Fasting plasma chenodeoxycholic acid and cholic acid concentrations are inversely correlated with insulin sensitivity in adults
Background Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and to increase energy expenditure in mice. Here, we investigated the relationship between fasting plasma BAs concentrations and metabo...
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Published in | Nutrition & metabolism Vol. 8; no. 1; pp. 48 - 344 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
BioMed Central
07.07.2011
BioMed Central Ltd BMC |
Subjects | |
Online Access | Get full text |
ISSN | 1743-7075 1743-7075 |
DOI | 10.1186/1743-7075-8-48 |
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Abstract | Background
Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and to increase energy expenditure in mice. Here, we investigated the relationship between fasting plasma BAs concentrations and metabolic parameters in humans.
Findings
Fasting plasma glucose, insulin and lipid profile were measured in 14 healthy volunteers, 20 patients with type 2 diabetes (T2D), and 22 non-diabetic abdominally obese subjects. Insulin sensitivity was also assessed by the determination of the glucose infusion rate (GIR) during a hyperinsulinemic-euglycemic clamp in a subgroup of patients (9 healthy and 16 T2D subjects). Energy expenditure was measured by indirect calorimetry. Plasma cholic acid (CA), chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) concentrations were analyzed by gas chromatograph-mass spectrometry. In univariable analysis, a positive association was found between HOMA-IR and plasma CDCA (β = 0.09, p = 0.001), CA (β = 0.03, p = 0.09) and DCA concentrations (β = 0.07, p < 0.0001). Spearman analysis retrieved an inverse relationship between plasma CDCA (r = -0.44, p = 0.03), CA (r = -0.65, p = 0.001) and the GIR. HOMA-IR remained positively associated with CDCA (β = 0.11, p = 0.01), CA (β = 0.04, p = 0.01) and DCA (β = 0.06, p = 0.007) in multivariable analysis, after adjustment for age, gender, BMI, HbA1C and plasma lipid parameters. In contrast, HbA1c, energy expenditure and plasma lipid concentrations were not correlated with plasma BAs levels in multivariable analysis.
Conclusions
Both plasma CDCA, CA and DCA concentrations were negatively associated with insulin sensitivity in a wide range of subjects. |
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AbstractList | Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and to increase energy expenditure in mice. Here, we investigated the relationship between fasting plasma BAs concentrations and metabolic parameters in humans.BACKGROUNDAccumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and to increase energy expenditure in mice. Here, we investigated the relationship between fasting plasma BAs concentrations and metabolic parameters in humans.Fasting plasma glucose, insulin and lipid profile were measured in 14 healthy volunteers, 20 patients with type 2 diabetes (T2D), and 22 non-diabetic abdominally obese subjects. Insulin sensitivity was also assessed by the determination of the glucose infusion rate (GIR) during a hyperinsulinemic-euglycemic clamp in a subgroup of patients (9 healthy and 16 T2D subjects). Energy expenditure was measured by indirect calorimetry. Plasma cholic acid (CA), chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) concentrations were analyzed by gas chromatograph-mass spectrometry. In univariable analysis, a positive association was found between HOMA-IR and plasma CDCA (β = 0.09, p = 0.001), CA (β = 0.03, p = 0.09) and DCA concentrations (β = 0.07, p < 0.0001). Spearman analysis retrieved an inverse relationship between plasma CDCA (r = -0.44, p = 0.03), CA (r = -0.65, p = 0.001) and the GIR. HOMA-IR remained positively associated with CDCA (β = 0.11, p = 0.01), CA (β = 0.04, p = 0.01) and DCA (β = 0.06, p = 0.007) in multivariable analysis, after adjustment for age, gender, BMI, HbA1C and plasma lipid parameters. In contrast, HbA1c, energy expenditure and plasma lipid concentrations were not correlated with plasma BAs levels in multivariable analysis.FINDINGSFasting plasma glucose, insulin and lipid profile were measured in 14 healthy volunteers, 20 patients with type 2 diabetes (T2D), and 22 non-diabetic abdominally obese subjects. Insulin sensitivity was also assessed by the determination of the glucose infusion rate (GIR) during a hyperinsulinemic-euglycemic clamp in a subgroup of patients (9 healthy and 16 T2D subjects). Energy expenditure was measured by indirect calorimetry. Plasma cholic acid (CA), chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) concentrations were analyzed by gas chromatograph-mass spectrometry. In univariable analysis, a positive association was found between HOMA-IR and plasma CDCA (β = 0.09, p = 0.001), CA (β = 0.03, p = 0.09) and DCA concentrations (β = 0.07, p < 0.0001). Spearman analysis retrieved an inverse relationship between plasma CDCA (r = -0.44, p = 0.03), CA (r = -0.65, p = 0.001) and the GIR. HOMA-IR remained positively associated with CDCA (β = 0.11, p = 0.01), CA (β = 0.04, p = 0.01) and DCA (β = 0.06, p = 0.007) in multivariable analysis, after adjustment for age, gender, BMI, HbA1C and plasma lipid parameters. In contrast, HbA1c, energy expenditure and plasma lipid concentrations were not correlated with plasma BAs levels in multivariable analysis.Both plasma CDCA, CA and DCA concentrations were negatively associated with insulin sensitivity in a wide range of subjects.CONCLUSIONSBoth plasma CDCA, CA and DCA concentrations were negatively associated with insulin sensitivity in a wide range of subjects. BACKGROUND: Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and to increase energy expenditure in mice. Here, we investigated the relationship between fasting plasma BAs concentrations and metabolic parameters in humans. FINDINGS: Fasting plasma glucose, insulin and lipid profile were measured in 14 healthy volunteers, 20 patients with type 2 diabetes (T2D), and 22 non-diabetic abdominally obese subjects. Insulin sensitivity was also assessed by the determination of the glucose infusion rate (GIR) during a hyperinsulinemic-euglycemic clamp in a subgroup of patients (9 healthy and 16 T2D subjects). Energy expenditure was measured by indirect calorimetry. Plasma cholic acid (CA), chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) concentrations were analyzed by gas chromatograph-mass spectrometry. In univariable analysis, a positive association was found between HOMA-IR and plasma CDCA (beta=0.09, p=0.001), CA (beta=0.03, p=0.09) and DCA concentrations (beta=0.07, p<0.0001). Spearman analysis retrieved an inverse relationship between plasma CDCA (r=-0.44, p=0.03), CA (r=-0.65, p=0.001) and the GIR. HOMA-IR remained positively associated with CDCA (beta=0.11, p=0.01), CA (beta=0.04, p=0.01) and DCA (beta=0.06, p=0.007) in multivariable analysis, after adjustment for age, gender, BMI, HbA1C and plasma lipid parameters. In contrast, HbA1c, energy expenditure and plasma lipid concentrations were not correlated with plasma BAs levels in multivariable analysis. CONCLUSIONS: Both plasma CDCA, CA and DCA concentrations were negatively associated with insulin sensitivity in a wide range of subjects. BACKGROUND: Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and to increase energy expenditure in mice. Here, we investigated the relationship between fasting plasma BAs concentrations and metabolic parameters in humans. FINDINGS: Fasting plasma glucose, insulin and lipid profile were measured in 14 healthy volunteers, 20 patients with type 2 diabetes (T2D), and 22 non-diabetic abdominally obese subjects. Insulin sensitivity was also assessed by the determination of the glucose infusion rate (GIR) during a hyperinsulinemic-euglycemic clamp in a subgroup of patients (9 healthy and 16 T2D subjects). Energy expenditure was measured by indirect calorimetry. Plasma cholic acid (CA), chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) concentrations were analyzed by gas chromatograph-mass spectrometry. In univariable analysis, a positive association was found between HOMA-IR and plasma CDCA (β = 0.09, p = 0.001), CA (β = 0.03, p = 0.09) and DCA concentrations (β = 0.07, p < 0.0001). Spearman analysis retrieved an inverse relationship between plasma CDCA (r = -0.44, p = 0.03), CA (r = -0.65, p = 0.001) and the GIR. HOMA-IR remained positively associated with CDCA (β = 0.11, p = 0.01), CA (β = 0.04, p = 0.01) and DCA (β = 0.06, p = 0.007) in multivariable analysis, after adjustment for age, gender, BMI, HbA1C and plasma lipid parameters. In contrast, HbA1c, energy expenditure and plasma lipid concentrations were not correlated with plasma BAs levels in multivariable analysis. CONCLUSIONS: Both plasma CDCA, CA and DCA concentrations were negatively associated with insulin sensitivity in a wide range of subjects. Background Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and to increase energy expenditure in mice. Here, we investigated the relationship between fasting plasma BAs concentrations and metabolic parameters in humans. Findings Fasting plasma glucose, insulin and lipid profile were measured in 14 healthy volunteers, 20 patients with type 2 diabetes (T2D), and 22 non-diabetic abdominally obese subjects. Insulin sensitivity was also assessed by the determination of the glucose infusion rate (GIR) during a hyperinsulinemic-euglycemic clamp in a subgroup of patients (9 healthy and 16 T2D subjects). Energy expenditure was measured by indirect calorimetry. Plasma cholic acid (CA), chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) concentrations were analyzed by gas chromatograph-mass spectrometry. In univariable analysis, a positive association was found between HOMA-IR and plasma CDCA ([beta] = 0.09, p = 0.001), CA ([beta] = 0.03, p = 0.09) and DCA concentrations ([beta] = 0.07, p [less than] 0.0001). Spearman analysis retrieved an inverse relationship between plasma CDCA (r = -0.44, p = 0.03), CA (r = -0.65, p = 0.001) and the GIR. HOMA-IR remained positively associated with CDCA ([beta] = 0.11, p = 0.01), CA ([beta] = 0.04, p = 0.01) and DCA ([beta] = 0.06, p = 0.007) in multivariable analysis, after adjustment for age, gender, BMI, HbA1C and plasma lipid parameters. In contrast, HbA1c, energy expenditure and plasma lipid concentrations were not correlated with plasma BAs levels in multivariable analysis. Conclusions Both plasma CDCA, CA and DCA concentrations were negatively associated with insulin sensitivity in a wide range of subjects. Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and to increase energy expenditure in mice. Here, we investigated the relationship between fasting plasma BAs concentrations and metabolic parameters in humans. Fasting plasma glucose, insulin and lipid profile were measured in 14 healthy volunteers, 20 patients with type 2 diabetes (T2D), and 22 non-diabetic abdominally obese subjects. Insulin sensitivity was also assessed by the determination of the glucose infusion rate (GIR) during a hyperinsulinemic-euglycemic clamp in a subgroup of patients (9 healthy and 16 T2D subjects). Energy expenditure was measured by indirect calorimetry. Plasma cholic acid (CA), chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) concentrations were analyzed by gas chromatograph-mass spectrometry. In univariable analysis, a positive association was found between HOMA-IR and plasma CDCA ([beta] = 0.09, p = 0.001), CA ([beta] = 0.03, p = 0.09) and DCA concentrations ([beta] = 0.07, p [less than] 0.0001). Spearman analysis retrieved an inverse relationship between plasma CDCA (r = -0.44, p = 0.03), CA (r = -0.65, p = 0.001) and the GIR. HOMA-IR remained positively associated with CDCA ([beta] = 0.11, p = 0.01), CA ([beta] = 0.04, p = 0.01) and DCA ([beta] = 0.06, p = 0.007) in multivariable analysis, after adjustment for age, gender, BMI, HbA1C and plasma lipid parameters. In contrast, HbA1c, energy expenditure and plasma lipid concentrations were not correlated with plasma BAs levels in multivariable analysis. Both plasma CDCA, CA and DCA concentrations were negatively associated with insulin sensitivity in a wide range of subjects. Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and to increase energy expenditure in mice. Here, we investigated the relationship between fasting plasma BAs concentrations and metabolic parameters in humans. Fasting plasma glucose, insulin and lipid profile were measured in 14 healthy volunteers, 20 patients with type 2 diabetes (T2D), and 22 non-diabetic abdominally obese subjects. Insulin sensitivity was also assessed by the determination of the glucose infusion rate (GIR) during a hyperinsulinemic-euglycemic clamp in a subgroup of patients (9 healthy and 16 T2D subjects). Energy expenditure was measured by indirect calorimetry. Plasma cholic acid (CA), chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) concentrations were analyzed by gas chromatograph-mass spectrometry. In univariable analysis, a positive association was found between HOMA-IR and plasma CDCA (β = 0.09, p = 0.001), CA (β = 0.03, p = 0.09) and DCA concentrations (β = 0.07, p < 0.0001). Spearman analysis retrieved an inverse relationship between plasma CDCA (r = -0.44, p = 0.03), CA (r = -0.65, p = 0.001) and the GIR. HOMA-IR remained positively associated with CDCA (β = 0.11, p = 0.01), CA (β = 0.04, p = 0.01) and DCA (β = 0.06, p = 0.007) in multivariable analysis, after adjustment for age, gender, BMI, HbA1C and plasma lipid parameters. In contrast, HbA1c, energy expenditure and plasma lipid concentrations were not correlated with plasma BAs levels in multivariable analysis. Both plasma CDCA, CA and DCA concentrations were negatively associated with insulin sensitivity in a wide range of subjects. Abstract Background Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and to increase energy expenditure in mice. Here, we investigated the relationship between fasting plasma BAs concentrations and metabolic parameters in humans. Findings Fasting plasma glucose, insulin and lipid profile were measured in 14 healthy volunteers, 20 patients with type 2 diabetes (T2D), and 22 non-diabetic abdominally obese subjects. Insulin sensitivity was also assessed by the determination of the glucose infusion rate (GIR) during a hyperinsulinemic-euglycemic clamp in a subgroup of patients (9 healthy and 16 T2D subjects). Energy expenditure was measured by indirect calorimetry. Plasma cholic acid (CA), chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) concentrations were analyzed by gas chromatograph-mass spectrometry. In univariable analysis, a positive association was found between HOMA-IR and plasma CDCA (β = 0.09, p = 0.001), CA (β = 0.03, p = 0.09) and DCA concentrations (β = 0.07, p < 0.0001). Spearman analysis retrieved an inverse relationship between plasma CDCA (r = -0.44, p = 0.03), CA (r = -0.65, p = 0.001) and the GIR. HOMA-IR remained positively associated with CDCA (β = 0.11, p = 0.01), CA (β = 0.04, p = 0.01) and DCA (β = 0.06, p = 0.007) in multivariable analysis, after adjustment for age, gender, BMI, HbA1C and plasma lipid parameters. In contrast, HbA1c, energy expenditure and plasma lipid concentrations were not correlated with plasma BAs levels in multivariable analysis. Conclusions Both plasma CDCA, CA and DCA concentrations were negatively associated with insulin sensitivity in a wide range of subjects. Background Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and to increase energy expenditure in mice. Here, we investigated the relationship between fasting plasma BAs concentrations and metabolic parameters in humans. Findings Fasting plasma glucose, insulin and lipid profile were measured in 14 healthy volunteers, 20 patients with type 2 diabetes (T2D), and 22 non-diabetic abdominally obese subjects. Insulin sensitivity was also assessed by the determination of the glucose infusion rate (GIR) during a hyperinsulinemic-euglycemic clamp in a subgroup of patients (9 healthy and 16 T2D subjects). Energy expenditure was measured by indirect calorimetry. Plasma cholic acid (CA), chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) concentrations were analyzed by gas chromatograph-mass spectrometry. In univariable analysis, a positive association was found between HOMA-IR and plasma CDCA (β = 0.09, p = 0.001), CA (β = 0.03, p = 0.09) and DCA concentrations (β = 0.07, p < 0.0001). Spearman analysis retrieved an inverse relationship between plasma CDCA (r = -0.44, p = 0.03), CA (r = -0.65, p = 0.001) and the GIR. HOMA-IR remained positively associated with CDCA (β = 0.11, p = 0.01), CA (β = 0.04, p = 0.01) and DCA (β = 0.06, p = 0.007) in multivariable analysis, after adjustment for age, gender, BMI, HbA1C and plasma lipid parameters. In contrast, HbA1c, energy expenditure and plasma lipid concentrations were not correlated with plasma BAs levels in multivariable analysis. Conclusions Both plasma CDCA, CA and DCA concentrations were negatively associated with insulin sensitivity in a wide range of subjects. |
Audience | Academic |
Author | Zaïr, Yassine Laville, Martine Guyomarc'h-Delasalle, Béatrice Krempf, Michel Cariou, Bertrand Chetiveaux, Maud Pouteau, Etienne Disse, Emmanuel |
AuthorAffiliation | 2 Nestlé Research Center, R&D Santiago, 9260075 Maipú Santiago, Chile 1 INSERM, UMR915; Université de Nantes; CHU Nantes, Clinique d'Endocrinologie, Maladies Métaboliques et Nutrition, l'Institut du Thorax, Nantes, CRNH Nantes, F-44000 France 3 CRNH Rhone-Alpes; INSERM Unit -1060, CarMeN Laboratory and CENS, Lyon1 University; Hospices Civils de Lyon, France Centre Hospitalier Lyon-Sud, F-69310 Pierre Bénite, France |
AuthorAffiliation_xml | – name: 2 Nestlé Research Center, R&D Santiago, 9260075 Maipú Santiago, Chile – name: 1 INSERM, UMR915; Université de Nantes; CHU Nantes, Clinique d'Endocrinologie, Maladies Métaboliques et Nutrition, l'Institut du Thorax, Nantes, CRNH Nantes, F-44000 France – name: 3 CRNH Rhone-Alpes; INSERM Unit -1060, CarMeN Laboratory and CENS, Lyon1 University; Hospices Civils de Lyon, France Centre Hospitalier Lyon-Sud, F-69310 Pierre Bénite, France |
Author_xml | – sequence: 1 givenname: Bertrand surname: Cariou fullname: Cariou, Bertrand email: bertrand.cariou@univ-nantes.fr organization: INSERM, UMR915; Université de Nantes; CHU Nantes, Clinique d'Endocrinologie, Maladies Métaboliques et Nutrition – sequence: 2 givenname: Maud surname: Chetiveaux fullname: Chetiveaux, Maud organization: INSERM, UMR915; Université de Nantes; CHU Nantes, Clinique d'Endocrinologie, Maladies Métaboliques et Nutrition – sequence: 3 givenname: Yassine surname: Zaïr fullname: Zaïr, Yassine organization: INSERM, UMR915; Université de Nantes; CHU Nantes, Clinique d'Endocrinologie, Maladies Métaboliques et Nutrition – sequence: 4 givenname: Etienne surname: Pouteau fullname: Pouteau, Etienne organization: Nestlé Research Center, R&D Santiago – sequence: 5 givenname: Emmanuel surname: Disse fullname: Disse, Emmanuel organization: CRNH Rhone-Alpes; INSERM Unit -1060, CarMeN Laboratory and CENS, Lyon1 University; Hospices Civils de Lyon – sequence: 6 givenname: Béatrice surname: Guyomarc'h-Delasalle fullname: Guyomarc'h-Delasalle, Béatrice organization: INSERM, UMR915; Université de Nantes; CHU Nantes, Clinique d'Endocrinologie, Maladies Métaboliques et Nutrition – sequence: 7 givenname: Martine surname: Laville fullname: Laville, Martine organization: CRNH Rhone-Alpes; INSERM Unit -1060, CarMeN Laboratory and CENS, Lyon1 University; Hospices Civils de Lyon – sequence: 8 givenname: Michel surname: Krempf fullname: Krempf, Michel organization: INSERM, UMR915; Université de Nantes; CHU Nantes, Clinique d'Endocrinologie, Maladies Métaboliques et Nutrition |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21736725$$D View this record in MEDLINE/PubMed https://inserm.hal.science/inserm-00611430$$DView record in HAL |
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Cites_doi | 10.1016/j.cmet.2009.08.001 10.1038/nature04330 10.1186/1743-7075-7-73 10.1016/S0092-8674(00)00062-3 10.1074/jbc.M306309200 10.2337/diabetes.31.10.903 10.1073/pnas.0506982103 10.1172/JCI25604 10.1074/jbc.M510258200 10.1016/j.biochi.2004.11.018 10.2337/db11-0030 10.1074/jbc.M209706200 10.1002/hep.23831 10.2165/00003495-200767100-00001 10.1152/physrev.00010.2008 10.1016/S0006-291X(02)02550-0 |
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References | 10.1186/1743-7075-8-48-B11 10.1186/1743-7075-8-48-B12 10.1186/1743-7075-8-48-B20 10.1186/1743-7075-8-48-B10 - 10.1186/1743-7075-8-48-B5 10.1186/1743-7075-8-48-B3 10.1186/1743-7075-8-48-B2 10.1186/1743-7075-8-48-B1 10.1186/1743-7075-8-48-B13 10.1186/1743-7075-8-48-B9 10.1186/1743-7075-8-48-B19 10.1186/1743-7075-8-48-B8 10.1186/1743-7075-8-48-B7 10.1186/1743-7075-8-48-B6 10.1186/1743-7075-8-48-B18 12524422 - J Biol Chem. 2003 Mar 14;278(11):9435-40 12419312 - Biochem Biophys Res Commun. 2002 Nov 15;298(5):714-9 16400329 - Nature. 2006 Jan 26;439(7075):484-9 11030617 - Cell. 2000 Sep 15;102(6):731-44 19126757 - Physiol Rev. 2009 Jan;89(1):147-91 20815878 - Nutr Metab (Lond). 2010 Sep 03;7:73 15733743 - Biochimie. 2005 Jan;87(1):93-8 6759223 - Diabetes. 1982 Oct;31(10):903-10 382871 - Am J Physiol. 1979 Sep;237(3):E214-23 12917447 - J Biol Chem. 2003 Oct 24;278(43):41930-7 16446356 - J Biol Chem. 2006 Apr 21;281(16):11039-49 18682704 - Mol Syst Biol. 2008;4:214 21593203 - Diabetes. 2011 Jul;60(7):1861-71 16410358 - Proc Natl Acad Sci U S A. 2006 Jan 24;103(4):1006-11 17412431 - Trends Pharmacol Sci. 2007 May;28(5):236-43 19723493 - Cell Metab. 2009 Sep;10(3):167-77 17600387 - Drugs. 2007;67(10):1383-92 20725912 - Hepatology. 2010 Oct;52(4):1455-64 16557297 - J Clin Invest. 2006 Apr;116(4):1102-9 2614267 - J Lipid Res. 1989 Oct;30(10):1647-52 870827 - N Engl J Med. 1977 Jun 16;296(24):1365-71 |
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Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose... Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose tolerance and... Background Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose... BACKGROUND: Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve glucose... Abstract Background Accumulating data suggest a novel role for bile acids (BAs) in modulating metabolic homeostasis. BA treatment has been shown to improve... |
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SubjectTerms | adults Bile acids blood glucose blood lipids Blood sugar body mass index Brief Communication calorimetry Chenodeoxycholic acid Cholic acid Clinical Nutrition deoxycholic acid energy expenditure Food and Nutrition FXR gas chromatography gender glucose glucose tolerance homeostasis Human health and pathology humans hyperinsulinemic-euglycemic clamp insulin insulin resistance Life Sciences lipid content lipids mass spectrometry Medicine Medicine & Public Health Metabolic Diseases mice multivariate analysis noninsulin-dependent diabetes mellitus patients Physiological aspects TGR5 Tissues and Organs type 2 diabetes volunteers |
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Title | Fasting plasma chenodeoxycholic acid and cholic acid concentrations are inversely correlated with insulin sensitivity in adults |
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