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Article ; Online: John Denis McGarry, PhD: A Remembrance of a Master Metabolic Physiologist.

Newgard, Christopher B

2018 Volume 41, Issue 7, Page(s) 1330–1336

Language	English
Publishing date	2018
Publishing country	United States
Document type	Journal Article
ZDB-ID	441231-x
ISSN	1935-5548 ; 0149-5992
ISSN (online)	1935-5548
ISSN	0149-5992
DOI	10.2337/dci18-0022
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Article ; Online: Mechanisms controlling pancreatic islet cell function in insulin secretion.

Campbell, Jonathan E / Newgard, Christopher B

Nature reviews. Molecular cell biology

2021 Volume 22, Issue 2, Page(s) 142–158

Abstract: Metabolic homeostasis in mammals is tightly regulated by the complementary actions of insulin and glucagon. The secretion of these hormones from pancreatic β-cells and α-cells, respectively, is controlled by metabolic, endocrine, and paracrine regulatory ...

Abstract	Metabolic homeostasis in mammals is tightly regulated by the complementary actions of insulin and glucagon. The secretion of these hormones from pancreatic β-cells and α-cells, respectively, is controlled by metabolic, endocrine, and paracrine regulatory mechanisms and is essential for the control of blood levels of glucose. The deregulation of these mechanisms leads to various pathologies, most notably type 2 diabetes, which is driven by the combined lesions of impaired insulin action and a loss of the normal insulin secretion response to glucose. Glucose stimulates insulin secretion from β-cells in a bi-modal fashion, and new insights about the underlying mechanisms, particularly relating to the second or amplifying phase of this secretory response, have been recently gained. Other recent work highlights the importance of α-cell-produced proglucagon-derived peptides, incretin hormones from the gastrointestinal tract and other dietary components, including certain amino acids and fatty acids, in priming and potentiation of the β-cell glucose response. These advances provide a new perspective for the understanding of the β-cell failure that triggers type 2 diabetes.
MeSH term(s)	Animals ; Diabetes Mellitus, Type 2/physiopathology ; Glucose/metabolism ; Homeostasis ; Humans ; Insulin Secretion ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/physiology
Chemical Substances	Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-01-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2031313-5
ISSN	1471-0080 ; 1471-0072
ISSN (online)	1471-0080
ISSN	1471-0072
DOI	10.1038/s41580-020-00317-7
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Zs.A 5446: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Metabolomics and Metabolic Diseases: Where Do We Stand?

Newgard, Christopher B

Cell metabolism

2016 Volume 25, Issue 1, Page(s) 43–56

Abstract: Metabolomics, or the comprehensive profiling of small molecule metabolites in cells, tissues, or whole organisms, has undergone a rapid technological evolution in the past two decades. These advances have led to the application of metabolomics to ... ...

Abstract	Metabolomics, or the comprehensive profiling of small molecule metabolites in cells, tissues, or whole organisms, has undergone a rapid technological evolution in the past two decades. These advances have led to the application of metabolomics to defining predictive biomarkers for incident cardiometabolic diseases and, increasingly, as a blueprint for understanding those diseases' pathophysiologic mechanisms. Progress in this area and challenges for the future are reviewed here.
MeSH term(s)	Animals ; Disease Models, Animal ; Humans ; Metabolic Diseases/metabolism ; Metabolome ; Metabolomics ; Models, Biological ; Treatment Outcome
Language	English
Publishing date	2016-10-27
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2016.09.018
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Article ; Online: Branched-chain amino acids in disease.

White, Phillip J / Newgard, Christopher B

Science (New York, N.Y.)

2018 Volume 363, Issue 6427, Page(s) 582–583

MeSH term(s)	Amino Acids, Branched-Chain/blood ; Amino Acids, Branched-Chain/metabolism ; Animals ; Diabetes Mellitus, Type 2/physiopathology ; Diet ; Dietary Carbohydrates ; Disease Models, Animal ; Dyslipidemias/physiopathology ; Humans ; Insulin Resistance ; Obesity/physiopathology
Chemical Substances	Amino Acids, Branched-Chain ; Dietary Carbohydrates
Language	English
Publishing date	2018-12-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.aav0558
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Zs.A 27: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Improving human β-cell maturation in vitro.

Hohmeier, Hans E / An, Jie / Newgard, Christopher B

Nature cell biology

2019 Volume 21, Issue 2, Page(s) 119–121

MeSH term(s)	Cell Differentiation ; Endocrine Cells ; Humans ; Stem Cells
Language	English
Publishing date	2019-01-31
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/s41556-019-0277-6
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Article ; Online: Metabolomic and genetic architecture of gestational diabetes subtypes.

Lee, Kristen / Kuang, Alan / Bain, James R / Hayes, M Geoffrey / Muehlbauer, Michael J / Ilkayeva, Olga R / Newgard, Christopher B / Powe, Camille E / Hivert, Marie-France / Scholtens, Denise M / Lowe, William L

Diabetologia

2024 Volume 67, Issue 5, Page(s) 895–907

Abstract: Aims/hypothesis: Physiological gestational diabetes mellitus (GDM) subtypes that may confer different risks for adverse pregnancy outcomes have been defined. The aim of this study was to characterise the metabolome and genetic architecture of GDM ... ...

Abstract	Aims/hypothesis: Physiological gestational diabetes mellitus (GDM) subtypes that may confer different risks for adverse pregnancy outcomes have been defined. The aim of this study was to characterise the metabolome and genetic architecture of GDM subtypes to address the hypothesis that they differ between GDM subtypes. Methods: This was a cross-sectional study of participants in the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study who underwent an OGTT at approximately 28 weeks' gestation. GDM was defined retrospectively using International Association of Diabetes and Pregnancy Study Groups/WHO criteria, and classified as insulin-deficient GDM (insulin secretion <25th percentile with preserved insulin sensitivity) or insulin-resistant GDM (insulin sensitivity <25th percentile with preserved insulin secretion). Metabolomic analyses were performed on fasting and 1 h serum samples in 3463 individuals (576 with GDM). Genome-wide genotype data were obtained for 8067 individuals (1323 with GDM). Results: Regression analyses demonstrated striking differences between the metabolomes for insulin-deficient or insulin-resistant GDM compared to those with normal glucose tolerance. After adjustment for covariates, 33 fasting metabolites, including 22 medium- and long-chain acylcarnitines, were uniquely associated with insulin-deficient GDM; 23 metabolites, including the branched-chain amino acids and their metabolites, were uniquely associated with insulin-resistant GDM; two metabolites (glycerol and 2-hydroxybutyrate) were associated with the same direction of association with both subtypes. Subtype differences were also observed 1 h after a glucose load. In genome-wide association studies, variants within MTNR1B (rs10830963, p=3.43×10 Conclusions/interpretation: This study demonstrates that physiological GDM subtypes differ in their metabolome and genetic architecture. These findings require replication in additional cohorts, but suggest that these differences may contribute to subtype-related adverse pregnancy outcomes.
MeSH term(s)	Female ; Pregnancy ; Humans ; Diabetes, Gestational ; Blood Glucose/metabolism ; Insulin Resistance/genetics ; Hyperglycemia ; Pregnancy Outcome ; Glucose Tolerance Test ; Genome-Wide Association Study ; Cross-Sectional Studies ; Retrospective Studies ; Insulin/metabolism ; Glucose/metabolism
Chemical Substances	Blood Glucose ; Insulin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2024-02-17
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-024-06110-x
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Article ; Online: Interplay between lipids and branched-chain amino acids in development of insulin resistance.

Newgard, Christopher B

Cell metabolism

2012 Volume 15, Issue 5, Page(s) 606–614

Abstract: Fatty acids (FA) and FA-derived metabolites have long been implicated in the development of insulin resistance and type 2 diabetes. Surprisingly, application of metabolomics technologies has revealed that branched-chain amino acids (BCAA) and related ... ...

Abstract	Fatty acids (FA) and FA-derived metabolites have long been implicated in the development of insulin resistance and type 2 diabetes. Surprisingly, application of metabolomics technologies has revealed that branched-chain amino acids (BCAA) and related metabolites are more strongly associated with insulin resistance than many common lipid species. Moreover, the BCAA-related signature is predictive of incident diabetes and intervention outcomes and uniquely responsive to therapeutic interventions. Nevertheless, in animal feeding studies, BCAA supplementation requires the background of a high-fat diet to promote insulin resistance. This Perspective develops a model to explain how lipids and BCAA may synergize to promote metabolic diseases.
MeSH term(s)	Amino Acids, Branched-Chain/metabolism ; Animals ; Humans ; Insulin Resistance/physiology ; Lipid Metabolism/physiology ; Metabolic Diseases/metabolism
Chemical Substances	Amino Acids, Branched-Chain
Language	English
Publishing date	2012-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2012.01.024
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Article ; Online: Circulating metabolic profile in idiopathic pulmonary fibrosis: data from the IPF-PRO Registry.

Summer, Ross / Todd, Jamie L / Neely, Megan L / Lobo, L Jason / Namen, Andrew / Newby, L Kristin / Shafazand, Shirin / Suliman, Sally / Hesslinger, Christian / Keller, Sascha / Leonard, Thomas B / Palmer, Scott M / Ilkayeva, Olga / Muehlbauer, Michael J / Newgard, Christopher B / Roman, Jesse

Respiratory research

2024 Volume 25, Issue 1, Page(s) 58

Abstract: Background: The circulating metabolome, reflecting underlying cellular processes and disease biology, has not been fully characterized in patients with idiopathic pulmonary fibrosis (IPF). We evaluated whether circulating levels of metabolites correlate ...

Abstract	Background: The circulating metabolome, reflecting underlying cellular processes and disease biology, has not been fully characterized in patients with idiopathic pulmonary fibrosis (IPF). We evaluated whether circulating levels of metabolites correlate with the presence of IPF, with the severity of IPF, or with the risk of clinically relevant outcomes among patients with IPF. Methods: We analyzed enrollment plasma samples from 300 patients with IPF in the IPF-PRO Registry and 100 individuals without known lung disease using a set of targeted metabolomics and clinical analyte modules. Linear regression was used to compare metabolite and clinical analyte levels between patients with IPF and controls and to determine associations between metabolite levels and measures of disease severity in patients with IPF. Unadjusted and adjusted univariable Cox regression models were used to evaluate associations between circulating metabolites and the risk of mortality or disease progression among patients with IPF. Results: Levels of 64 metabolites and 5 clinical analytes were significantly different between patients with IPF and controls. Among analytes with greatest differences were non-esterified fatty acids, multiple long-chain acylcarnitines, and select ceramides, levels of which were higher among patients with IPF versus controls. Levels of the branched-chain amino acids valine and leucine/isoleucine were inversely correlated with measures of disease severity. After adjusting for clinical factors known to influence outcomes, higher levels of the acylcarnitine C:16-OH/C:14-DC were associated with all-cause mortality, lower levels of the acylcarnitine C16:1-OH/C14:1DC were associated with all-cause mortality, respiratory death, and respiratory death or lung transplant, and higher levels of the sphingomyelin d43:2 were associated with the risk of respiratory death or lung transplantation. Conclusions: IPF has a distinct circulating metabolic profile characterized by increased levels of non-esterified fatty acids, long-chain acylcarnitines, and ceramides, which may suggest a more catabolic environment that enhances lipid mobilization and metabolism. We identified select metabolites that were highly correlated with measures of disease severity or the risk of disease progression and that may be developed further as biomarkers. Trial registration: ClinicalTrials.gov; No: NCT01915511; URL: www. Clinicaltrials: gov .
MeSH term(s)	Humans ; Carnitine/analogs & derivatives ; Ceramides ; Disease Progression ; Fatty Acids ; Idiopathic Pulmonary Fibrosis/metabolism ; Metabolome ; Registries
Chemical Substances	acylcarnitine ; Carnitine (S7UI8SM58A) ; Ceramides ; Fatty Acids
Language	English
Publishing date	2024-01-25
Publishing country	England
Document type	Clinical Study ; Journal Article
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-993X
ISSN (online)	1465-993X
ISSN	1465-993X
DOI	10.1186/s12931-023-02644-7
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Article ; Online: Targeted Metabolomic Profiling of Dapagliflozin in Heart Failure With Preserved Ejection Fraction: The PRESERVED-HF Trial.

Selvaraj, Senthil / Patel, Shachi / Sauer, Andrew J / McGarrah, Robert W / Jones, Philip / Kwee, Lydia Coulter / Windsor, Sheryl L / Ilkayeva, Olga / Muehlbauer, Michael J / Newgard, Christopher B / Borlaug, Barry A / Kitzman, Dalane W / Shah, Sanjiv J / Shah, Svati H / Kosiborod, Mikhail N

JACC. Heart failure

2024

Abstract: ... associated with changes in N-terminal pro-B-type natriuretic peptide; changes in medium-/long-chain ... acylcarnitines were positively associated with changes in N-terminal pro-B-type natriuretic peptide and ...

Abstract	Background: Although sodium glucose co-transporter 2 inhibitors (SGLT2is) improve heart failure (HF)-related symptoms and outcomes in HF with preserved ejection fraction (HFpEF), underlying mechanisms remain unclear. In HF with reduced EF, dapagliflozin altered ketone and fatty acid metabolites vs placebo; however, metabolite signatures of SGLT2is have not been well elucidated in HFpEF. Objectives: The goal of this study was to assess whether SGLT2i treatment altered systemic metabolic pathways and their relationship to outcomes in HFpEF. Methods: Targeted profiling of 64 metabolites was performed from 293 participants in PRESERVED-HF (Dapagliflozin in PRESERVED Ejection Fraction Heart Failure), a 12-week, placebo-controlled trial of dapagliflozin. Linear regression assessed changes in metabolite factors defined by principal components analysis (PCA) with dapagliflozin vs placebo. The relationship between changes in metabolite factors with changes in study endpoints was also assessed. Results: The mean age was 70 ± 11 years, 58% were female, and 29% were Black. There were no significant differences in 12 PCA-derived metabolite factors between treatment arms, including metabolites reflecting ketone, fatty acid, or branched-chain amino acid (BCAA) pathways. Combining treatment arms, changes in BCAAs and branched-chain ketoacids were negatively associated with changes in N-terminal pro-B-type natriuretic peptide; changes in medium-/long-chain acylcarnitines were positively associated with changes in N-terminal pro-B-type natriuretic peptide and negatively associated with changes in 6-minute walk test distance; and changes in ketones were negatively associated with changes in weight, without treatment interaction. Conclusions: Leveraging targeted metabolomics in a placebo-controlled SGLT2i trial of HFpEF, dapagliflozin did not alter systemic metabolic as reflected by circulating metabolites, in contrast with reported effects in HF with reduced ejection fraction. Metabolite biomarkers reflecting BCAA, ketone, and fatty acid metabolism were associated with markers of disease severity, suggesting a role for potential novel treatment targets. (Dapagliflozin in PRESERVED Ejection Fraction Heart Failure [PRESERVED-HF]; NCT03030235).
Language	English
Publishing date	2024-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2705621-1
ISSN	2213-1787 ; 2213-1779
ISSN (online)	2213-1787
ISSN	2213-1779
DOI	10.1016/j.jchf.2024.02.018
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Article ; Online: BCAA Supplementation in Mice with Diet-induced Obesity Alters the Metabolome Without Impairing Glucose Homeostasis.

Lee, Jennifer / Vijayakumar, Archana / White, Phillip J / Xu, Yuping / Ilkayeva, Olga / Lynch, Christopher J / Newgard, Christopher B / Kahn, Barbara B

Endocrinology

2021 Volume 162, Issue 7

Abstract: Circulating branched chain amino acid (BCAA) levels are elevated in obese humans and genetically obese rodents. However, the relationship of BCAAs to insulin resistance in diet-induced obese mice, a commonly used model to study glucose homeostasis, is ... ...

Abstract	Circulating branched chain amino acid (BCAA) levels are elevated in obese humans and genetically obese rodents. However, the relationship of BCAAs to insulin resistance in diet-induced obese mice, a commonly used model to study glucose homeostasis, is still ill-defined. Here we examined how high-fat high-sucrose (HFHS) or high-fat diet (HFD) feeding, with or without BCAA supplementation in water, alters the metabolome in serum/plasma and tissues in mice and whether raising circulating BCAA levels worsens insulin resistance and glucose intolerance. Neither HFHS nor HFD feeding raised circulating BCAA levels in insulin-resistant diet-induced obese mice. BCAA supplementation raised circulating BCAA and branched-chain α-keto acid levels and C5-OH/C3-DC acylcarnitines (AC) in muscle from mice fed an HFHS diet or HFD, but did not worsen insulin resistance. A set of short- and long-chain acyl CoAs were elevated by diet alone in muscle, liver, and white adipose tissue (WAT), but not increased further by BCAA supplementation. HFD feeding reduced valine and leucine oxidation in WAT but not in muscle. BCAA supplementation markedly increased valine oxidation in muscle from HFD-fed mice, while leucine oxidation was unaffected by diet or BCAA treatment. Here we establish an extensive metabolome database showing tissue-specific changes in mice on 2 different HFDs, with or without BCAA supplementation. We conclude that mildly elevating circulating BCAAs and a subset of ACs by BCAA supplementation does not worsen insulin resistance or glucose tolerance in mice. This work highlights major differences in the effects of BCAAs on glucose homeostasis in diet-induced obese mice versus data reported in obese rats and in humans.
MeSH term(s)	Amino Acids, Branched-Chain/administration & dosage ; Amino Acids, Branched-Chain/blood ; Amino Acids, Branched-Chain/metabolism ; Animals ; Blood Glucose/metabolism ; Diet/adverse effects ; Diet, High-Fat ; Dietary Sucrose/administration & dosage ; Dietary Supplements ; Female ; Glucose Intolerance/blood ; Homeostasis/drug effects ; Insulin Resistance/physiology ; Lipid Metabolism/drug effects ; Liver/metabolism ; Male ; Metabolomics ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/metabolism ; Obesity/etiology ; Obesity/metabolism ; Oxidation-Reduction
Chemical Substances	Amino Acids, Branched-Chain ; Blood Glucose ; Dietary Sucrose
Language	English
Publishing date	2021-03-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqab062
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