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Article ; Online: Angiotensin Type-2 Receptors: Transducers of Natriuresis in the Renal Proximal Tubule.

Carey, Robert M / Siragy, Helmy M / Gildea, John J / Keller, Susanna R

International journal of molecular sciences

2022 Volume 23, Issue 4

Abstract: Angiotensin II (Ang II) type-2 receptors ( ... ...

Abstract	Angiotensin II (Ang II) type-2 receptors (AT
MeSH term(s)	Animals ; Humans ; Hypertension/metabolism ; Kidney Tubules, Proximal/metabolism ; Natriuresis/physiology ; Receptor, Angiotensin, Type 2/metabolism ; Transducers
Chemical Substances	Receptor, Angiotensin, Type 2
Language	English
Publishing date	2022-02-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23042317
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Article ; Online: Insulin-regulated aminopeptidase is required for water excretion in response to acute hypotonic stress.

Zuchowski, Yvonne / Carty, Joshua / Terker, Andrew S / Bock, Fabian / Trapani, Jonathan B / Bhave, Gautam / Watts, Jason A / Keller, Susanna / Zhang, Mingzhi / Zent, Roy / Harris, Raymond C / Arroyo, Juan Pablo

American journal of physiology. Renal physiology

2023 Volume 324, Issue 6, Page(s) F521–F531

Abstract: The objective of this study was to understand the response of mice lacking insulin-regulated aminopeptidase (IRAP) to an acute water load. For mammals to respond appropriately to acute water loading, vasopressin activity needs to decrease. IRAP degrades ... ...

Abstract	The objective of this study was to understand the response of mice lacking insulin-regulated aminopeptidase (IRAP) to an acute water load. For mammals to respond appropriately to acute water loading, vasopressin activity needs to decrease. IRAP degrades vasopressin in vivo. Therefore, we hypothesized that mice lacking IRAP have an impaired ability to degrade vasopressin and, thus, have persistent urinary concentration. Age-matched 8- to 12-wk-old IRAP wild-type (WT) and knockout (KO) male mice were used for all experiments. Blood electrolytes and urine osmolality were measured before and 1 h after water load (∼2 mL sterile water via intraperitoneal injection). Urine was collected from IRAP WT and KO mice for urine osmolality measurements at baseline and after 1 h administration of the vasopressin type 2 receptor antagonist OPC-31260 (10 mg/kg ip). Immunofluorescence and immunoblot analysis were performed on kidneys at baseline and after 1 h acute water load. IRAP was expressed in the glomerulus, thick ascending loop of Henle, distal tubule, connecting duct, and collecting duct. IRAP KO mice had elevated urine osmolality compared with WT mice due to higher membrane expression of aquaporin 2 (AQP2), which was restored to that of controls after administration of OPC-31260. IRAP KO mice developed hyponatremia after an acute water load because they were unable to increase free water excretion due to increased surface expression of AQP2. In conclusion, IRAP is required to increase water excretion in response to an acute water load due to persistent vasopressin stimulation of AQP2.
MeSH term(s)	Animals ; Male ; Mice ; Aminopeptidases/genetics ; Aminopeptidases/metabolism ; Aquaporin 2/genetics ; Aquaporin 2/metabolism ; Insulin/metabolism ; Mammals/metabolism ; Osmotic Pressure ; Vasopressins/pharmacology ; Vasopressins/metabolism ; Water/metabolism
Chemical Substances	Aminopeptidases (EC 3.4.11.-) ; Aquaporin 2 ; Insulin ; Vasopressins (11000-17-2) ; Water (059QF0KO0R) ; leucyl-cystinyl aminopeptidase (EC 3.4.11.3)
Language	English
Publishing date	2023-03-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00318.2022
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Article: Module Anchored Network Inference: A Sequential Module-Based Approach to Novel Gene Network Construction from Genomic Expression Data on Human Disease Mechanism.

Muthiah, Annamalai / Keller, Susanna R / Lee, Jae K

International journal of genomics

2017 Volume 2017, Page(s) 8514071

Abstract: Different computational approaches have been examined and compared for inferring network relationships from time-series genomic data on human disease mechanisms under the recent Dialogue on Reverse Engineering Assessment and Methods (DREAM) challenge. ... ...

Abstract	Different computational approaches have been examined and compared for inferring network relationships from time-series genomic data on human disease mechanisms under the recent Dialogue on Reverse Engineering Assessment and Methods (DREAM) challenge. Many of these approaches infer all possible relationships among all candidate genes, often resulting in extremely crowded candidate network relationships with many more False Positives than True Positives. To overcome this limitation, we introduce a novel approach, Module Anchored Network Inference (MANI), that constructs networks by analyzing sequentially small adjacent building blocks (modules). Using MANI, we inferred a 7-gene adipogenesis network based on time-series gene expression data during adipocyte differentiation. MANI was also applied to infer two 10-gene networks based on time-course perturbation datasets from DREAM3 and DREAM4 challenges. MANI well inferred and distinguished serial, parallel, and time-dependent gene interactions and network cascades in these applications showing a superior performance to other in silico network inference techniques for discovering and reconstructing gene network relationships.
Language	English
Publishing date	2017-01-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2711883-6
ISSN	2314-4378 ; 2314-436X
ISSN (online)	2314-4378
ISSN	2314-436X
DOI	10.1155/2017/8514071
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Article ; Online: Identification of a Primary Renal AT

Kemp, Brandon A / Howell, Nancy L / Gildea, John J / Keller, Susanna R / Carey, Robert M

Circulation research

2020 Volume 126, Issue 5, Page(s) 644–659

Abstract: Rationale: Previous studies identified a defect in Ang III (angiotensin III [des-aspartyl: Objective: This study aimed to delineate in prehypertensive SHR kidneys the receptor or postreceptor defect causing impaired AT: Methods and results: Female ...

Abstract	Rationale: Previous studies identified a defect in Ang III (angiotensin III [des-aspartyl Objective: This study aimed to delineate in prehypertensive SHR kidneys the receptor or postreceptor defect causing impaired AT Methods and results: Female 4-week-old Wistar Kyoto and SHR rats were studied after 24-hour systemic AT Conclusions: The results demonstrate a primary renal proximal tubule cell AT
MeSH term(s)	Angiotensin II Type 2 Receptor Blockers/pharmacology ; Animals ; Cell Adhesion Molecules/metabolism ; Cyclic GMP/metabolism ; Extracellular Fluid/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Hypertension/genetics ; Hypertension/metabolism ; Kidney Tubules, Proximal/drug effects ; Kidney Tubules, Proximal/metabolism ; Microfilament Proteins/metabolism ; Natriuresis ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Transport ; Rats ; Rats, Inbred SHR ; Rats, Wistar ; Receptor, Angiotensin, Type 2/metabolism ; Sodium/metabolism ; Sodium-Hydrogen Exchangers/metabolism ; Sodium-Potassium-Exchanging ATPase/metabolism ; src-Family Kinases/metabolism
Chemical Substances	Angiotensin II Type 2 Receptor Blockers ; Cell Adhesion Molecules ; Microfilament Proteins ; Phosphoproteins ; Receptor, Angiotensin, Type 2 ; Sodium-Hydrogen Exchangers ; vasodilator-stimulated phosphoprotein ; Sodium (9NEZ333N27) ; src-Family Kinases (EC 2.7.10.2) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2020-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.119.316193
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Article ; Online: Evidence That Binding of Cyclic GMP to the Extracellular Domain of NKA (Sodium-Potassium ATPase) Mediates Natriuresis.

Kemp, Brandon A / Howell, Nancy L / Gildea, John J / Hinkle, Josh D / Shabanowitz, Jeffrey / Hunt, Donald F / Conaway, Mark R / Keller, Susanna R / Carey, Robert M

Circulation research

2023 Volume 132, Issue 9, Page(s) 1127–1140

Abstract: Background: Extracellular renal interstitial guanosine cyclic 3',5'-monophosphate (cGMP) inhibits renal proximal tubule (RPT) sodium (Na: Methods: Urine Na: Results: Renal interstitial cGMP and raised renal perfusion pressure induced natriuresis ... ...

Abstract	Background: Extracellular renal interstitial guanosine cyclic 3',5'-monophosphate (cGMP) inhibits renal proximal tubule (RPT) sodium (Na Methods: Urine Na Results: Renal interstitial cGMP and raised renal perfusion pressure induced natriuresis and increased phosphorylated Src Conclusions: cGMP can bind to NKA and thereby mediate natriuresis.
MeSH term(s)	Animals ; Female ; Rats ; Adenosine Triphosphatases/metabolism ; Biotin/metabolism ; Cyclic GMP/chemistry ; Cyclic GMP/metabolism ; Natriuresis/physiology ; Ouabain/pharmacology ; Potassium/metabolism ; Rats, Sprague-Dawley ; Sodium/metabolism ; Sodium-Potassium-Exchanging ATPase/chemistry ; Sodium-Potassium-Exchanging ATPase/metabolism
Chemical Substances	4,4-difluoro-4-bora-3a,4a-diaza-s-indacene ; Adenosine Triphosphatases (EC 3.6.1.-) ; Biotin (6SO6U10H04) ; Cyclic GMP (H2D2X058MU) ; Ouabain (5ACL011P69) ; Potassium (RWP5GA015D) ; Sodium (9NEZ333N27) ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13)
Language	English
Publishing date	2023-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.122.321693
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Article ; Online: Knockout of Nephron ATP6AP2 Impairs Proximal Tubule Function and Prevents High-Fat Diet-Induced Obesity in Male Mice.

Culver, Silas A / Akhtar, Safia / Rountree-Jablin, Callie / Keller, Susanna R / Cathro, Helen P / Gildea, John J / Siragy, Helmy M

Endocrinology

2021 Volume 162, Issue 12

Abstract: ATP6AP2 expression is increased in the nephron during high-fat diet (HFD) and its knockout (ATP6AP2 KO) reduces body weight (WT) in mice. We evaluated the contribution of ATP6AP2 to urinary glucose (UG) and albumin (Ualb) handling during HFD. We ... ...

Abstract	ATP6AP2 expression is increased in the nephron during high-fat diet (HFD) and its knockout (ATP6AP2 KO) reduces body weight (WT) in mice. We evaluated the contribution of ATP6AP2 to urinary glucose (UG) and albumin (Ualb) handling during HFD. We hypothesized that nephron ATP6AP2 KO increases UG and Ualb and minimizes HFD-induced obesity. Eight-week-old male C57BL/6J mice with inducible nephron-specific ATP6AP2 KO and noninduced controls were fed either normal diet (ND, 12% kcal fat) or HFD (45% kcal fat) for 6 months. ATP6AP2 KO mice on ND had 20% (P < 0.01) lower WT compared with controls. HFD-fed mice had 41% (P < 0.05) greater WT than ND-fed control mice. In contrast, ATP6AP2 KO abrogated the increase in WT induced by HFD by 40% (P < 0.05). Mice on HFD had less caloric intake compared with ND controls (P < 0.01). There were no significant differences in metabolic rate between all groups. UG and Ualb was significantly increased in ATP6AP2 KO mice on both ND and HFD. ATP6AP2 KO showed greater levels of proximal tubule apoptosis and histologic evidence of proximal tubule injury. In conclusion, our results demonstrate that nephron-specific ATP6AP2 KO is associated with glucosuria and albuminuria, most likely secondary to renal proximal tubule injury and/or dysfunction. Urinary loss of nutrients may have contributed to the reduced WT of knockout mice on ND and lack of WT gain in response to HFD. Future investigation should elucidate the mechanisms by which loss of renal ATP6AP2 causes proximal tubule injury and dysfunction.
MeSH term(s)	Animals ; Diet, High-Fat ; Energy Metabolism/genetics ; Kidney Tubules, Proximal/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nephrons/metabolism ; Obesity/genetics ; Obesity/metabolism ; Obesity/prevention & control ; Organ Specificity/genetics ; Proton-Translocating ATPases/genetics ; Proton-Translocating ATPases/metabolism ; Proton-Translocating ATPases/physiology ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Receptors, Cell Surface/physiology ; Renal Insufficiency/genetics ; Renal Insufficiency/metabolism ; Renal Insufficiency/pathology
Chemical Substances	ATP6AP2 protein, mouse ; Receptors, Cell Surface ; Proton-Translocating ATPases (EC 3.6.3.14)
Language	English
Publishing date	2021-09-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqab200
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Article ; Online: Renal AT

Kemp, Brandon A / Howell, Nancy L / Gildea, John J / Keller, Susanna R / Brautigan, David L / Carey, Robert M

Circulation research

2021 Volume 130, Issue 1, Page(s) 96–111

Abstract: Background: How signals from activated angiotensin type-2 receptors (AT: Methods and results: In Wistar-Kyoto rats, direct renal interstitial administration of selective AT: Conclusions: In renal proximal tubule cells of Wistar-Kyoto rats, PP2A is ...

Abstract	Background: How signals from activated angiotensin type-2 receptors (AT Methods and results: In Wistar-Kyoto rats, direct renal interstitial administration of selective AT Conclusions: In renal proximal tubule cells of Wistar-Kyoto rats, PP2A is activated and PP2A subunits AB55αC are recruited to C-21-activated AT
MeSH term(s)	Animals ; Cells, Cultured ; Cyclic GMP/metabolism ; Female ; Kidney/metabolism ; Natriuresis ; Protein Phosphatase 2/metabolism ; Rats ; Rats, Wistar ; Receptor, Angiotensin, Type 2/metabolism ; Sodium/metabolism
Chemical Substances	Receptor, Angiotensin, Type 2 ; Sodium (9NEZ333N27) ; Protein Phosphatase 2 (EC 3.1.3.16) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2021-11-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.121.319519
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Article ; Online: Rab GAPs AS160 and Tbc1d1 play nonredundant roles in the regulation of glucose and energy homeostasis in mice.

Hargett, Stefan R / Walker, Natalie N / Keller, Susanna R

American journal of physiology. Endocrinology and metabolism

2016 Volume 310, Issue 4, Page(s) E276–88

Abstract: The related Rab GTPase-activating proteins (Rab GAPs) AS160 and Tbc1d1 regulate the trafficking of the glucose transporter GLUT4 that controls glucose uptake in muscle and fat cells and glucose homeostasis. AS160- and Tbc1d1-deficient mice exhibit ... ...

Abstract	The related Rab GTPase-activating proteins (Rab GAPs) AS160 and Tbc1d1 regulate the trafficking of the glucose transporter GLUT4 that controls glucose uptake in muscle and fat cells and glucose homeostasis. AS160- and Tbc1d1-deficient mice exhibit different adipocyte- and skeletal muscle-specific defects in glucose uptake, GLUT4 expression and trafficking, and glucose homeostasis. A recent study analyzed male mice with simultaneous deletion of AS160 and Tbc1d1 (AS160(-/-)/Tbc1d1(-/-) mice). Herein, we describe abnormalities in male and female AS160(-/-)/Tbc1d1(-/-) mice on another strain background. We confirm the earlier observation that GLUT4 expression and glucose uptake defects of single-knockout mice join in AS160(-/-)/Tbc1d1(-/-) mice to affect all skeletal muscle and adipose tissues. In large mixed fiber-type skeletal muscles, changes in relative basal GLUT4 plasma membrane association in AS160(-/-) and Tbc1d1(-/-) mice also combine in AS160(-/-)/Tbc1d1(-/-) mice. However, we found different glucose uptake abnormalities in isolated skeletal muscles and adipocytes than reported previously, resulting in different interpretations of how AS160 and Tbc1d1 regulate GLUT4 translocation to the cell surface. In support of a larger role for AS160 in glucose homeostasis, in contrast with the previous study, we find similarly impaired glucose and insulin tolerance in AS160(-/-)/Tbc1d1(-/-) and AS160(-/-) mice. However, in vivo glucose uptake abnormalities in AS160(-/-)/Tbc1d1(-/-) skeletal muscles differ from those observed previously in AS160(-/-) mice, indicating additional defects due to Tbc1d1 deletion. Similar to AS160- and Tbc1d1-deficient mice, AS160(-/-)/Tbc1d1(-/-) mice show sex-specific abnormalities in glucose and energy homeostasis. In conclusion, our study supports nonredundant functions for AS160 and Tbc1d1.
MeSH term(s)	Adipocytes/metabolism ; Adipose Tissue/metabolism ; Animals ; Blood Glucose/metabolism ; Energy Metabolism/genetics ; Female ; GTPase-Activating Proteins/genetics ; Glucose/metabolism ; Glucose Transporter Type 4/metabolism ; Homeostasis/genetics ; Insulin/metabolism ; Insulin Resistance ; Male ; Mice ; Mice, Knockout ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; Sex Factors
Chemical Substances	Blood Glucose ; GTPase-Activating Proteins ; Glucose Transporter Type 4 ; Insulin ; Slc2a4 protein, mouse ; Tbc1d1 protein, mouse ; Tbc1d4 protein, mouse ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2016-02-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00342.2015
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Article ; Online: Progressive Cardiac Metabolic Defects Accompany Diastolic and Severe Systolic Dysfunction in Spontaneously Hypertensive Rat Hearts.

Li, Jie / Minczuk, Krzysztof / Huang, Qiao / Kemp, Brandon A / Howell, Nancy L / Chordia, Mahendra D / Roy, R Jack / Patrie, James T / Qureshi, Zoraiz / Kramer, Christopher M / Epstein, Frederick H / Carey, Robert M / Kundu, Bijoy K / Keller, Susanna R

Journal of the American Heart Association

2023 Volume 12, Issue 10, Page(s) e026950

Abstract: Background Cardiac metabolic abnormalities are present in heart failure. Few studies have followed metabolic changes accompanying diastolic and systolic heart failure in the same model. We examined metabolic changes during the development of diastolic ... ...

Abstract	Background Cardiac metabolic abnormalities are present in heart failure. Few studies have followed metabolic changes accompanying diastolic and systolic heart failure in the same model. We examined metabolic changes during the development of diastolic and severe systolic dysfunction in spontaneously hypertensive rats (SHR). Methods and Results We serially measured myocardial glucose uptake rates with dynamic 2-[
MeSH term(s)	Rats ; Animals ; Rats, Inbred SHR ; Hypertension ; Tomography, X-Ray Computed ; Heart Failure ; Rats, Inbred WKY ; Glucose ; Deoxyglucose ; Blood Pressure
Chemical Substances	Glucose (IY9XDZ35W2) ; Deoxyglucose (9G2MP84A8W)
Language	English
Publishing date	2023-05-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.122.026950
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Article ; Online: Adipocyte-Specific Modulation of KLF14 Expression in Mice Leads to Sex-Dependent Impacts on Adiposity and Lipid Metabolism.

Yang, Qianyi / Hinkle, Jameson / Reed, Jordan N / Aherrahrou, Redouane / Xu, Zhiwen / Harris, Thurl E / Stephenson, Erin J / Musunuru, Kiran / Keller, Susanna R / Civelek, Mete

Diabetes

2022 Volume 71, Issue 4, Page(s) 677–693

Abstract: Genome-wide association studies identified single nucleotide polymorphisms on chromosome 7 upstream of KLF14 to be associated with metabolic syndrome traits and increased risk for type 2 diabetes (T2D). The associations were more significant in women ... ...

Abstract	Genome-wide association studies identified single nucleotide polymorphisms on chromosome 7 upstream of KLF14 to be associated with metabolic syndrome traits and increased risk for type 2 diabetes (T2D). The associations were more significant in women than in men. The risk allele carriers expressed lower levels of the transcription factor KLF14 in adipose tissues than nonrisk allele carriers. To investigate how adipocyte KLF14 regulates metabolic traits in a sex-dependent manner, we characterized high-fat diet-fed male and female mice with adipocyte-specific Klf14 deletion or overexpression. Klf14 deletion resulted in increased fat mass in female mice and decreased fat mass in male mice. Female Klf14-deficient mice had overall smaller adipocytes in subcutaneous fat depots but larger adipocytes in parametrial depots, indicating a shift in lipid storage from subcutaneous to visceral fat depots. They had reduced metabolic rates and increased respiratory exchange ratios consistent with increased use of carbohydrates as an energy source. Fasting- and isoproterenol-induced adipocyte lipolysis was defective in female Klf14-deficient mice, and concomitantly, adipocyte triglycerides lipase mRNA levels were downregulated. Female Klf14-deficient mice cleared blood triglyceride and nonesterified fatty acid less efficiently than wild-type. Finally, adipocyte-specific overexpression of Klf14 resulted in lower total body fat in female but not male mice. Taken together, consistent with human studies, adipocyte KLF14 deficiency in female but not in male mice causes increased adiposity and redistribution of lipid storage from subcutaneous to visceral adipose tissues. Increasing KLF14 abundance in adipocytes of females with obesity and T2D may provide a novel treatment option to alleviate metabolic abnormalities.
MeSH term(s)	Adipocytes/metabolism ; Adiposity/genetics ; Animals ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Female ; Genome-Wide Association Study ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Lipid Metabolism/genetics ; Male ; Mice ; Obesity/genetics ; Obesity/metabolism ; Sex Factors
Chemical Substances	Klf14 protein, mouse ; Kruppel-Like Transcription Factors
Language	English
Publishing date	2022-01-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db21-0674
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