but decreased CB1 receptor in the N Acc and PFC. After fat withdrawal, the reduction of CB1 receptor in the N Acc was maintained. Gene expression of GHSR in the VTA decreased during the HFD and increased after withdrawal. Following fat discontinuation, mice exhibited increased anxiety, augmented locomotor response to cocaine, and developed CPP for 1 mg/kg cocaine. HFD reduced the number of sessions required to extinguish the preference and decreased sensitivity to drug priming-induced reinstatement. CONCLUSION: Our results suggest that consumption of a HFD during adolescence induces neurobiochemical changes that increased sensitivity to cocaine when fat is withdrawn, acting as an alternative reward.
[Mh] Termos MeSH primário: Cocaína/farmacologia
Dieta Hiperlipídica/psicologia
Dieta Hiperlipídica/tendências
Receptor CB1 de Canabinoide/biossíntese
Receptor CB1 de Canabinoide/genética
Recompensa
[Mh] Termos MeSH secundário: Animais
Condicionamento Clássico/efeitos dos fármacos
Condicionamento Clássico/fisiologia
Expressão Gênica
Masculino
Camundongos
Núcleo Accumbens/efeitos dos fármacos
Núcleo Accumbens/metabolismo
Córtex Pré-Frontal/efeitos dos fármacos
Córtex Pré-Frontal/metabolismo
Receptores de Grelina/metabolismo
Receptores Opioides mu/metabolismo
Reforço (Psicologia)
Área Tegmentar Ventral/efeitos dos fármacos
Área Tegmentar Ventral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, Cannabinoid, CB1); 0 (Receptors, Ghrelin); 0 (Receptors, Opioid, mu); I5Y540LHVR (Cocaine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE
[do] DOI:10.1007/s00213-017-4630-9


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[PMID]:29351550
[Au] Autor:Rachid TL; Silva-Veiga FM; Graus-Nunes F; Bringhenti I; Mandarim-de-Lacerda CA; Souza-Mello V
[Ad] Endereço:Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
[Ti] Título:Differential actions of PPAR-α and PPAR-ß/δ on beige adipocyte formation: A study in the subcutaneous white adipose tissue of obese male mice.
[So] Source:PLoS One;13(1):e0191365, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Obesity compromises adipocyte physiology. PPARs are essential to adipocyte plasticity, but its isolated role in the browning phenomenon is not clear. This study aimed to examine whether activation of PPAR-α or PPAR-ß/δ could induce beige cell depots in the subcutaneous white adipose tissue of diet-induced obese mice. MATERIAL AND METHODS: Sixty animals were randomly assigned to receive a control diet (C, 10% lipids) or a high-fat diet (HF, 50% lipids) for ten weeks. Then each group was re-divided to begin the treatments that lasted 4 weeks, totalizing six groups: C, C-α (C plus PPAR-α agonist, 2.5 mg/kg BM), C-ß (C plus PPAR-ß/δ agonist, 1 mg/kg BM), HF, HF-α (HF plus PPAR-α agonist), HF-ß (HF plus PPAR-ß/δ agonist). RESULTS: HF animals presented with overweight, glucose intolerance and subcutaneous white adipocyte hypertrophy. Both treatments significantly attenuated these parameters. Browning, verified by UCP1 positive beige cells and enhanced body temperature, was just observed in PPAR-α treated groups. PPAR-α agonism also elicited an enhanced gene expression of the thermogenesis effector UCP1, the beige-selective gene TMEM26 and the PRDM16, an essential gene for brown-like phenotype maintenance in the beige adipocytes when compared to their counterparts. The enhanced CIDEA and the reduced UCP1 gene levels might justify the white phenotype predominance after the treatment with the PPAR-ß/δ agonist. CONCLUSIONS: This work provides evidence that the PPAR-ß/δ agonist ameliorated metabolic disorders through enhanced beta-oxidation and better tolerance to glucose, whereas the PPAR-α agonism was confirmed as a promising therapeutic target for treating metabolic diseases via beige cell induction and enhanced thermogenesis.
[Mh] Termos MeSH primário: Adipócitos Bege/efeitos dos fármacos
Obesidade/tratamento farmacológico
PPAR alfa/agonistas
PPAR delta/agonistas
PPAR beta/agonistas
[Mh] Termos MeSH secundário: Adipócitos Bege/metabolismo
Adipócitos Bege/patologia
Tecido Adiposo Branco/efeitos dos fármacos
Tecido Adiposo Branco/metabolismo
Tecido Adiposo Branco/patologia
Adiposidade/efeitos dos fármacos
Animais
Glicemia/metabolismo
Peso Corporal/efeitos dos fármacos
Tamanho Celular/efeitos dos fármacos
Dieta Hiperlipídica/efeitos adversos
Ingestão de Energia/efeitos dos fármacos
Expressão Gênica/efeitos dos fármacos
Intolerância à Glucose/tratamento farmacológico
Hiperinsulinismo/tratamento farmacológico
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Obesidade/metabolismo
Obesidade/patologia
Termogênese/efeitos dos fármacos
Proteína Desacopladora 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (PPAR alpha); 0 (PPAR delta); 0 (PPAR-beta); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191365


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[PMID]:29348470
[Au] Autor:Li H; Wu G; Fang Q; Zhang M; Hui X; Sheng B; Wu L; Bao Y; Li P; Xu A; Jia W
[Ad] Endereço:Department of Endocrinology and Metabolism, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Center of Diabetes, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
[Ti] Título:Fibroblast growth factor 21 increases insulin sensitivity through specific expansion of subcutaneous fat.
[So] Source:Nat Commun;9(1):272, 2018 01 18.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Although the pharmacological effects of fibroblast growth factor 21 (FGF21) are well-documented, uncertainty about its role in regulating excessive energy intake remains. Here, we show that FGF21 improves systemic insulin sensitivity by promoting the healthy expansion of subcutaneous adipose tissue (SAT). Serum FGF21 levels positively correlate with the SAT area in insulin-sensitive obese individuals. FGF21 knockout mice (FGF21KO) show less SAT mass and are more insulin-resistant when fed a high-fat diet. Replenishment of recombinant FGF21 to a level equivalent to that in obesity restores SAT mass and reverses insulin resistance in FGF21KO, but not in adipose-specific ßklotho knockout mice. Moreover, transplantation of SAT from wild-type to FGF21KO mice improves insulin sensitivity in the recipients. Mechanistically, circulating FGF21 upregulates adiponectin in SAT, accompanied by an increase of M2 macrophage polarization. We propose that elevated levels of endogenous FGF21 in obesity serve as a defense mechanism to protect against systemic insulin resistance.
[Mh] Termos MeSH primário: Fatores de Crescimento de Fibroblastos/genética
Resistência à Insulina/genética
Obesidade/genética
Gordura Subcutânea/metabolismo
[Mh] Termos MeSH secundário: Adiponectina/metabolismo
Animais
Dieta Hiperlipídica
Fatores de Crescimento de Fibroblastos/sangue
Fatores de Crescimento de Fibroblastos/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Obesidade/sangue
Obesidade/metabolismo
Proteínas Recombinantes/farmacologia
Gordura Subcutânea/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adiponectin); 0 (Recombinant Proteins); 0 (fibroblast growth factor 21); 62031-54-3 (Fibroblast Growth Factors)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02677-9


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[PMID]:29385178
[Au] Autor:Parvaresh Rizi E; Loh TP; Baig S; Chhay V; Huang S; Caleb Quek J; Tai ES; Toh SA; Khoo CM
[Ad] Endereço:Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
[Ti] Título:A high carbohydrate, but not fat or protein meal attenuates postprandial ghrelin, PYY and GLP-1 responses in Chinese men.
[So] Source:PLoS One;13(1):e0191609, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It is known that the macronutrient content of a meal has different impacts on the postprandial satiety and appetite hormonal responses. Whether obesity interacts with such nutrient-dependent responses is not well characterized. We examined the postprandial appetite and satiety hormonal responses after a high-protein (HP), high-carbohydrate (HC), or high-fat (HF) mixed meal. This was a randomized cross-over study of 9 lean insulin-sensitive (mean±SEM HOMA-IR 0.83±0.10) and 9 obese insulin-resistant (HOMA-IR 4.34±0.41) young (age 21-40 years), normoglycaemic Chinese men. We measured fasting and postprandial plasma concentration of glucose, insulin, active glucagon-like peptide-1 (GLP-1), total peptide-YY (PYY), and acyl-ghrelin in response to HP, HF, or HC meals. Overall postprandial plasma insulin response was more robust in the lean compared to obese subjects. The postprandial GLP-1 response after HF or HP meal was higher than HC meal in both lean and obese subjects. In obese subjects, HF meal induced higher response in postprandial PYY compared to HC meal. HP and HF meals also suppressed ghrelin greater compared to HC meal in the obese than lean subjects. In conclusion, a high-protein or high-fat meal induces a more favorable postprandial satiety and appetite hormonal response than a high-carbohydrate meal in obese insulin-resistant subjects.
[Mh] Termos MeSH primário: Carboidratos da Dieta/administração & dosagem
Gorduras na Dieta/administração & dosagem
Proteínas na Dieta/administração & dosagem
Grelina/sangue
Peptídeo 1 Semelhante ao Glucagon/sangue
Peptídeo YY/sangue
[Mh] Termos MeSH secundário: Adulto
Grupo com Ancestrais do Continente Asiático
Glicemia/metabolismo
Estudos Cross-Over
Dieta Hiperlipídica
Dieta Rica em Proteínas
Seres Humanos
Insulina/sangue
Resistência à Insulina
Masculino
Obesidade/sangue
Obesidade/dietoterapia
Período Pós-Prandial/fisiologia
Resposta de Saciedade/fisiologia
Singapura
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Dietary Carbohydrates); 0 (Dietary Fats); 0 (Dietary Proteins); 0 (Ghrelin); 0 (Insulin); 106388-42-5 (Peptide YY); 89750-14-1 (Glucagon-Like Peptide 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191609


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[PMID]:29352300
[Au] Autor:Wang Z; Koonen D; Hofker M; Bao Z
[Ad] Endereço:Department of Geriatrics and Gastroenterology, Huadong Hospital, Shanghai Medical College, Fudan University, Shanghai Key Laboratory of Clinical Geriatric Medicine, Shanghai, P.R. China.
[Ti] Título:5-aminosalicylic acid improves lipid profile in mice fed a high-fat cholesterol diet through its dual effects on intestinal PPARγ and PPARα.
[So] Source:PLoS One;13(1):e0191485, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obesity is associated with a series of metabolic complications, including dyslipidemia and insulin resistance (IR) that lack effective therapies. In recent years, intestinal inflammation has been suggested to contribute to obesity related metabolic syndrome and targeting gut inflammation with 5-ASA improves diet induced IR, however, its role in dyslipidemia is unknown and has never been explored. In the present study, we reported for the first time that administration of 5-ASA for 12 weeks significantly improved lipid profile by repressing plasma triglycerides and free cholesterol levels in mice fed high-fat cholesterol diet (HFC). In addition, liver lipids were significantly reduced by 5-ASA treatment in HFC-fed mice. Mechanistically, anti-inflammatory genes peroxisome proliferator-activated receptor-γ (Pparγ) and M2 marker, such as Mrc1 and Ym1, were remarkably upregulated, while pro-inflammation gene monocyte chemoattractant protein-1 (Mcp-1) were downregulated in small intestine of mice treated by 5-ASA. Further, 5-ASA improved gastrointestinal barrier by increasing the expression of the tight junction marker ZO-1. 5-ASA also enhanced cholesterol translocation by elevating genes expression of Npc1l1 and Abcg5/8. Moreover, mice fed HFC 5-ASA expressed increased Pparα in small intestinal and its target genes function in lipid oxidation and hydrolysis were remarkable elevated. Taken together, we reported a novel role of 5-ASA which may serve as a therapy target intestinal inflammation induced dyslipidemia.
[Mh] Termos MeSH primário: Colesterol na Dieta/administração & dosagem
Dieta Hiperlipídica/efeitos adversos
Intestinos/efeitos dos fármacos
Intestinos/metabolismo
Metabolismo dos Lipídeos/efeitos dos fármacos
Mesalamina/farmacologia
PPAR alfa/metabolismo
PPAR gama/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/farmacologia
Dislipidemias/tratamento farmacológico
Dislipidemias/genética
Dislipidemias/metabolismo
Ácidos Graxos/metabolismo
Hipolipemiantes/farmacologia
Inflamação/tratamento farmacológico
Inflamação/genética
Inflamação/metabolismo
Metabolismo dos Lipídeos/genética
Lipídeos/sangue
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
PPAR gama/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cholesterol, Dietary); 0 (Fatty Acids); 0 (Hypolipidemic Agents); 0 (Lipids); 0 (PPAR alpha); 0 (PPAR gamma); 0 (RNA, Messenger); 4Q81I59GXC (Mesalamine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191485


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[PMID]:29254298
[Au] Autor:Khawar MB; Sheikh N
[Ad] Endereço:Cell and Molecular Biology Laboratory, Department of Zoology, University of the Punjab, Lahore-Pakistan.
[Ti] Título:Alterations in transaminase activity and serum level of leptin and hepcidin induced by high fat diet in albino rats.
[So] Source:J Biol Regul Homeost Agents;31(4):951-956, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Obesity is a commonly growing life-threatening problem of the modern world. The present study was aimed to assess alterations in transaminase levels as well as leptin and hepcidin levels of sera through ELISA after high fat diet consumption for sixteen weeks by albino rats (n=5). Three groups were established: experimental groups 1 and 2 and a control group. Group 1 was fed on a high fat diet having a composition of 33% rat chow +33% sucrose +33% milk powder. Similarly, group 2 was fed with another high fat diet with a mixture of rat chow and milk powder ad libitum. The control group was fed on normal rat chow and water ad libitum. After sixteen weeks, the rats were euthanized and blood was collected for serum separation. Serum levels of alanine aminotransferase showed a positive significant increase (P=0.0325) while a significant negative change (P=0.0006) was noted in aspartate aminotransferase levels in both the experimental groups compared to the control group. Serum leptin levels were found to be increased up to 10.06-fold in Group 1 and 6.11-fold in Group 2 when compared to controls. On the other hand, serum hepcidin levels showed up to 1-fold and 2.59-fold changes in Group 1 and Group 2, respectively, compared to controls. Taken together, from these results it can be concluded that a high fat diet not only disturbs normal metabolism, but it also leads to liver inflammation which is obvious by the changes in transaminase activity as well as leptin and hepcidin levels.
[Mh] Termos MeSH primário: Alanina Transaminase/sangue
Aspartato Aminotransferases/sangue
Gorduras na Dieta/efeitos adversos
Hepcidinas/sangue
Leptina/sangue
Obesidade/genética
[Mh] Termos MeSH secundário: Alanina Transaminase/genética
Animais
Aspartato Aminotransferases/genética
Dieta Hiperlipídica
Expressão Gênica
Hepcidinas/genética
Leptina/genética
Fígado/metabolismo
Fígado/patologia
Masculino
Obesidade/sangue
Obesidade/etiologia
Obesidade/patologia
Ratos
Desmame
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Fats); 0 (Hamp protein, rat); 0 (Hepcidins); 0 (Leptin); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:29293679
[Au] Autor:Bauters D; Bedossa P; Lijnen HR; Hemmeryckx B
[Ad] Endereço:Center for Molecular and Vascular Biology, Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium.
[Ti] Título:Functional role of ADAMTS5 in adiposity and metabolic health.
[So] Source:PLoS One;13(1):e0190595, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies with gene-deficient mice (ADAMTS5-P) revealed that ADAMTS5 (A Disintegrin And Metalloproteinase with Thrombospondin type 1 motifs, member 5) plays a functional role in adiposity and metabolic health. To confirm these observations, we have performed similar studies with an independently generated strain of ADAMTS5 deficient mice (ADAMTS5-J). Upon cold exposure as well as after high-fat diet feeding (diet-induced obesity or DIO model), these knockout (KO) mice developed less subcutaneous and gonadal white adipose tissue (WAT) as compared to their wild-type (WT) littermates (reduction was more pronounced in ADAMTS5-P mice). Enhanced browning of WAT, as monitored by expression of UCP-1 was seen in the ADAMTS5-J KO mice upon cold exposure but not in the DIO model (seen in both conditions with the ADAMTS5-P mice). Brown adipose tissue (BAT) mass was not different between KO and WT ADAMTS5-J mice, either upon cold exposure or in the DIO model (in contrast to the enhanced BAT mass with the ADAMTS5-P mice). Energy expenditure and thermogenesis were not significantly different between KO and WT ADAMTS5-J mice (in contrast to somewhat enhanced levels in ADAMTS5-P mice). Insulin sensitivity was improved in the ADAMTS5-J KO mice, and they were protected against non-alcoholic steatohepatitis in the DIO model (as the ADAMTS5-P mice). These data are thus similar for both strains of KO mice, confirming specificity of the phenotype, but some quantitative and qualitative differences are also observed.
[Mh] Termos MeSH primário: Proteína ADAMTS5/fisiologia
Adiposidade/fisiologia
[Mh] Termos MeSH secundário: Proteína ADAMTS5/genética
Tecido Adiposo Marrom/metabolismo
Animais
Western Blotting
Calorimetria
Temperatura Baixa
Dieta Hiperlipídica
Metabolismo Energético
Regulação da Expressão Gênica
Camundongos
Camundongos Knockout
Termogênese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.4.24.- (ADAMTS5 Protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190595


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[PMID]:29300916
[Au] Autor:Kougias DG; Cortes LR; Moody L; Rhoads S; Pan YX; Juraska JM
[Ad] Endereço:Neuroscience Program, University of Illinois, Champaign, Illinois.
[Ti] Título:Effects of Perinatal Exposure to Phthalates and a High-Fat Diet on Maternal Behavior and Pup Development and Social Play.
[So] Source:Endocrinology;159(2):1088-1105, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Humans are ubiquitously exposed to many phthalates, a class of endocrine-disrupting chemicals commonly used in many consumer goods, and diet, especially fatty food, is presumed to be a major source of exposure. Here, we use a rat model of human prenatal exposure to investigate the potential interactive effects of an environmentally relevant mixture of phthalates and a maternal high-fat diet (HFD). From gestation through postnatal day (P)10, dams consumed the mixture of phthalates (0, 200, or 1000 µg/kg/d) and were fed a control diet or HFD. In males, perinatal exposure to the mixture of phthalates decreased prepubertal body weight and, in a dose-specific manner, periadolescent social play behavior. A dose-specific effect from phthalates with HFD was also seen in increased time alone in females during social play. HFD resulted in dams consuming more calories, having greater gestational weight gain, and licking and nursing their pups more, such that an early postnatal HFD generally increased pup body weight. There also was a tendency for increased oxidative stress markers at P10 within the medial prefrontal cortex of males exposed to the relatively high dose of phthalates and HFD. Effects on gene expression were inconsistent at P10 and P90 in both the medial prefrontal cortex and hypothalamus. Overall, this study demonstrates that phthalates and a maternal HFD only rarely interacted, except in oxidative stress markers in males. Additionally, perinatal exposure to an environmentally relevant mixture of phthalates can have a modest, but lasting, impact on social behaviors in both males and females.
[Mh] Termos MeSH primário: Dieta Hiperlipídica
Crescimento/efeitos dos fármacos
Comportamento Materno/efeitos dos fármacos
Ácidos Ftálicos/toxicidade
Jogos e Brinquedos
Efeitos Tardios da Exposição Pré-Natal
Comportamento Social
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Dieta Hiperlipídica/efeitos adversos
Feminino
Masculino
Fenômenos Fisiológicos da Nutrição Materna
Jogos e Brinquedos/psicologia
Gravidez
Efeitos Tardios da Exposição Pré-Natal/fisiopatologia
Efeitos Tardios da Exposição Pré-Natal/psicologia
Ratos
Ratos Long-Evans
Maturidade Sexual/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Phthalic Acids); 6O7F7IX66E (phthalic acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180105
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03047



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