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  1. Article ; Online: Acute Activation of GFRAL in the Area Postrema Contributes to Glucose Regulation Independent of Weight.

    Zhang, Song-Yang / Danaei, Zahra / Bruce, Kyla / Chiu, Jennifer F M / Lam, Tony K T

    Diabetes

    2023  Volume 73, Issue 3, Page(s) 426–433

    MeSH term(s) Rats ; Animals ; Area Postrema/metabolism ; Glucose/metabolism ; Metformin/pharmacology ; Brain ; Insulins/metabolism
    Chemical Substances Glucose (IY9XDZ35W2) ; Metformin (9100L32L2N) ; Insulins
    Language English
    Publishing date 2023-12-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/db23-0705
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.175: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: A glucose-sensing mechanism with glucose transporter 1 and pyruvate kinase in the area postrema regulates hepatic glucose production in rats.

    Li, Rosa J W / Chiu, Jennifer F M / Bruce, Kyla / Zhang, Song-Yang / Barros, Daniel R / Yue, Jessica T Y / Lam, Tony K T

    The Journal of biological chemistry

    2023  Volume 299, Issue 5, Page(s) 104633

    Abstract: The area postrema (AP) of the brain is exposed to circulating metabolites and hormones. However, whether AP detects glucose changes to exert biological responses remains unknown. Its neighboring nuclei, the nucleus tractus solitarius (NTS), responds to ... ...

    Abstract The area postrema (AP) of the brain is exposed to circulating metabolites and hormones. However, whether AP detects glucose changes to exert biological responses remains unknown. Its neighboring nuclei, the nucleus tractus solitarius (NTS), responds to acute glucose infusion by inhibiting hepatic glucose production, but the mechanism also remains elusive. Herein, we characterized AP and NTS glucose-sensing mechanisms. Infusion of glucose into the AP, like the NTS, of chow rats suppressed glucose production during the pancreatic (basal insulin)-euglycemic clamps. Glucose transporter 1 or pyruvate kinase lentiviral-mediated knockdown in the AP negated AP glucose infusion to lower glucose production, while the glucoregulatory effect of NTS glucose infusion was also negated by knocking down glucose transporter 1 or pyruvate kinase in the NTS. Furthermore, we determined that high-fat (HF) feeding disrupts glucose infusion to lower glucose production in association with a modest reduction in the expression of glucose transporter 1, but not pyruvate kinase, in the AP and NTS. However, pyruvate dehydrogenase activator dichloroacetate infusion into the AP or NTS that enhanced downstream pyruvate metabolism and recapitulated the glucoregulatory effect of glucose in chow rats still failed to lower glucose production in HF rats. We discovered that a glucose transporter 1- and pyruvate kinase-dependent glucose-sensing mechanism in the AP (as well as the NTS) lowers glucose production in chow rats and that HF disrupts the glucose-sensing mechanism that is downstream of pyruvate metabolism in the AP and NTS. These findings highlight the role of AP and NTS in mediating glucose to regulate hepatic glucose production.
    MeSH term(s) Animals ; Rats ; Area Postrema/metabolism ; Glucose/metabolism ; Glucose Transporter Type 1/genetics ; Glucose Transporter Type 1/metabolism ; Solitary Nucleus/metabolism ; Pyruvate Kinase/metabolism ; Gene Knockdown Techniques ; Lentivirus/metabolism ; Pyruvic Acid/metabolism ; Male ; Diet, High-Fat
    Chemical Substances Glucose (IY9XDZ35W2) ; Glucose Transporter Type 1 ; Pyruvate Kinase (EC 2.7.1.40) ; Pyruvic Acid (8558G7RUTR)
    Language English
    Publishing date 2023-03-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2023.104633
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.108: Show issues Location:
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  3. Article ; Online: Metformin triggers a kidney GDF15-dependent area postrema axis to regulate food intake and body weight.

    Zhang, Song-Yang / Bruce, Kyla / Danaei, Zahra / Li, Rosa J W / Barros, Daniel R / Kuah, Rachel / Lim, Yu-Mi / Mariani, Laura H / Cherney, David Z / Chiu, Jennifer F M / Reich, Heather N / Lam, Tony K T

    Cell metabolism

    2023  Volume 35, Issue 5, Page(s) 875–886.e5

    Abstract: Metformin, the most widely prescribed medication for obesity-associated type 2 diabetes (T2D), lowers plasma glucose levels, food intake, and body weight in rodents and humans, but the mechanistic site(s) of action remain elusive. Metformin increases ... ...

    Abstract Metformin, the most widely prescribed medication for obesity-associated type 2 diabetes (T2D), lowers plasma glucose levels, food intake, and body weight in rodents and humans, but the mechanistic site(s) of action remain elusive. Metformin increases plasma growth/differentiation factor 15 (GDF15) levels to regulate energy balance, while GDF15 administration activates GDNF family receptor α-like (GFRAL) that is highly expressed in the area postrema (AP) and the nucleus of the solitary tract (NTS) of the hindbrain to lower food intake and body weight. However, the tissue-specific contribution of plasma GDF15 levels after metformin treatment is still under debate. Here, we found that metformin increased plasma GDF15 levels in high-fat (HF) fed male rats through the upregulation of GDF15 synthesis in the kidney. Importantly, the kidney-specific knockdown of GDF15 expression as well as the AP-specific knockdown of GFRAL expression negated the ability of metformin to lower food intake and body weight gain. Taken together, we unveil the kidney as a target of metformin to regulate energy homeostasis through a kidney GDF15-dependent AP axis.
    MeSH term(s) Humans ; Male ; Rats ; Animals ; Metformin/pharmacology ; Area Postrema/metabolism ; Weight Loss ; Diabetes Mellitus, Type 2/metabolism ; Body Weight/physiology ; Eating ; Kidney/metabolism ; Growth Differentiation Factor 15/metabolism
    Chemical Substances Metformin (9100L32L2N) ; GDF15 protein, human ; Growth Differentiation Factor 15
    Language English
    Publishing date 2023-04-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2023.03.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6169: Show issues Location:
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