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  1. Article ; Online: Estradiol Protects Female ApoE KO Mice against Western-Diet-Induced Non-Alcoholic Steatohepatitis

    Layanne C. C. Araujo / Alessandra G. Cruz / Felipe N. Camargo / Felipe G. Sucupira / Gabriela V. Moreira / Sandro L. Matos / Andressa G. Amaral / Gilson Masahiro Murata / Carla R. O. Carvalho / Joao Paulo Camporez

    International Journal of Molecular Sciences, Vol 24, Iss 9845, p

    2023  Volume 9845

    Abstract: The prevalence of non-alcoholic fatty liver disease (NAFLD) and its severe form, non-alcoholic steatohepatitis (NASH), is higher in men than in women of reproductive age, and postmenopausal women are especially susceptible to developing the disease. Aim: ...

    Abstract The prevalence of non-alcoholic fatty liver disease (NAFLD) and its severe form, non-alcoholic steatohepatitis (NASH), is higher in men than in women of reproductive age, and postmenopausal women are especially susceptible to developing the disease. Aim: we evaluated if female apolipoprotein E (ApoE) KO mice were protected against Western-diet (WD)-induced NASH. Methods: Female ovariectomized (OVX) ApoE KO mice or sham-operated (SHAM) mice were fed either a WD or a regular chow (RC) for 7 weeks. Additionally, OVX mice fed a WD were treated with either estradiol (OVX + E2) or vehicle (OVX). Results: Whole-body fat, plasma glucose, and plasma insulin were increased and associated with increased glucose intolerance in OVX mice fed a WD (OVX + WD). Plasma and hepatic triglycerides, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) hepatic enzymes were also increased in the plasma of OVX + WD group, which was associated with hepatic fibrosis and inflammation. Estradiol replacement in OVX mice reduced body weight, body fat, glycemia, and plasma insulin associated with reduced glucose intolerance. Treatment also reduced hepatic triglycerides, ALT, AST, hepatic fibrosis, and inflammation in OVX mice. Conclusions: These data support the hypothesis that estradiol protects OVX ApoE KO mice from NASH and glucose intolerance.
    Keywords estradiol ; NASH ; Western diet ; ovariectomy ; female ApoE KO mice ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 630
    Language English
    Publishing date 2023-06-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Evaluation of Hepatic Steatosis in Rodents by Time-Domain Nuclear Magnetic Resonance

    João A.B. Pedroso / João Paulo Camporez / Luciana T. Belpiede / Rafaela S. Pinto / José Cipolla-Neto / Jose Donato

    Diagnostics, Vol 9, Iss 4, p

    2019  Volume 198

    Abstract: Devices that analyze body composition of rodents by time-domain nuclear magnetic resonance (TD-NMR) are becoming popular in research centers that study metabolism. Theoretically, TD-NMR devices can also evaluate lipid content in isolated tissues. However, ...

    Abstract Devices that analyze body composition of rodents by time-domain nuclear magnetic resonance (TD-NMR) are becoming popular in research centers that study metabolism. Theoretically, TD-NMR devices can also evaluate lipid content in isolated tissues. However, the accuracy of TD-NMR to determine hepatic steatosis in the liver of small laboratory animals has not been evaluated in detail. We observed that TD-NMR was able to detect increased lipid content in the liver of rats consuming high-fat diet (HFD) for 12 weeks and in genetically obese ( Lep ob/ob and Lepr db/db ) mice. The lipid content determined by TD-NMR showed a positive correlation with triglyceride content measured by colorimetric assays. In contrast, TD-NMR did not detect hepatic steatosis in C57BL/6 mice consuming HFD for 4 or 12 weeks, despite their obesity and increased liver triglyceride content. These findings indicate that tissue mass and the severity of hepatic steatosis affect the sensitivity of TD-NMR to detect liver lipid content.
    Keywords obesity ; hepatic steatosis ; liver ; Medicine (General) ; R5-920
    Language English
    Publishing date 2019-11-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Genetic Ablation of miR-33 Increases Food Intake, Enhances Adipose Tissue Expansion, and Promotes Obesity and Insulin Resistance

    Nathan L. Price / Abhishek K. Singh / Noemi Rotllan / Leigh Goedeke / Allison Wing / Alberto Canfrán-Duque / Alberto Diaz-Ruiz / Elisa Araldi / Ángel Baldán / Joao-Paulo Camporez / Yajaira Suárez / Matthew S. Rodeheffer / Gerald I. Shulman / Rafael de Cabo / Carlos Fernández-Hernando

    Cell Reports, Vol 22, Iss 8, Pp 2133-

    2018  Volume 2145

    Abstract: Summary: While therapeutic modulation of miRNAs provides a promising approach for numerous diseases, the promiscuous nature of miRNAs raises concern over detrimental off-target effects. miR-33 has emerged as a likely target for treatment of ... ...

    Abstract Summary: While therapeutic modulation of miRNAs provides a promising approach for numerous diseases, the promiscuous nature of miRNAs raises concern over detrimental off-target effects. miR-33 has emerged as a likely target for treatment of cardiovascular diseases. However, the deleterious effects of long-term anti-miR-33 therapies and predisposition of miR-33−/− mice to obesity and metabolic dysfunction exemplify the possible pitfalls of miRNA-based therapies. Our work provides an in-depth characterization of miR-33−/− mice and explores the mechanisms by which loss of miR-33 promotes insulin resistance in key metabolic tissues. Contrary to previous reports, our data do not support a direct role for SREBP-1-mediated lipid synthesis in promoting these effects. Alternatively, in adipose tissue of miR-33−/− mice, we observe increased pre-adipocyte proliferation, enhanced lipid uptake, and impaired lipolysis. Moreover, we demonstrate that the driving force behind these abnormalities is increased food intake, which can be prevented by pair feeding with wild-type animals.
    Keywords miR-33 ; obesity ; insulin-resistance ; food-consumption ; metabolism ; micro-RNA ; Biology (General) ; QH301-705.5
    Subject code 616
    Language English
    Publishing date 2018-02-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Absence of Carbohydrate Response Element Binding Protein in Adipocytes Causes Systemic Insulin Resistance and Impairs Glucose Transport

    Archana Vijayakumar / Pratik Aryal / Jennifer Wen / Ismail Syed / Reema P. Vazirani / Pedro M. Moraes-Vieira / Joao Paulo Camporez / Molly R. Gallop / Rachel J. Perry / Odile D. Peroni / Gerald I. Shulman / Alan Saghatelian / Timothy E. McGraw / Barbara B. Kahn

    Cell Reports, Vol 21, Iss 4, Pp 1021-

    2017  Volume 1035

    Abstract: Summary: Lower adipose-ChREBP and de novo lipogenesis (DNL) are associated with insulin resistance in humans. Here, we generated adipose-specific ChREBP knockout (AdChREBP KO) mice with negligible sucrose-induced DNL in adipose tissue (AT). Chow-fed ... ...

    Abstract Summary: Lower adipose-ChREBP and de novo lipogenesis (DNL) are associated with insulin resistance in humans. Here, we generated adipose-specific ChREBP knockout (AdChREBP KO) mice with negligible sucrose-induced DNL in adipose tissue (AT). Chow-fed AdChREBP KO mice are insulin resistant with impaired insulin action in the liver, muscle, and AT and increased AT inflammation. HFD-fed AdChREBP KO mice are also more insulin resistant than controls. Surprisingly, adipocytes lacking ChREBP display a cell-autonomous reduction in insulin-stimulated glucose transport that is mediated by impaired Glut4 translocation and exocytosis, not lower Glut4 levels. AdChREBP KO mice have lower levels of palmitic acid esters of hydroxy stearic acids (PAHSAs) in serum, and AT. 9-PAHSA supplementation completely rescues their insulin resistance and AT inflammation. 9-PAHSA also normalizes impaired glucose transport and Glut4 exocytosis in ChREBP KO adipocytes. Thus, loss of adipose-ChREBP is sufficient to cause insulin resistance, potentially by regulating AT glucose transport and flux through specific lipogenic pathways. : ChREBP expression in fat strongly correlates with insulin sensitivity in people. Vijayakumar et al. demonstrate that fat-specific knockout of ChREBP in mice is sufficient to cause insulin resistance and cell-autonomous impairments in glucose transport and Glut4 trafficking, potentially by altering substrate flux through specific lipogenic pathways. Keywords: adipose-carbohydrate response element binding protein, ChREBP, de novo lipogenesis, systemic insulin resistance, glucose transport, adipose tissue inflammation, palmitic acid hydroxy stearic acid, PAHSA, Glut4 trafficking
    Keywords Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2017-10-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: DHEA supplementation in ovariectomized rats reduces impaired glucose-stimulated insulin secretion induced by a high-fat diet

    Katherine Veras / Felipe Natali Almeida / Renato Tadeu Nachbar / Daniel Simões de Jesus / João Paulo Camporez / Ângelo Rafael Carpinelli / Julia H. Goedecke / Carla Roberta de Oliveira Carvalho

    FEBS Open Bio, Vol 4, Iss C, Pp 141-

    2014  Volume 146

    Abstract: Dehydroepiandrosterone (DHEA) and the dehydroepiandrosterone sulfate (DHEA-S) are steroids produced mainly by the adrenal cortex. There is evidence from both human and animal models suggesting beneficial effects of these steroids for obesity, diabetes ... ...

    Abstract Dehydroepiandrosterone (DHEA) and the dehydroepiandrosterone sulfate (DHEA-S) are steroids produced mainly by the adrenal cortex. There is evidence from both human and animal models suggesting beneficial effects of these steroids for obesity, diabetes mellitus, hypertension, and osteoporosis, conditions associated with the post-menopausal period. Accordingly, we hypothesized that DHEA supplementation in ovariectomized (OVX) female rats fed a high-fat diet would maintain glucose-induced insulin secretion (GSIS) and pancreatic islet function. OVX resulted in a 30% enlargement of the pancreatic islets area compared to the control rats, which was accompanied by a 50% reduction in the phosphorylation of AKT protein in the pancreatic islets. However, a short-term high-fat diet induced insulin resistance, accompanied by impaired GSIS in isolated pancreatic islets. These effects were reversed by DHEA treatment, with improved insulin sensitivity to levels similar to the control group, and with increased serine phosphorylation of the AKT protein. These data confirm the protective effect of DHEA on the endocrine pancreas in a situation of diet-induced overweight and low estrogen concentrations, a phenotype similar to that of the post-menopausal period.
    Keywords High fat diet ; Menopause ; Pancreatic islets ; Insulin sensitivity ; Insulin secretion ; p-Akt/Akt ; Biology (General) ; QH301-705.5
    Subject code 500
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Wiley
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article: Selective Chemical Inhibition of PGC-1α Gluconeogenic Activity Ameliorates Type 2 Diabetes

    Sharabi, Kfir / Amy K. Rines / Clint D.J. Tavares / Gerald I. Shulman / Hua Lin / Jaemin Lee / Joao Paulo Camporez / John E. Dominy / José Perez / Joshua A. Bittker / Marc Hickey / Mark P. Jedrychowski / Melissa Bennion / Michelle Palmer / Partha P. Nag / Patrick R. Griffin / Pere Puigserver / Rachel J. Perry / Roger Schilling /
    Steve P. Gygi / Stuart L. Schreiber / Theodore M. Kamenecka / Umut Ozcan

    Cell. 2017 Mar. 23, v. 169, no. 1

    2017  

    Abstract: Type 2 diabetes (T2D) is a worldwide epidemic with a medical need for additional targeted therapies. Suppression of hepatic glucose production (HGP) effectively ameliorates diabetes and can be exploited for its treatment. We hypothesized that targeting ... ...

    Abstract Type 2 diabetes (T2D) is a worldwide epidemic with a medical need for additional targeted therapies. Suppression of hepatic glucose production (HGP) effectively ameliorates diabetes and can be exploited for its treatment. We hypothesized that targeting PGC-1α acetylation in the liver, a chemical modification known to inhibit hepatic gluconeogenesis, could be potentially used for treatment of T2D. Thus, we designed a high-throughput chemical screen platform to quantify PGC-1α acetylation in cells and identified small molecules that increase PGC-1α acetylation, suppress gluconeogenic gene expression, and reduce glucose production in hepatocytes. On the basis of potency and bioavailability, we selected a small molecule, SR-18292, that reduces blood glucose, strongly increases hepatic insulin sensitivity, and improves glucose homeostasis in dietary and genetic mouse models of T2D. These studies have important implications for understanding the regulatory mechanisms of glucose metabolism and treatment of T2D.
    Keywords acetylation ; animal models ; bioavailability ; blood glucose ; gene expression ; gluconeogenesis ; glucose ; hepatocytes ; homeostasis ; insulin resistance ; liver ; noninsulin-dependent diabetes mellitus
    Language English
    Dates of publication 2017-0323
    Size p. 148-160.e15.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2017.03.001
    Database NAL-Catalogue (AGRICOLA)

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