2024
A kidney-hypothalamus axis promotes compensatory glucose production in response to glycosuria
Faniyan T, Zhang X, Morgan D, Robles J, Bathina S, Brookes P, Rahmouni K, Perry R, Chhabra K. A kidney-hypothalamus axis promotes compensatory glucose production in response to glycosuria. ELife 2024, 12 DOI: 10.7554/elife.91540.4.Peer-Reviewed Original ResearchGlucose productionEndogenous glucose productionReabsorption of nutrientsLoss of glucoseHypothalamic-pituitary-adrenal axisNormal energy supplyProteomic analysisCompensatory increaseAfferent renal nervesAfferent renal denervationPlasma proteomic analysisDefense mechanismsAcute phase proteinsRenal denervationKO miceSGLT2 inhibitorsKnockout miceRenal nervesAfferent nervesEfficiency of drugsBody's defense mechanismsGlycosuriaGlucosePhase proteinsTreat hyperglycemiaA kidney-hypothalamus axis promotes compensatory glucose production in response to glycosuria
Faniyan T, Zhang X, Morgan D, Robles J, Bathina S, Brookes P, Rahmouni K, Perry R, Chhabra K. A kidney-hypothalamus axis promotes compensatory glucose production in response to glycosuria. ELife 2024, 12: rp91540. PMID: 39082939, PMCID: PMC11290820, DOI: 10.7554/elife.91540.Peer-Reviewed Original ResearchConceptsGlucose productionEndogenous glucose productionReabsorption of nutrientsLoss of glucoseHypothalamic-pituitary-adrenal axisNormal energy supplyProteomic analysisCompensatory increaseAfferent renal nervesAfferent renal denervationPlasma proteomic analysisDefense mechanismsAcute phase proteinsRenal denervationKO miceSGLT2 inhibitorsKnockout miceRenal nervesAfferent nervesEfficiency of drugsBody's defense mechanismsGlycosuriaGlucosePhase proteinsTreat hyperglycemia
2023
THU123 Knockout Of Renal Glut2 Gene Activates The Hypothalamic-pituitary-adrenal Axis To Increase Glucose Production In Mice
Faniyan T, Robles J, Zhang X, Bathina S, Brookes P, Perry R, Chhabra K. THU123 Knockout Of Renal Glut2 Gene Activates The Hypothalamic-pituitary-adrenal Axis To Increase Glucose Production In Mice. Journal Of The Endocrine Society 2023, 7: bvad114.1201. PMCID: PMC10554224, DOI: 10.1210/jendso/bvad114.1201.Peer-Reviewed Original ResearchKnockout miceAdrenocorticotrophic hormoneHPA axisEndogenous glucose productionCorticotropin-releasing hormone geneSystemic glucose homeostasisHypothalamic-pituitary-adrenal (HPA) axisStreptozocin-induced diabetesCirculating adrenocorticotrophic hormoneGlucose homeostasisElevated blood glucose levelsGlucose productionGLUT2 geneFluorescence in situ hybridizationEfficacy of drugsRegulating systemic glucose homeostasisHigh-fat dietBlood glucose levelsHypothalamic CRHRenal glucose productionAdrenal glandExcess blood glucoseLoss of glucoseMouse modelGlucose tolerance
2017
Pathogenesis of hypothyroidism-induced NAFLD is driven by intra- and extrahepatic mechanisms
Ferrandino G, Kaspari RR, Spadaro O, Reyna-Neyra A, Perry RJ, Cardone R, Kibbey RG, Shulman GI, Dixit VD, Carrasco N. Pathogenesis of hypothyroidism-induced NAFLD is driven by intra- and extrahepatic mechanisms. Proceedings Of The National Academy Of Sciences Of The United States Of America 2017, 114: e9172-e9180. PMID: 29073114, PMCID: PMC5664516, DOI: 10.1073/pnas.1707797114.Peer-Reviewed Original ResearchConceptsNonalcoholic fatty liver diseaseDe novo lipogenesisAdipose tissue lipolysisHepatic insulin resistanceThyroid hormonesHypothyroid miceImpaired suppressionInsulin resistanceTissue lipolysisInsulin secretionHigh thyroid-stimulating hormone levelsRegulation of THThyroid-stimulating hormone levelsLipid utilizationFatty liver diseaseSerum glucose levelsEndogenous glucose productionLow thyroid hormoneFatty acidsHepatic lipid utilizationLiver diseaseSevere hypothyroidismHormone levelsProfound suppressionGlucose levels