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  • 1
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    Online Resource
    Relation of Lipoprotein(a) Levels to Incident Type 2 Diabetes and Modification by Alirocumab Treatment
    American Diabetes Association ; 2021
    In:  Diabetes Care Vol. 44, No. 5 ( 2021-05-01), p. 1219-1227
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 44, No. 5 ( 2021-05-01), p. 1219-1227
    Abstract: In observational data, lower levels of lipoprotein(a) have been associated with greater prevalence of type 2 diabetes. Whether pharmacologic lowering of lipoprotein(a) influences incident type 2 diabetes is unknown. We determined the relationship of lipoprotein(a) concentration with incident type 2 diabetes and effects of treatment with alirocumab, a PCSK9 inhibitor. RESEARCH DESIGN AND METHODS In the ODYSSEY OUTCOMES trial alirocumab was compared with placebo in patients with acute coronary syndrome. Incident diabetes was determined from laboratory, medication, and adverse event data. RESULTS Among 13,480 patients without diabetes at baseline, 1,324 developed type 2 diabetes over a median 2.7 years. Median baseline lipoprotein(a) was 21.9 mg/dL. With placebo, 10 mg/dL lower baseline lipoprotein(a) was associated with hazard ratio 1.04 (95% CI 1.02−1.06, P & lt; 0.001) for incident type 2 diabetes. Alirocumab reduced lipoprotein(a) by a median 23.2% with greater absolute reductions from higher baseline levels and no overall effect on incident type 2 diabetes (hazard ratio 0.95, 95% CI 0.85–1.05). At low baseline lipoprotein(a) levels, alirocumab tended to reduce incident type 2 diabetes, while at high baseline lipoprotein(a) alirocumab tended to increase incident type 2 diabetes compared with placebo (treatment–baseline lipoprotein(a) interaction P = 0.006). In the alirocumab group, a 10 mg/dL decrease in lipoprotein(a) from baseline was associated with hazard ratio 1.07 (95% CI 1.03−1.12; P = 0.0002) for incident type 2 diabetes. CONCLUSIONS In patients with acute coronary syndrome, baseline lipoprotein(a) concentration associated inversely with incident type 2 diabetes. Alirocumab had neutral overall effect on incident type 2 diabetes. However, treatment-related reductions in lipoprotein(a), more pronounced from high baseline levels, were associated with increased risk of incident type 2 diabetes. Whether these findings pertain to other therapies that reduce lipoprotein(a) is undetermined.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc20-2842
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2021
    detail.hit.zdb_id: 1490520-6
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  • 2
    Online Resource
    Online Resource
    Receptor binding and tyrosine kinase activation by insulin analogues with extreme affinities studied in human hepatoma HepG2 cells
    American Diabetes Association ; 1991
    In:  Diabetes Vol. 40, No. 11 ( 1991-11-01), p. 1488-1495
    Details
    In: Diabetes, American Diabetes Association, Vol. 40, No. 11 ( 1991-11-01), p. 1488-1495
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 0012-1797
    URL: Article
    DOI: 10.2337/diabetes.40.11.1488
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 1991
    detail.hit.zdb_id: 1501252-9
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  • 3
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    Online Resource
    3-Hydroxyisobutyrate, A Strong Marker of Insulin Resistance in Type 2 Diabetes and Obesity That Modulates White and Brown Adipocyte Metabolism
    American Diabetes Association ; 2020
    In:  Diabetes Vol. 69, No. 9 ( 2020-09-01), p. 1903-1916
    Details
    In: Diabetes, American Diabetes Association, Vol. 69, No. 9 ( 2020-09-01), p. 1903-1916
    Abstract: Circulating branched-chain amino acids (BCAAs) associate with insulin resistance and type 2 diabetes. 3-Hydroxyisobutyrate (3-HIB) is a catabolic intermediate of the BCAA valine. In this study, we show that in a cohort of 4,942 men and women, circulating 3-HIB is elevated according to levels of hyperglycemia and established type 2 diabetes. In complementary cohorts with measures of insulin resistance, we found positive correlates for circulating 3-HIB concentrations with HOMA2 of insulin resistance, as well as a transient increase in 3-HIB followed by a marked decrease after bariatric surgery and weight loss. During differentiation, both white and brown adipocytes upregulate BCAA utilization and release increasing amounts of 3-HIB. Knockdown of the 3-HIB–forming enzyme 3-hydroxyisobutyryl-CoA hydrolase decreases release of 3-HIB and lipid accumulation in both cell types. Conversely, addition of 3-HIB to white and brown adipocyte cultures increases fatty acid uptake and modulated insulin-stimulated glucose uptake in a time-dependent manner. Finally, 3-HIB treatment decreases mitochondrial oxygen consumption and generation of reactive oxygen species in white adipocytes, while increasing these measures in brown adipocytes. Our data establish 3-HIB as a novel adipocyte-derived regulator of adipocyte subtype-specific functions strongly linked to obesity, insulin resistance, and type 2 diabetes.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db19-1174
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2020
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  • 4
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    Online Resource
    Metabolic Syndrome, Independent of Its Components, Is a Risk Factor for Stroke and Death But Not for Coronary Heart Disease Among Hypertensive Patients in the ASCOT-BPLA
    American Diabetes Association ; 2010
    In:  Diabetes Care Vol. 33, No. 7 ( 2010-07-01), p. 1647-1651
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 33, No. 7 ( 2010-07-01), p. 1647-1651
    Abstract: To evaluate whether in hypertensive patients the risk of cardiovascular disease is greater in association with the metabolic syndrome (MetS) or the sum of its individual components. RESEARCH DESIGN AND METHODS Cox regression analysis models were developed to assess the influence of age, sex, ethnicity, and the individual components of MetS on risk associated with the MetS (using several definitions) of coronary outcomes, stroke, and all-cause mortality. RESULTS MetS was significantly associated with coronary outcomes, stroke, and all-cause mortality after adjusting for age, sex, and ethnicity. However, when the model was further adjusted for the individual components, MetS was associated with significantly increased risk of stroke (hazard ratio 1.34 [95% CI 1.07–1.68]) and all-cause mortality (1.35 [1.16–1.58] ) but not coronary outcomes (fatal coronary heart disease plus nonfatal myocardial infarction 1.16 [0.95–1.43] and total coronary events 1.06 [0.91–1.24] ). CONCLUSIONS MetS, independent of its individual components, is associated with increased risk of stroke and all-cause mortality but not coronary outcomes.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc09-2208
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2010
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  • 5
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    Online Resource
    Role of the Neutral Amino Acid Transporter SLC7A10 in Adipocyte Lipid Storage, Obesity, and Insulin Resistance
    American Diabetes Association ; 2021
    In:  Diabetes Vol. 70, No. 3 ( 2021-03-01), p. 680-695
    Details
    In: Diabetes, American Diabetes Association, Vol. 70, No. 3 ( 2021-03-01), p. 680-695
    Abstract: Elucidation of mechanisms that govern lipid storage, oxidative stress, and insulin resistance may lead to improved therapeutic options for type 2 diabetes and other obesity-related diseases. Here, we find that adipose expression of the small neutral amino acid transporter SLC7A10, also known as alanine-serine-cysteine transporter-1 (ASC-1), shows strong inverse correlates with visceral adiposity, insulin resistance, and adipocyte hypertrophy across multiple cohorts. Concordantly, loss of Slc7a10 function in zebrafish in vivo accelerates diet-induced body weight gain and adipocyte enlargement. Mechanistically, SLC7A10 inhibition in human and murine adipocytes decreases adipocyte serine uptake and total glutathione levels and promotes reactive oxygen species (ROS) generation. Conversely, SLC7A10 overexpression decreases ROS generation and increases mitochondrial respiratory capacity. RNA sequencing revealed consistent changes in gene expression between human adipocytes and zebrafish visceral adipose tissue following loss of SLC7A10, e.g., upregulation of SCD (lipid storage) and downregulation of CPT1A (lipid oxidation). Interestingly, ROS scavenger reduced lipid accumulation and attenuated the lipid-storing effect of SLC7A10 inhibition. These data uncover adipocyte SLC7A10 as a novel important regulator of adipocyte resilience to nutrient and oxidative stress, in part by enhancing glutathione levels and mitochondrial respiration, conducive to decreased ROS generation, lipid accumulation, adipocyte hypertrophy, insulin resistance, and type 2 diabetes.
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db20-0096
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2021
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  • 6
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    Online Resource
    Comparable Rates of Severe Hypoglycemia in People with Type 2 Diabetes (T2DM) at High Risk of Hypoglycemia Switching to either Insulin Glargine 300 U/mL (Gla-300) or Insulin Degludec (IDeg)—The Lightning Real-World Predictive Modeling Study
    American Diabetes Association ; 2018
    In:  Diabetes Vol. 67, No. Supplement_1 ( 2018-07-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 67, No. Supplement_1 ( 2018-07-01)
    Abstract: Hypoglycemic events during basal insulin (BI) treatment, recorded by physicians in U.S. electronic health records in real-life practice, were used to predict hypoglycemia rates in people with T2DM prescribed BI analogs. Based on large-scale real-world data (Optum Humedica), a predictive model (implementing machine learning and controlling for & gt;160 baseline demographic and clinical variables) was developed and validated for each drug-specific cohort (patients treated with a specific BI). Overall, models predicted similar severe hypoglycemia rates when switching from another BI to second-generation BI analogs Gla-300 or IDeg. This subanalysis focuses on severe hypoglycemia rates in clinically vulnerable subgroups of patients. Numerically, the highest rates were found in the subgroup with prior hypoglycemic events (Table). The models predicted no statistically significant differences in severe hypoglycemia rates between Gla-300 and IDeg in any of the at-risk subgroups (Table). In summary, using real-world data, these predictive modeling results show similar rates of severe hypoglycemia when switching to either Gla-300 or IDeg, in subgroups of patients with T2DM at high risk of hypoglycemia. Disclosure L. Meneghini: Advisory Panel; Self; Novo Nordisk Inc., Sanofi US. Consultant; Self; Sanofi US, Novo Nordisk Inc.. Advisory Panel; Self; Intarcia Therapeutics, Inc.. Other Relationship; Self; American Diabetes Association. R. Roussel: Advisory Panel; Self; AbbVie Inc., Abbott, Eli Lilly and Company, Sanofi, Novo Nordisk A/S, AstraZeneca. Speaker's Bureau; Self; Servier. Consultant; Self; Bayer AG. Advisory Panel; Self; Merck Sharp & Dohme Corp.. Research Support; Self; Amgen Inc., Sanofi, Novo Nordisk A/S, Danone Research. Stock/Shareholder; Self; Iriade. Advisory Panel; Self; Physiogenex S.A.S. F.L. Zhou: Employee; Self; Sanofi. Stock/Shareholder; Self; Sanofi. Employee; Spouse/Partner; Lexicon Pharmaceuticals, Inc.. Stock/Shareholder; Spouse/Partner; Lexicon Pharmaceuticals, Inc. Z. Bosnyak: Employee; Self; Sanofi. Stock/Shareholder; Self; Sanofi. J. Westerbacka: Employee; Self; Sanofi. Stock/Shareholder; Self; Sanofi. R. Berria: Employee; Self; Sanofi. Stock/Shareholder; Self; Sanofi. J. Jimenez: Employee; Self; Sanofi. Stock/Shareholder; Self; Sanofi. B. Eliasson: Advisory Panel; Self; Amgen Inc.. Speaker's Bureau; Self; AstraZeneca. Advisory Panel; Self; Boehringer Ingelheim GmbH. Speaker's Bureau; Self; Eli Lilly and Company. Advisory Panel; Self; Merck Sharp & Dohme Corp.. Speaker's Bureau; Self; Novo Nordisk A/S. Consultant; Self; Sanofi. I. Hramiak: Advisory Panel; Self; AstraZeneca. Research Support; Self; AstraZeneca. Advisory Panel; Self; Eli Lilly and Company. Research Support; Self; Eli Lilly and Company. Advisory Panel; Self; GlaxoSmithKline plc.. Research Support; Self; GlaxoSmithKline plc.. Advisory Panel; Self; Roche Pharma, Insulet Corporation, Janssen Pharmaceuticals, Inc.. Research Support; Self; Janssen Pharmaceuticals, Inc.. Speaker's Bureau; Self; Janssen Pharmaceuticals, Inc.. Research Support; Self; Lexicon Pharmaceuticals, Inc., Medtronic. Advisory Panel; Self; Merck & Co., Inc.. Research Support; Self; Merck & Co., Inc.. Speaker's Bureau; Self; Merck & Co., Inc.. Advisory Panel; Self; Novo Nordisk Inc.. Research Support; Self; Novo Nordisk Inc.. Speaker's Bureau; Self; Novo Nordisk Inc.. Advisory Panel; Self; Sanofi. Research Support; Self; Sanofi. T.S. Bailey: Research Support; Self; Abbott. Consultant; Self; Abbott. Speaker's Bureau; Self; Abbott. Research Support; Self; Ambra BioScience, Ascensia Diabetes Care, Becton, Dickinson and Company. Consultant; Self; Becton, Dickinson and Company. Research Support; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Calibra Medical. Consultant; Self; Calibra Medical. Research Support; Self; Companion Medical, Dexcom, Inc., Glooko, Inc., GlySens Incorporated, Lexicon Pharmaceuticals, Inc., Eli Lilly and Company. Consultant; Self; Eli Lilly and Company. Speaker's Bureau; Self; Eli Lilly and Company. Research Support; Self; Medtronic MiniMed, Inc.. Consultant; Self; Medtronic MiniMed, Inc.. Speaker's Bureau; Self; Medtronic MiniMed, Inc.. Research Support; Self; Novo Nordisk Inc.. Consultant; Self; Novo Nordisk Inc.. Speaker's Bureau; Self; Novo Nordisk Inc.. Research Support; Self; Sanofi. Consultant; Self; Sanofi. Speaker's Bureau; Self; Sanofi. Research Support; Self; Senseonics. Consultant; Self; Intarcia Therapeutics, Inc.. Research Support; Self; Versartis, Inc., Xeris Pharmaceuticals, Inc., MannKind Corporation.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db18-97-LB
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
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  • 7
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    Online Resource
    No Ljungan Virus RNA in Stool Samples From the Norwegian Environmental Triggers of Type 1 Diabetes (MIDIA) Cohort Study
    American Diabetes Association ; 2010
    In:  Diabetes Care Vol. 33, No. 5 ( 2010-05-01), p. 1069-1071
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 33, No. 5 ( 2010-05-01), p. 1069-1071
    Abstract: Ljungan virus (LjV) has been proposed as a potential environmental factor for type 1 diabetes. The objective was to test for any association of LjV with type 1 diabetes. RESEARCH DESIGN AND METHODS A nested case-control design was used to test for any association between the development of pre-diabetic autoimmunity and presence of LjV in stool samples (n = 3,803) in the Norwegian Environmental Triggers of Type 1 Diabetes (MIDIA) study. The children followed were 27 infants who developed pre-diabetic autoimmunity during or shortly after the sampling period, 54 matched control subjects, and 94 other children. RESULTS No LjV RNA was detected. CONCLUSIONS The results indicate that LjV is rare in young children. LjV does not seem to be involved in the development of human type 1 diabetes.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc09-1951
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2010
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  • 8
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    First Genome-Wide Association Study of Latent Autoimmune Diabetes in Adults Reveals Novel Insights Linking Immune and Metabolic Diabetes
    American Diabetes Association ; 2018
    In:  Diabetes Care Vol. 41, No. 11 ( 2018-11-01), p. 2396-2403
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 41, No. 11 ( 2018-11-01), p. 2396-2403
    Abstract: Latent autoimmune diabetes in adults (LADA) shares clinical features with both type 1 and type 2 diabetes; however, there is ongoing debate regarding the precise definition of LADA. Understanding its genetic basis is one potential strategy to gain insight into appropriate classification of this diabetes subtype. RESEARCH DESIGN AND METHODS We performed the first genome-wide association study of LADA in case subjects of European ancestry versus population control subjects (n = 2,634 vs. 5,947) and compared against both case subjects with type 1 diabetes (n = 2,454 vs. 968) and type 2 diabetes (n = 2,779 vs. 10,396). RESULTS The leading genetic signals were principally shared with type 1 diabetes, although we observed positive genetic correlations genome-wide with both type 1 and type 2 diabetes. Additionally, we observed a novel independent signal at the known type 1 diabetes locus harboring PFKFB3, encoding a regulator of glycolysis and insulin signaling in type 2 diabetes and inflammation and autophagy in autoimmune disease, as well as an attenuation of key type 1–associated HLA haplotype frequencies in LADA, suggesting that these are factors that distinguish childhood-onset type 1 diabetes from adult autoimmune diabetes. CONCLUSIONS Our results support the need for further investigations of the genetic factors that distinguish forms of autoimmune diabetes as well as more precise classification strategies.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc18-1032
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
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  • 9
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    Online Resource
    Determinants of New-Onset Diabetes Among 19,257 Hypertensive Patients Randomized in the Anglo-Scandinavian Cardiac Outcomes Trial–Blood Pressure Lowering Arm and the Relative Influence of Antihypertensive Medication
    American Diabetes Association ; 2008
    In:  Diabetes Care Vol. 31, No. 5 ( 2008-05-01), p. 982-988
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 31, No. 5 ( 2008-05-01), p. 982-988
    Abstract: OBJECTIVE—The purpose of this study was to determine the baseline predictors of new-onset diabetes (NOD) in hypertensive patients and to develop a risk score to identify those at high risk of NOD. RESEARCH DESIGN AND METHODS—Among 19,257 hypertensive patients in the Anglo-Scandinavian Cardiac Outcomes Trial–Blood Pressure Lowering Arm (ASCOT-BPLA) who were randomly assigned to receive one of two antihypertensive regimens (atenolol ± thiazide or amlodipine ± perindopril), 14,120 were at risk of developing diabetes at baseline. Of these, 1,366 (9.7%) subsequently developed NOD during median follow-up of 5.5 years. A multivariate Cox model was developed to identify the independent predictors of NOD and individual risk scores. RESULTS—NOD was significantly associated with an increase in baseline fasting plasma glucose (FPG), BMI, serum triglycerides, and systolic blood pressure. In contrast, amlodipine ± perindopril in comparison with atenolol ± thiazide treatment (hazard ratio 0.66 [95% CI 0.59–0.74]), high HDL cholesterol, alcohol use, and age & gt;55 years were found to be significantly protective factors. FPG was the most powerful predictor with risk increasing by 5.8 times (95% CI 5.23–6.43) for each millimole per liter rise & gt;5 mmol/l. The risk of NOD increased steadily with increasing quartile of risk score, with a 19-fold increase (95% CI 14.3–25.4) among those in the highest compared with those in the lowest quartile. The model showed excellent internal validity and discriminative ability. CONCLUSIONS—Baseline FPG & gt;5 mmol/l, BMI, and use of an atenolol ± diuretic regimen were among the major determinants of NOD in hypertensive patients. The model developed from these data allows accurate prediction of NOD among hypertensive subjects.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc07-1768
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2008
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  • 10
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    Online Resource
    Common Missense Variant in the Glucokinase Regulatory Protein Gene Is Associated With Increased Plasma Triglyceride and C-Reactive Protein but Lower Fasting Glucose Concentrations
    American Diabetes Association ; 2008
    In:  Diabetes Vol. 57, No. 11 ( 2008-11-01), p. 3112-3121
    Details
    In: Diabetes, American Diabetes Association, Vol. 57, No. 11 ( 2008-11-01), p. 3112-3121
    Abstract: OBJECTIVE—Using the genome-wide association approach, we recently identified the glucokinase regulatory protein gene (GCKR, rs780094) region as a novel quantitative trait locus for plasma triglyceride concentration in Europeans. Here, we sought to study the association of GCKR variants with metabolic phenotypes, including measures of glucose homeostasis, to evaluate the GCKR locus in samples of non-European ancestry and to fine- map across the associated genomic interval. RESEARCH DESIGN AND METHODS—We performed association studies in 12 independent cohorts comprising & gt;45,000 individuals representing several ancestral groups (whites from Northern and Southern Europe, whites from the U.S., African Americans from the U.S., Hispanics of Caribbean origin, and Chinese, Malays, and Asian Indians from Singapore). We conducted genetic fine-mapping across the ∼417-kb region of linkage disequilibrium spanning GCKR and 16 other genes on chromosome 2p23 by imputing untyped HapMap single nucleotide polymorphisms (SNPs) and genotyping 104 SNPs across the associated genomic interval. RESULTS—We provide comprehensive evidence that GCKR rs780094 is associated with opposite effects on fasting plasma triglyceride (Pmeta = 3 × 10−56) and glucose (Pmeta = 1 × 10−13) concentrations. In addition, we confirmed recent reports that the same SNP is associated with C-reactive protein (CRP) level (P = 5 × 10−5). Both fine-mapping approaches revealed a common missense GCKR variant (rs1260326, Pro446Leu, 34% frequency, r2 = 0.93 with rs780094) as the strongest association signal in the region. CONCLUSIONS—These findings point to a molecular mechanism in humans by which higher triglycerides and CRP can be coupled with lower plasma glucose concentrations and position GCKR in central pathways regulating both hepatic triglyceride and glucose metabolism.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db08-0516
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2008
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