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The effect of the EP3 antagonist DG-041 on male mice with diet-induced obesity.
Ceddia RP, Downey JD, Morrison RD, Kraemer MP, Davis SE, Wu J, Lindsley CW, Yin H, Daniels JS, Breyer RM
(2019) Prostaglandins Other Lipid Mediat 144: 106353
MeSH Terms: Acrylamides, Animals, Blood Pressure, Body Weight, Diet, High-Fat, HEK293 Cells, Humans, Insulin Resistance, Male, Mice, Muscle, Skeletal, Obesity, Phenotype, Receptors, Prostaglandin E, EP3 Subtype, Sulfones, Triglycerides
Show Abstract · Added September 4, 2019
BACKGROUND/AIMS - The prostaglandin E (PGE) EP3 receptor has a multifaceted role in metabolism. Drugs targeting EP3 have been proposed as therapeutics for diabetes; however, studies utilizing global EP3 knockout mice suggest that EP3 blockade increases obesity and insulin resistance. The present studies attempt to determine the effect of acute EP3 antagonist treatment on the diabetic phenotype.
METHODS - DG-041 was confirmed to be a high affinity antagonist at the mouse EP3 receptor by competition radioligand binding and by blockade of EP3-mediated responses. DG-041 pharmacokinetic studies were performed to determine the most efficacious route of administration. Male C57BL/6 × BALB/c (CB6F1) mice were fed diets containing 10%, 45%, or 60% calories from fat to induce obesity. Changes to the metabolic phenotype in these mice were evaluated after one week treatment with DG-041.
RESULTS - Subcutaneous injections of DG-041 at 20 mg/kg blocked the sulprostone-evoked rise in mean arterial pressure confirming the efficacy of this administration regime. Seven day treatment with DG-041 had minimal effect on body composition or glycemic control. DG-041 administration caused a reduction in skeletal muscle triglyceride content while showing a trend toward increased hepatic triglycerides.
CONCLUSION - Short term EP3 administration of DG-041 produced effective blockade of the EP3 receptor and decreased skeletal muscle triglyceride content but had no significant effects on the diabetic phenotype.
Published by Elsevier Inc.
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FcγRIIb on CD11c cells modulates serum cholesterol and triglyceride levels and differentially affects atherosclerosis in male and female Ldlr mice.
Marvin J, Rhoads JP, Major AS
(2019) Atherosclerosis 285: 108-119
MeSH Terms: Animals, Atherosclerosis, CD11 Antigens, Cholesterol, Dendritic Cells, Female, Male, Mice, Mice, Inbred C57BL, Receptors, IgG, Sex Factors, Triglycerides
Show Abstract · Added March 30, 2020
BACKGROUND AND AIMS - Circulating levels of oxidized lipoprotein (oxLDL) correlate with myocardial infarction risk and atherosclerosis severity. Our previous study demonstrates that oxLDL immune complexes (oxLDL-ICs) can signal through FcγRs on bone marrow-derived dendritic cells (BMDCs) and enhance their activation and inflammatory cytokine secretion. While global FcγR studies have shown that activating FcγRs are proatherogenic, the role of the inhibitory FcγRIIb is unclear. We sought to determine the role of DC-specific FcγRIIb in atherosclerosis.
METHODS - Bone marrow chimeras were generated by rescuing lethally irradiated Ldlr mice with hematopoietic cells from littermate CD11c-Cre or CD11c-CreFcgr2b donors. Four weeks following transplant, recipients were placed on a Western diet for eight weeks. Various tissues and organs were analyzed for differences in inflammation.
RESULTS - Quantitation of atherosclerosis in the proximal aorta demonstrated a 58% increase in female CD11c-CreFcgr2b recipients, but a surprising 44% decrease in male recipients. Hepatic cholesterol and triglycerides were increased in female CD11c-CreFcgr2b recipients. This was associated with an increase in CD36 and MHC Class II expression on hepatic CD11cCD11b DCs in female livers. In contrast, male CD11c-CreFcgr2b recipients had decreased hepatic lipids with a corresponding decrease in CD36 and MHC Class II expression on CD11c cells. Interestingly, both sexes of CD11c-CreFcgr2b recipients had significant decreases in serum cholesterol and TGs with corresponding decreases in liver Fasn transcripts.
CONCLUSIONS - The absence of FcγRIIb expression on CD11c cells results in sex-dependent alteration in liver inflammation influencing atherogenesis and sex-independent modulation of serum cholesterol and TGs.
Published by Elsevier B.V.
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Administration of N-Acyl-Phosphatidylethanolamine Expressing Bacteria to Low Density Lipoprotein Receptor Mice Improves Indices of Cardiometabolic Disease.
May-Zhang LS, Chen Z, Dosoky NS, Yancey PG, Boyd KL, Hasty AH, Linton MF, Davies SS
(2019) Sci Rep 9: 420
MeSH Terms: Animals, Cardiovascular Diseases, Escherichia coli, Fatty Acids, Gastrointestinal Microbiome, Liver, Liver Cirrhosis, Mice, Phosphatidylethanolamines, Receptors, LDL, Triglycerides
Show Abstract · Added January 30, 2019
Obesity increases the risk for cardiometabolic diseases. N-acyl phosphatidylethanolamines (NAPEs) are precursors of N-acylethanolamides, which are endogenous lipid satiety factors. Incorporating engineered bacteria expressing NAPEs into the gut microbiota retards development of diet induced obesity in wild-type mice. Because NAPEs can also exert anti-inflammatory effects, we hypothesized that administering NAPE-expressing bacteria to low-density lipoprotein receptor (Ldlr) mice fed a Western diet would improve various indices of cardiometabolic disease manifested by these mice. NAPE-expressing E. coli Nissle 1917 (pNAPE-EcN), control Nissle 1917 (pEcN), or vehicle (veh) were given via drinking water to Ldlr mice for 12 weeks. Compared to pEcN or veh treatment, pNAPE-EcN significantly reduced body weight and adiposity, hepatic triglycerides, fatty acid synthesis genes, and increased expression of fatty acid oxidation genes. pNAPE-EcN also significantly reduced markers for hepatic inflammation and early signs of fibrotic development. Serum cholesterol was reduced with pNAPE-EcN, but atherosclerotic lesion size showed only a non-significant trend for reduction. However, pNAPE-EcN treatment reduced lesion necrosis by 69% indicating an effect on preventing macrophage inflammatory death. Our results suggest that incorporation of NAPE expressing bacteria into the gut microbiota can potentially serve as an adjuvant therapy to retard development of cardiometabolic disease.
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Longer lactation duration is associated with decreased prevalence of non-alcoholic fatty liver disease in women.
Ajmera VH, Terrault NA, VanWagner LB, Sarkar M, Lewis CE, Carr JJ, Gunderson EP
(2019) J Hepatol 70: 126-132
MeSH Terms: Adolescent, Adult, Biomarkers, Blood Glucose, Breast Feeding, Disease Progression, Female, Follow-Up Studies, Humans, Insulin, Lactation, Non-alcoholic Fatty Liver Disease, Prevalence, Prognosis, Retrospective Studies, Risk Factors, Time Factors, Triglycerides, United States, Young Adult
Show Abstract · Added January 10, 2020
BACKGROUND & AIMS - Lactation lowers blood glucose and triglycerides, and increases insulin sensitivity. We hypothesized that a longer duration of lactation would be associated with lower prevalence of non-alcoholic fatty liver disease (NAFLD), which is the leading cause of chronic liver disease in the United States.
METHODS - Participants from the Coronary Artery Risk Development in Young Adults cohort study who delivered ≥ 1 child post-baseline (Y0: 1985-1986), and underwent CT quantification of hepatic steatosis 25 years following cohort entry (Y25: 2010-2011) were included (n = 844). The duration of lactation was summed for all post-baseline births, and NAFLD at Y25 was assessed by central review of CT images and defined by liver attenuation ≤ 40 Hounsfield Units after exclusion of other causes of hepatic steatosis. Unadjusted and multivariable logistic regression analyses were performed using an a priori set of confounding variables; age, race, education, and baseline body mass index.
RESULTS - Of 844 women who delivered after baseline (48% black, 52% white, mean age 49 years at Y25 exam), 32% reported lactation duration of 0 to 1 month, 25% reported >1 to 6 months, 43% reported more than 6 months, while 54 (6%) had NAFLD. Longer lactation duration was inversely associated with NAFLD in unadjusted logistic regression. For women who reported >6 months lactation compared to those reporting 0-1 month, the odds ratio for NAFLD was 0.48 (95% CI 0.25-0.94; p = 0.03) and the association remained after adjustment for confounders (adjusted odds ratio 0.46; 95% CI 0.22-0.97; p = 0.04).
CONCLUSIONS - A longer duration of lactation, particularly greater than 6 months, is associated with lower odds of NAFLD in mid-life and may represent a modifiable risk factor for NAFLD.
LAY SUMMARY - A longer duration of breastfeeding has been associated with multiple potential health benefits for the mother including reduction in heart disease, diabetes and certain cancers. In this study we found that breastfeeding for longer than 6 months was associated with a lower risk of non-alcoholic fatty liver disease in mid-life.
Copyright © 2018 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
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Exome Sequencing Identifies Genetic Variants Associated with Circulating Lipid Levels in Mexican Americans: The Insulin Resistance Atherosclerosis Family Study (IRASFS).
Gao C, Tabb KL, Dimitrov LM, Taylor KD, Wang N, Guo X, Long J, Rotter JI, Watanabe RM, Curran JE, Blangero J, Langefeld CD, Bowden DW, Palmer ND
(2018) Sci Rep 8: 5603
MeSH Terms: Adult, Apolipoprotein A-V, Atherosclerosis, Carrier Proteins, Female, Genetic Linkage, Genetic Variation, Genome-Wide Association Study, Humans, Insulin Resistance, Lipids, Lipoproteins, HDL, Mexican Americans, Middle Aged, Polymorphism, Single Nucleotide, Triglycerides, Whole Exome Sequencing
Show Abstract · Added April 10, 2018
Genome-wide association studies have identified numerous variants associated with lipid levels; yet, the majority are located in non-coding regions with unclear mechanisms. In the Insulin Resistance Atherosclerosis Family Study (IRASFS), heritability estimates suggest a strong genetic basis: low-density lipoprotein (LDL, h = 0.50), high-density lipoprotein (HDL, h = 0.57), total cholesterol (TC, h = 0.53), and triglyceride (TG, h = 0.42) levels. Exome sequencing of 1,205 Mexican Americans (90 pedigrees) from the IRASFS identified 548,889 variants and association and linkage analyses with lipid levels were performed. One genome-wide significant signal was detected in APOA5 with TG (rs651821, P = 3.67 × 10, LOD = 2.36, MAF = 14.2%). In addition, two correlated SNPs (r = 1.0) rs189547099 (P = 6.31 × 10, LOD = 3.13, MAF = 0.50%) and chr4:157997598 (P = 6.31 × 10, LOD = 3.13, MAF = 0.50%) reached exome-wide significance (P < 9.11 × 10). rs189547099 is an intronic SNP in FNIP2 and SNP chr4:157997598 is intronic in GLRB. Linkage analysis revealed 46 SNPs with a LOD > 3 with the strongest signal at rs1141070 (LOD = 4.30, P = 0.33, MAF = 21.6%) in DFFB. A total of 53 nominally associated variants (P < 5.00 × 10, MAF ≥ 1.0%) were selected for replication in six Mexican-American cohorts (N = 3,280). The strongest signal observed was a synonymous variant (rs1160983, P = 4.44 × 10, MAF = 2.7%) in TOMM40. Beyond primary findings, previously reported lipid loci were fine-mapped using exome sequencing in IRASFS. These results support that exome sequencing complements and extends insights into the genetics of lipid levels.
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A case of severe acquired hypertriglyceridemia in a 7-year-old girl.
Lilley JS, Linton MF, Kelley JC, Graham TB, Fazio S, Tavori H
(2017) J Clin Lipidol 11: 1480-1484
MeSH Terms: Autoantibodies, Autoimmunity, Child, Female, Heterozygote, Humans, Hyperlipoproteinemia Type I, Lipoprotein Lipase, Mutation, Prednisone, Sjogren's Syndrome, Triglycerides
Show Abstract · Added April 10, 2018
We report a case of severe type I hyperlipoproteinemia caused by autoimmunity against lipoprotein lipase (LPL) in the context of presymptomatic Sjögren's syndrome. A 7-year-old mixed race (Caucasian/African American) girl was admitted to the intensive care unit at Vanderbilt Children's Hospital with acute pancreatitis and shock. She was previously healthy aside from asthma and history of Hashimoto's thyroiditis. Admission triglycerides (TGs) were 2191 mg/dL but returned to normal during the hospital stay and in the absence of food intake. At discharge, she was placed on a low-fat, low-sugar diet. She did not respond to fibrates, prescription fish oil, metformin, or orlistat, and during the following 2 years, she was hospitalized several times with recurrent pancreatitis. Except for a heterozygous mutation in the promoter region of LPL, predicted to have no clinical significance, she had no further mutations in genes known to affect TG metabolism and to cause inherited type I hyperlipoproteinemia, such as APOA5, APOC2, GPIHBP1, or LMF1. When her TG levels normalized after incidental use of prednisone, an autoimmune mechanism was suspected. Immunoblot analyses showed the presence of autoantibodies to LPL in the patient's plasma. Autoantibodies to LPL decreased by 37% while patient was on prednisone, and by 68% as she subsequently transitioned to hydroxychloroquine monotherapy. While on hydroxychloroquine, she underwent a supervised high-fat meal challenge and showed normal ability to metabolize TG. For the past 3 years and 6 months, she has had TG consistently <250 mg/dL, and no symptoms of, or readmissions for, pancreatitis.
Copyright © 2017 National Lipid Association. Published by Elsevier Inc. All rights reserved.
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Association analyses of East Asian individuals and trans-ancestry analyses with European individuals reveal new loci associated with cholesterol and triglyceride levels.
Spracklen CN, Chen P, Kim YJ, Wang X, Cai H, Li S, Long J, Wu Y, Wang YX, Takeuchi F, Wu JY, Jung KJ, Hu C, Akiyama K, Zhang Y, Moon S, Johnson TA, Li H, Dorajoo R, He M, Cannon ME, Roman TS, Salfati E, Lin KH, Guo X, Sheu WHH, Absher D, Adair LS, Assimes TL, Aung T, Cai Q, Chang LC, Chen CH, Chien LH, Chuang LM, Chuang SC, Du S, Fan Q, Fann CSJ, Feranil AB, Friedlander Y, Gordon-Larsen P, Gu D, Gui L, Guo Z, Heng CK, Hixson J, Hou X, Hsiung CA, Hu Y, Hwang MY, Hwu CM, Isono M, Juang JJ, Khor CC, Kim YK, Koh WP, Kubo M, Lee IT, Lee SJ, Lee WJ, Liang KW, Lim B, Lim SH, Liu J, Nabika T, Pan WH, Peng H, Quertermous T, Sabanayagam C, Sandow K, Shi J, Sun L, Tan PC, Tan SP, Taylor KD, Teo YY, Toh SA, Tsunoda T, van Dam RM, Wang A, Wang F, Wang J, Wei WB, Xiang YB, Yao J, Yuan JM, Zhang R, Zhao W, Chen YI, Rich SS, Rotter JI, Wang TD, Wu T, Lin X, Han BG, Tanaka T, Cho YS, Katsuya T, Jia W, Jee SH, Chen YT, Kato N, Jonas JB, Cheng CY, Shu XO, He J, Zheng W, Wong TY, Huang W, Kim BJ, Tai ES, Mohlke KL, Sim X
(2017) Hum Mol Genet 26: 1770-1784
MeSH Terms: Adult, Alleles, Asian Continental Ancestry Group, Cholesterol, Ethnic Groups, European Continental Ancestry Group, Female, Gene Frequency, Genetic Association Studies, Genome-Wide Association Study, Humans, Linkage Disequilibrium, Lipids, Lipoproteins, HDL, Lipoproteins, LDL, Male, Middle Aged, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Triglycerides
Show Abstract · Added April 3, 2018
Large-scale meta-analyses of genome-wide association studies (GWAS) have identified >175 loci associated with fasting cholesterol levels, including total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG). With differences in linkage disequilibrium (LD) structure and allele frequencies between ancestry groups, studies in additional large samples may detect new associations. We conducted staged GWAS meta-analyses in up to 69,414 East Asian individuals from 24 studies with participants from Japan, the Philippines, Korea, China, Singapore, and Taiwan. These meta-analyses identified (P < 5 × 10-8) three novel loci associated with HDL-C near CD163-APOBEC1 (P = 7.4 × 10-9), NCOA2 (P = 1.6 × 10-8), and NID2-PTGDR (P = 4.2 × 10-8), and one novel locus associated with TG near WDR11-FGFR2 (P = 2.7 × 10-10). Conditional analyses identified a second signal near CD163-APOBEC1. We then combined results from the East Asian meta-analysis with association results from up to 187,365 European individuals from the Global Lipids Genetics Consortium in a trans-ancestry meta-analysis. This analysis identified (log10Bayes Factor ≥6.1) eight additional novel lipid loci. Among the twelve total loci identified, the index variants at eight loci have demonstrated at least nominal significance with other metabolic traits in prior studies, and two loci exhibited coincident eQTLs (P < 1 × 10-5) in subcutaneous adipose tissue for BPTF and PDGFC. Taken together, these analyses identified multiple novel lipid loci, providing new potential therapeutic targets.
© The Author 2017. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
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Testosterone Levels in Pre-Menopausal Women are Associated With Nonalcoholic Fatty Liver Disease in Midlife.
Sarkar M, Wellons M, Cedars MI, VanWagner L, Gunderson EP, Ajmera V, Torchen L, Siscovick D, Carr JJ, Terry JG, Rinella M, Lewis CE, Terrault N
(2017) Am J Gastroenterol 112: 755-762
MeSH Terms: Adult, Body Mass Index, Diabetes Mellitus, Follow-Up Studies, Humans, Insulin Resistance, Intra-Abdominal Fat, Lipoproteins, HDL, Middle Aged, Multidetector Computed Tomography, Non-alcoholic Fatty Liver Disease, Premenopause, Prevalence, Risk Factors, Testosterone, Triglycerides, Waist Circumference, Young Adult
Show Abstract · Added September 11, 2017
OBJECTIVES - Young women with hyperandrogenism have high risk of metabolic co-morbidities, including increased risk of nonalcoholic fatty liver disease (NAFLD). Whether testosterone (the predominant androgen) is associated with NAFLD independent of metabolic co-factors is unclear. Additionally, whether testosterone confers increased risk of NAFLD in women without hyperandrogenism is unknown.
METHODS - Among women in the prospective population-based multicenter Coronary Artery Risk Development in Young Adults (CARDIA) study, we assessed whether free testosterone levels measured at Year 2 (1987-1988) were associated with prevalent NAFLD at Year 25 (2010-2011) (n=1052). NAFLD was defined using noncontrast abdominal CT scan with liver attenuation≤40 Hounsfield units after excluding other causes of hepatic fat. The association of free testosterone with prevalent NAFLD was assessed by logistic regression.
RESULTS - Increasing quintiles of free testosterone were associated with prevalent NAFLD at Year 25 (adjusted odds ratio (AOR) 1.25, 95% confidence interval (CI) 1.04-1.50, P=0.015), independent of insulin resistance, body mass index, waist circumference, and serum lipids. Importantly, the association persisted among n=955 women without androgen excess (AOR 1.27, 95% CI 1.05-1.53, P=0.016). Visceral adipose tissue (VAT) volume partially mediated the association of free testosterone with NAFLD (mediating effect 41.0%, 95% CI 22-119%).
CONCLUSIONS - Increasing free testosterone is associated with prevalent NAFLD in middle age, even in women without androgen excess. Visceral adiposity appears to play an important role in the relationship between testosterone and NAFLD in women. Testosterone may provide a potential novel target for NAFLD therapeutics, and future studies in pre-menopausal women should consider the importance of testosterone as a risk factor for NAFLD.
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Integrin-Linked Kinase Is Necessary for the Development of Diet-Induced Hepatic Insulin Resistance.
Williams AS, Trefts E, Lantier L, Grueter CA, Bracy DP, James FD, Pozzi A, Zent R, Wasserman DH
(2017) Diabetes 66: 325-334
MeSH Terms: Animals, Diet, High-Fat, Extracellular Matrix, Gene Deletion, Glucose Clamp Technique, Insulin Resistance, Liver, Mice, Mice, Transgenic, Protein-Serine-Threonine Kinases, Real-Time Polymerase Chain Reaction, Triglycerides
Show Abstract · Added April 26, 2017
The liver extracellular matrix (ECM) expands with high-fat (HF) feeding. This finding led us to address whether receptors for the ECM, integrins, are key to the development of diet-induced hepatic insulin resistance. Integrin-linked kinase (ILK) is a downstream integrin signaling molecule involved in multiple hepatic processes, including those related to differentiation, wound healing, and metabolism. We tested the hypothesis that deletion of ILK in mice on an HF diet would disrupt the ECM-integrin signaling axis, thereby preventing the transformation into the insulin-resistant liver. To determine the role of ILK in hepatic insulin action in vivo, male C57BL/6J ILK mice were crossed with Albcre mice to produce a hepatocyte-specific ILK deletion (ILKAlbcre). Results from this study show that hepatic ILK deletion has no effect on insulin action in lean mice but sensitizes the liver to insulin during the challenge of HF feeding. This effect corresponds to changes in the expression and activation of key insulin signaling pathways as well as a greater capacity for hepatic mitochondrial glucose oxidation. This demonstrates that ILK contributes to hepatic insulin resistance and highlights the previously undefined role of integrin signaling in the pathogenesis of diet-induced hepatic insulin resistance.
© 2017 by the American Diabetes Association.
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Physical activity and metabolic health in chronic kidney disease: a cross-sectional study.
Bowlby W, Zelnick LR, Henry C, Himmelfarb J, Kahn SE, Kestenbaum B, Robinson-Cohen C, Utzschneider KM, de Boer IH
(2016) BMC Nephrol 17: 187
MeSH Terms: Absorptiometry, Photon, Accelerometry, Adipose Tissue, Aged, Aged, 80 and over, Blood Pressure, C-Reactive Protein, Case-Control Studies, Cholesterol, HDL, Cross-Sectional Studies, Exercise, Female, Glomerular Filtration Rate, Homeostasis, Humans, Insulin Resistance, Male, Middle Aged, Renal Insufficiency, Chronic, Triglycerides
Show Abstract · Added September 19, 2017
BACKGROUND - Patients with chronic kidney disease (CKD) are at high risk of progression to end stage renal disease and cardiovascular events. Physical activity may reduce these risks by improving metabolic health. We tested associations of physical activity with central components of metabolic health among people with moderate-severe non-diabetic CKD.
METHODS - We performed a cross-sectional study of 47 people with CKD (estimated GFR <60 ml/min/1.73 m) and 29 healthy control subjects. Accelerometry was used to measured physical activity over 7 days, the hyperinsulinemic-euglycemic clamp was used to measure insulin sensitivity, and DXA was used to measured fat mass. We tested associations of physical activity with insulin sensitivity, fat mass, blood pressure, serum lipid concentrations, and serum high sensitivity C-reactive protein concentration using multivariable linear regression, adjusting for possible confounding factors.
RESULTS - Participants with CKD were less active than participants without CKD (mean (SD) 468.1 (233.1) versus 662.3 (292.5) counts per minute) and had lower insulin sensitivity (4.1 (2.1) versus 5.2 (2.0 (mg/min)/(μU/mL)), higher fat mass (32.0 (11.4) versus 29.4 (14.8) kg), and higher triglyceride concentrations (153.2 (91.6) versus 99.6 (66.8) mg/dL). With adjustment for demographics, comorbidity, medications, and estimated GFR, each two-fold higher level of physical activity was associated with a 0.9 (mg/min)/(μU/mL) higher insulin sensitivity (95% CI 0.2, 1.5, p = 0.006), an 8.0 kg lower fat mass (-12.9, -3.1, p = 0.001), and a 37.9 mg/dL lower triglyceride concentration (-71.9, -3.9, p = 0.03). Associations of physical activity with insulin sensitivity and triglycerides did not differ significantly by CKD status (p-values for interaction >0.3).
CONCLUSIONS - Greater physical activity is associated with multiple manifestations of metabolic health among people with moderate-severe CKD.
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