White Adipose Tissue

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Timothy J Bartness - One of the best experts on this subject based on the ideXlab platform.

J P Dulor - One of the best experts on this subject based on the ideXlab platform.

  • expression of specific White Adipose Tissue genes in denervation induced skeletal muscle fatty degeneration
    FEBS Letters, 1998
    Co-Authors: J P Dulor, Brigitte Cambon, Pierre Vigneron, Yves Reyne, Jean Nougues, Louis Casteilla, Francis Bacou
    Abstract:

    Denervation of skeletal muscle results in rapid atrophy with loss of contractile mass and/or progressive degeneration of muscle fibers which are replaced to a greater or lesser degree by connective and fatty Tissues. In this study, we show that denervated rabbit muscles are transformed into a White Adipose Tissue, depending on their fiber types. This Tissue does express LPL, G3PDH and particularly the ob gene, a White Adipose Tissue-specific marker, and does not express the brown Adipose Tissue molecular marker UCP1 mRNA.

Masatsugu Horiuchi - One of the best experts on this subject based on the ideXlab platform.

  • Irbesartan increased PPARγ activity in vivo in White Adipose Tissue of atherosclerotic mice and improved Adipose Tissue dysfunction.
    Biochemical and biophysical research communications, 2011
    Co-Authors: Masaru Iwai, Harumi Kan-no, Izumi Senba, Hirotomo Nakaoka, Tomozo Moritani, Masatsugu Horiuchi
    Abstract:

    Research highlights: {yields} Atherosclerotic apolipoprotein E-deficient (ApoEKO) mice were treated with irbesartan. {yields} Irbesartan decreased White Adipose Tissue weight without affecting body weight. {yields} DNA-binding for PPAR{gamma} was increased in White Adipose Tissue in vivo by irbesartan. {yields} Irbesartan increased adipocyte number in White Adipose Tissue. {yields} Irbesatan increased the expression of adiponectin and leptin in White Adipose Tissue. -- Abstract: The effect of the PPAR{gamma} agonistic action of an AT{sub 1} receptor blocker, irbesartan, on Adipose Tissue dysfunction was explored using atherosclerotic model mice. Adult male apolipoprotein E-deficient (ApoEKO) mice at 9 weeks of age were treated with a high-cholesterol diet (HCD) with or without irbesartan at a dose of 50 mg/kg/day for 4 weeks. The weight of epididymal and retroperitoneal Adipose Tissue was decreased by irbesartan without changing food intake or body weight. Treatment with irbesartan increased the expression of PPAR{gamma} in White Adipose Tissue and the DNA-binding activity of PPAR{gamma} in nuclear extract prepared from Adipose Tissue. The expression of adiponectin, leptin and insulin receptor was also increased by irbesartan. These results suggest that irbesartan induced activation of PPAR{gamma} and improved Adipose Tissue dysfunction including insulin resistance.

  • Nifedipine, a Calcium-Channel Blocker, Attenuated Glucose Intolerance and White Adipose Tissue Dysfunction in Type 2 Diabetic KK-Ay Mice
    American journal of hypertension, 2010
    Co-Authors: Masaru Iwai, Harumi Kan-no, Shinji Inaba, Izumi Senba, Hisako Sone, Hirotomo Nakaoka, Masatsugu Horiuchi
    Abstract:

    BACKGROUND To explore the metabolic actions of nifedipine on diabetes, we examined glucose intolerance and White Adipose Tissue changes in type 2 diabetic KK-A y mice. METHODS Male KK-A y mice were treated with nifedipine (1.5 mg/kg/day in lab chow) for 5 weeks, which did not affect blood pressure or feeding of KK-A y mice. RESULTS After treatment with nifedipine, body weight tended to decrease and the weight of White Adipose Tissue was reduced. Without food restriction, nifedipine decreased plasma insulin level, while plasma glucose level tended to decrease. In oral glucose tolerance test, nifedipine suppressed the increase in glucose level after a glucose load without affecting plasma insulin concentration. Nifedipine also improved the result of insulin tolerance test. In White Adipose Tissue, nifedipine increased adipocyte number and the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and adipocyte fatty acid-binding protein related to adipocyte differentiation. In addition, expression of adiponectin, insulin receptor, insulin receptor substrate-1, and glucose transporter type-4 was also increased by nifedipine. Nifedipine also increased the expression of NO synthase in White Adipose Tissue. Nifedipine did not affect expression of angiotensin II type 1 (AT 1 ) and type 2 (AT 2 ) receptors in White Adipose Tissue. Such changes in White Adipose Tissue were apparent in retroperitoneal Adipose Tissue. Nifedipine did not change the expression of angiotensin receptors, renin receptor, and angiotensinogen in White Adipose Tissue. Moreover, nifedipine attenuated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and increased superoxide dismutase (SOD) activity in White Adipose Tissue. CONCLUSION These results suggest that nifedipine can enhance insulin sensitivity and reduce White Adipose Tissue, possibly related to stimulation of adipocyte differentiation.

Julian L. Griffin - One of the best experts on this subject based on the ideXlab platform.

  • inorganic nitrate promotes the browning of White Adipose Tissue through the nitrate nitrite nitric oxide pathway
    Diabetes, 2015
    Co-Authors: Lee D. Roberts, Julian L. Griffin, Tom Ashmore, Aleksandra O Kotwica, Steven A Murfitt, Bernadette O Fernandez, Martin Feelisch, Andrew J Murray
    Abstract:

    Inorganic nitrate was once considered an oxidation end product of nitric oxide metabolism with little biological activity. However, recent studies have demonstrated that dietary nitrate can modulate mitochondrial function in man and is effective in reversing features of the metabolic syndrome in mice. Using a combined histological, metabolomics, and transcriptional and protein analysis approach, we mechanistically defined that nitrate not only increases the expression of thermogenic genes in brown Adipose Tissue but also induces the expression of brown adipocyte–specific genes and proteins in White Adipose Tissue, substantially increasing oxygen consumption and fatty acid β-oxidation in adipocytes. Nitrate induces these phenotypic changes through a mechanism distinct from known physiological small molecule activators of browning, the recently identified nitrate-nitrite-nitric oxide pathway. The nitrate-induced browning effect was enhanced in hypoxia, a serious comorbidity affecting White Adipose Tissue in obese individuals, and corrected impaired brown adipocyte–specific gene expression in White Adipose Tissue in a murine model of obesity. Because resulting beige/brite cells exhibit antiobesity and antidiabetic effects, nitrate may be an effective means of inducing the browning response in Adipose Tissue to treat the metabolic syndrome.

  • Methods for performing lipidomics in White Adipose Tissue.
    Methods in enzymology, 2014
    Co-Authors: Lee D. Roberts, James A. West, Antonio Vidal-puig, Julian L. Griffin
    Abstract:

    Abstract Lipid metabolism is central to the function of White Adipose Tissue, with the Tissue having a central role in storing triacylglycerides following feeding and releasing free fatty acids and monoacylglycerides during periods of fasting. In addition, lipid species have been suggested to play a role in lipotoxicity and as signaling molecules during Adipose Tissue inflammation. This chapter details how mass spectrometry (MS) can be used to profile a range of lipid species found in Adipose Tissue. The initial step required in any MS-based approach is to extract the lipid fraction from the Tissue. We detail one commonly used method based on the Folch extraction procedure. The total fatty acid composition of the lipid fraction can readily be defined using gas chromatography–MS, and we provide a method routinely used for rodent and human Adipose Tissue samples. However, such approaches do not provide insight into what lipid classes the various fatty acids are associated with. To better understand the global lipid profile of the Tissue, we provide a general-purpose liquid chromatography–MS-based approach useful for processing phospholipids, free fatty acids, and triacylglycerides. In addition, we provide a method for profiling eicosanoids, a class of important lipid-signaling molecules, which have been implicated in White Adipose Tissue inflammation in rodent models of obesity, insulin resistance, and type 2 diabetes.

Rodrigo P A Barros - One of the best experts on this subject based on the ideXlab platform.