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  1. Article ; Online: Small intestinal CaSR-dependent and CaSR-independent protein sensing regulates feeding and glucose tolerance in rats.

    Li, Rosa J W / Barros, Daniel R / Kuah, Rachel / Lim, Yu-Mi / Gao, Anna / Beaudry, Jacqueline L / Zhang, Song-Yang / Lam, Tony K T

    Nature metabolism

    2024  Volume 6, Issue 1, Page(s) 39–49

    Abstract: Proteins activate small intestinal calcium sensing receptor (CaSR) and/or peptide transporter 1 (PepT1) to increase hormone ... ...

    Abstract Proteins activate small intestinal calcium sensing receptor (CaSR) and/or peptide transporter 1 (PepT1) to increase hormone secretion
    MeSH term(s) Animals ; Male ; Rats ; Caseins/metabolism ; Gastrointestinal Hormones/metabolism ; Glucose/metabolism ; Intestine, Small/metabolism ; Receptors, Calcium-Sensing/metabolism
    Chemical Substances Caseins ; Gastrointestinal Hormones ; Glucose (IY9XDZ35W2) ; Receptors, Calcium-Sensing ; extracellular calcium cation-sensing receptor, rat
    Language English
    Publishing date 2024-01-02
    Publishing country Germany
    Document type Journal Article
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-023-00942-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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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
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    Uc I Zs.108: Show issues Location:
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  3. Article ; Online: Interaction of glucose sensing and leptin action in the brain.

    Li, Rosa J W / Zhang, Song-Yang / Lam, Tony K T

    Molecular metabolism

    2020  Volume 39, Page(s) 101011

    Abstract: Background: In response to energy abundant or deprived conditions, nutrients and hormones activate hypothalamic pathways to maintain energy and glucose homeostasis. The underlying CNS mechanisms, however, remain elusive in rodents and humans.: Scope ... ...

    Abstract Background: In response to energy abundant or deprived conditions, nutrients and hormones activate hypothalamic pathways to maintain energy and glucose homeostasis. The underlying CNS mechanisms, however, remain elusive in rodents and humans.
    Scope of review: Here, we first discuss brain glucose sensing mechanisms in the presence of a rise or fall of plasma glucose levels, and highlight defects in hypothalamic glucose sensing disrupt in vivo glucose homeostasis in high-fat fed, obese, and/or diabetic conditions. Second, we discuss brain leptin signalling pathways that impact glucose homeostasis in glucose-deprived and excessed conditions, and propose that leptin enhances hypothalamic glucose sensing and restores glucose homeostasis in short-term high-fat fed and/or uncontrolled diabetic conditions.
    Major conclusions: In conclusion, we believe basic studies that investigate the interaction of glucose sensing and leptin action in the brain will address the translational impact of hypothalamic glucose sensing in diabetes and obesity.
    MeSH term(s) Animals ; Brain/physiology ; Disease Susceptibility ; Energy Metabolism ; Glucose/metabolism ; Homeostasis ; Humans ; Insulin/metabolism ; Leptin/metabolism ; Neurons/metabolism ; Signal Transduction
    Chemical Substances Insulin ; Leptin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2020-05-13
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2708735-9
    ISSN 2212-8778 ; 2212-8778
    ISSN (online) 2212-8778
    ISSN 2212-8778
    DOI 10.1016/j.molmet.2020.101011
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  4. 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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  5. Article ; Online: FXR in the dorsal vagal complex is sufficient and necessary for upper small intestinal microbiome-mediated changes of TCDCA to alter insulin action in rats.

    Zhang, Song-Yang / Li, Rosa J W / Lim, Yu-Mi / Batchuluun, Battsetseg / Liu, Huiying / Waise, T M Zaved / Lam, Tony K T

    Gut

    2020  Volume 70, Issue 9, Page(s) 1675–1683

    Abstract: Objective: Conjugated bile acids are metabolised by upper small intestinal microbiota, and serum levels of taurine-conjugated bile acids are elevated and correlated with insulin resistance in people with type 2 diabetes. However, whether changes in ... ...

    Abstract Objective: Conjugated bile acids are metabolised by upper small intestinal microbiota, and serum levels of taurine-conjugated bile acids are elevated and correlated with insulin resistance in people with type 2 diabetes. However, whether changes in taurine-conjugated bile acids are necessary for small intestinal microbiome to alter insulin action remain unknown.
    Design: We evaluated circulating and specifically brain insulin action using the pancreatic-euglycaemic clamps in high-fat (HF) versus chow fed rats with or without upper small intestinal healthy microbiome transplant. Chemical and molecular gain/loss-of-function experiments targeting specific taurine-conjugated bile acid-induced changes of farnesoid X receptor (FXR) in the brain were performed in parallel.
    Results: We found that short-term HF feeding increased the levels of taurochenodeoxycholic acid (TCDCA, an FXR ligand) in the upper small intestine, ileum, plasma and dorsal vagal complex (DVC) of the brain. Transplantation of upper small intestinal healthy microbiome into the upper small intestine of HF rats not only reversed the rise of TCDCA in all reported tissues but also enhanced the ability of either circulating hyperinsulinaemia or DVC insulin action to lower glucose production. Further, DVC infusion of TCDCA or FXR agonist negated the enhancement of insulin action, while genetic knockdown or chemical inhibition of FXR in the DVC of HF rats reversed insulin resistance.
    Conclusion: Our findings indicate that FXR in the DVC is sufficient and necessary for upper small intestinal microbiome-mediated changes of TCDCA to alter insulin action in rats, and highlight a previously unappreciated TCDCA-FXR axis linking gut microbiome and host insulin action.
    MeSH term(s) Animals ; Brain/metabolism ; Brain Chemistry ; Brain Stem/metabolism ; Brain Stem/physiology ; Diet, High-Fat ; Fecal Microbiota Transplantation ; Gastrointestinal Microbiome/physiology ; Gene Knockdown Techniques ; Glucose Clamp Technique ; Insulin Resistance/physiology ; Intestine, Small/metabolism ; Intestine, Small/microbiology ; Rats ; Receptors, Cytoplasmic and Nuclear/analysis ; Receptors, Cytoplasmic and Nuclear/metabolism ; Taurochenodeoxycholic Acid/analysis ; Taurochenodeoxycholic Acid/metabolism
    Chemical Substances Receptors, Cytoplasmic and Nuclear ; farnesoid X-activated receptor (0C5V0MRU6P) ; Taurochenodeoxycholic Acid (516-35-8)
    Language English
    Publishing date 2020-10-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2020-321757
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    Zs.A 160: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  6. Article ; Online: Nutrient infusion in the dorsal vagal complex controls hepatic lipid and glucose metabolism in rats.

    Li, Rosa J W / Batchuluun, Battsetseg / Zhang, Song-Yang / Abraham, Mona A / Wang, Beini / Lim, Yu-Mi / Yue, Jessica T Y / Lam, Tony K T

    iScience

    2021  Volume 24, Issue 4, Page(s) 102366

    Abstract: Hypothalamic regulation of lipid and glucose homeostasis is emerging, but whether the dorsal vagal complex (DVC) senses nutrients and regulates hepatic nutrient metabolism remains unclear. Here, we found in rats DVC oleic acid infusion suppressed hepatic ...

    Abstract Hypothalamic regulation of lipid and glucose homeostasis is emerging, but whether the dorsal vagal complex (DVC) senses nutrients and regulates hepatic nutrient metabolism remains unclear. Here, we found in rats DVC oleic acid infusion suppressed hepatic secretion of triglyceride-rich very-low-density lipoprotein (VLDL-TG), which was disrupted by inhibiting DVC long-chain fatty acyl-CoA synthetase that in parallel disturbed lipid homeostasis during intravenous lipid infusion. DVC glucose infusion elevated local glucose levels similarly as intravenous glucose infusion and suppressed hepatic glucose production. This was independent of lactate metabolism as inhibiting lactate dehydrogenase failed to disrupt glucose sensing and neither could DVC lactate infusion recapitulate glucose effect. DVC oleic acid and glucose infusion failed to lower VLDL-TG secretion and glucose production in high-fat fed rats, while inhibiting DVC farnesoid X receptor enhanced oleic acid but not glucose sensing. Thus, an impairment of DVC nutrient sensing may lead to the disruption of lipid and glucose homeostasis in metabolic syndrome.
    Language English
    Publishing date 2021-03-26
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2021.102366
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