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  • American Diabetes Association  (6)
  • 1
    Online Resource
    Online Resource
    Sterol Regulatory Element-Binding Factor 2 ( SREBF-2 ) Predicts 7-Year NAFLD Incidence and Severity of Liver Disease and Lipoprotein and Glucose Dysmetabolism
    American Diabetes Association ; 2013
    In:  Diabetes Vol. 62, No. 4 ( 2013-04-01), p. 1109-1120
    Details
    In: Diabetes, American Diabetes Association, Vol. 62, No. 4 ( 2013-04-01), p. 1109-1120
    Abstract: We prospectively assessed the impact of a sterol regulatory element-binding factor-2 (SREBF-2) polymorphism on the risk of developing nonalcoholic fatty liver disease (NAFLD) and on liver histology and lipoprotein and glucose metabolism in biopsy-proven NAFLD. In a population-based study, we followed 175 nonobese, nondiabetic participants without NAFLD or metabolic syndrome at baseline, characterized for the SREBF-2 rs133291 C/T polymorphism, dietary habits, physical activity, adipokines, C-reactive protein (CRP), and endothelial adhesion molecules. A comparable cohort of NAFLD patients underwent liver biopsy, an oral glucose tolerance test with minimal model analysis to yield glucose homeostasis parameters, and an oral fat tolerance test with measurement of plasma lipoproteins, adipokines, and cytokeratin-18 fragments. After 7 years, 27% of subjects developed NAFLD and 5% developed diabetes. SREBF-2 predicted incident NAFLD and diabetes and CRP and endothelial adhesion molecule changes. In biopsy-proven NAFLD patients, SREBF-2 predicted nonalcoholic steatohepatitis (odds ratio 2.92 [95% CI 2.08–4.18] , P = 0.002) and the severity of tissue insulin resistance, β-cell dysfunction, and oral fat intolerance (characterized by higher postprandial lipemia, cholesterol enrichment of triglyceride-rich lipoproteins and oxidized LDLs, HDL cholesterol fall, adipokine imbalance, and postprandial apoptosis activation). An SREBF-2 polymorphism predisposes individuals to NAFLD and associated cardiometabolic abnormalities and affects liver histology and glucose and lipid metabolism in biopsy-proven NAFLD.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db12-0858
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2013
    detail.hit.zdb_id: 1501252-9
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  • 2
    Online Resource
    Online Resource
    Transcription Factor 7-Like 2 ( TCF7L2 ) Polymorphism and Hyperglycemia in an Adult Italian Population-Based Cohort
    American Diabetes Association ; 2010
    In:  Diabetes Care Vol. 33, No. 6 ( 2010-06-01), p. 1233-1235
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 33, No. 6 ( 2010-06-01), p. 1233-1235
    Abstract: To assess whether TCF7L2 polymorphism has a role in the deterioration of glycemic control. RESEARCH DESIGN AND METHODS Metabolic variables were evaluated at baseline and after 6-year follow-up in 1,480 Caucasian subjects from a population-based cohort. RESULTS At baseline, T-allele carriers showed significantly lower BMI and homeostasis model assessment for β-cell function (HOMA-B) values and higher fasting glycemia and diabetes prevalence. At follow-up, fasting glucose and HOMA-B index were increased and reduced, respectively, in carriers of the T-allele. Incident impaired fasting glucose (IFG) and incident diabetes were 5.7, 10.7, 16.9% and 1.6, 1.7, 3.0% in the CC, CT, and TT genotypes, respectively. In a multiple logistic regression model, the association between incident IFG and the T-allele was significant (odds ratio [OR] 2.08 [95% CI 1.35–3.20] and 3.56 [2.11–5.98] in CT and TT genotypes, respectively). CONCLUSIONS The T-allele of TCF7L2 rs7903146 polymorphism was independently associated with increasing fasting glucose values toward hyperglycemia in the follow-up.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc09-1690
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2010
    detail.hit.zdb_id: 1490520-6
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  • 3
    Online Resource
    Online Resource
    Should Nonalcoholic Fatty Liver Disease Be Included in the Definition of Metabolic Syndrome? A Cross-Sectional Comparison With Adult Treatment Panel III Criteria in Nonobese Nondiabetic Subjects
    American Diabetes Association ; 2008
    In:  Diabetes Care Vol. 31, No. 5 ( 2008-05-01), p. e43-e43
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 31, No. 5 ( 2008-05-01), p. e43-e43
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc08-0223
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2008
    detail.hit.zdb_id: 1490520-6
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  • 4
    Online Resource
    Online Resource
    Obesity, Diabetes, and Gut Microbiota
    American Diabetes Association ; 2010
    In:  Diabetes Care Vol. 33, No. 10 ( 2010-10-01), p. 2277-2284
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 33, No. 10 ( 2010-10-01), p. 2277-2284
    Abstract: The connection between gut microbiota and energy homeostasis and inflammation and its role in the pathogenesis of obesity-related disorders are increasingly recognized. Animals models of obesity connect an altered microbiota composition to the development of obesity, insulin resistance, and diabetes in the host through several mechanisms: increased energy harvest from the diet, altered fatty acid metabolism and composition in adipose tissue and liver, modulation of gut peptide YY and glucagon-like peptide (GLP)-1 secretion, activation of the lipopolysaccharide toll-like receptor-4 axis, and modulation of intestinal barrier integrity by GLP-2. Instrumental for gut microbiota manipulation is the understanding of mechanisms regulating gut microbiota composition. Several factors shape the gut microflora during infancy: mode of delivery, type of infant feeding, hospitalization, and prematurity. Furthermore, the key importance of antibiotic use and dietary nutrient composition are increasingly recognized. The role of the Western diet in promoting an obesogenic gut microbiota is being confirmation in subjects. Following encouraging results in animals, several short-term randomized controlled trials showed the benefit of prebiotics and probiotics on insulin sensitivity, inflammatory markers, postprandial incretins, and glucose tolerance. Future research is needed to unravel the hormonal, immunomodulatory, and metabolic mechanisms underlying microbe-microbe and microbiota-host interactions and the specific genes that determine the health benefit derived from probiotics. While awaiting further randomized trials assessing long-term safety and benefits on clinical end points, a healthy lifestyle—including breast lactation, appropriate antibiotic use, and the avoidance of excessive dietary fat intake—may ensure a friendly gut microbiota and positively affect prevention and treatment of metabolic disorders.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc10-0556
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2010
    detail.hit.zdb_id: 1490520-6
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  • 5
    Online Resource
    Online Resource
    Should Nonalcoholic Fatty Liver Disease Be Included in the Definition of Metabolic Syndrome?
    American Diabetes Association ; 2008
    In:  Diabetes Care Vol. 31, No. 3 ( 2008-03-01), p. 562-568
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 31, No. 3 ( 2008-03-01), p. 562-568
    Abstract: OBJECTIVE—The ability of the Adult Treatment Panel III (ATP III) criteria of metabolic syndrome to identify insulin-resistant subjects at increased cardiovascular risk is suboptimal, especially in the absence of obesity and diabetes. Nonalcoholic fatty liver disease (NAFLD) is associated with insulin resistance and is emerging as an independent cardiovascular risk factor. We compared the strength of the associations of ATP III criteria and of NAFLD to insulin resistance, oxidative stress, and endothelial dysfunction in nonobese nondiabetic subjects. RESEARCH DESIGN AND METHODS—Homeostasis model assessment of insulin resistance (HOMA-IR) & gt;2, oxidative stress (nitrotyrosine), soluble adhesion molecules (intracellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin), and circulating adipokines (tumor necrosis factor-α, leptin, adiponectin, and resistin) were cross-sectionally correlated to ATP III criteria and to NAFLD in 197 unselected nonobese nondiabetic subjects. RESULTS—NAFLD more accurately predicted insulin resistance than ATP III criteria: sensitivity 73 vs. 38% (P = 0.0001); positive predictive value: 81 vs. 62% (P = 0.035); negative predictive value 87 vs. 74% (P = 0.012); positive likelihood ratio 4.39 vs. 1.64 (P = 0.0001); and negative likelihood ratio 0.14 vs. 0.35 (P = 0.0001). Adding NAFLD to ATP III criteria significantly improved their diagnostic accuracy for insulin resistance. Furthermore, NAFLD independently predicted HOMA-IR, nitrotyrosine, and soluble adhesion molecules on logistic regression analysis; the presence of NAFLD entailed more severe oxidative stress and endothelial dysfunction, independent of adiposity or any feature of the metabolic syndrome in insulin-resistant subjects. CONCLUSIONS—NAFLD is more tightly associated with insulin resistance and with markers of oxidative stress and endothelial dysfunction than with ATP III criteria in nonobese nondiabetic subjects and may help identify individuals with increased cardiometabolic risk in this population.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc07-1526
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2008
    detail.hit.zdb_id: 1490520-6
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  • 6
    Online Resource
    Online Resource
    Fatty Liver and Chronic Kidney Disease: Novel Mechanistic Insights and Therapeutic Opportunities
    American Diabetes Association ; 2016
    In:  Diabetes Care Vol. 39, No. 10 ( 2016-10-01), p. 1830-1845
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 39, No. 10 ( 2016-10-01), p. 1830-1845
    Abstract: Chronic kidney disease (CKD) is a risk factor for end-stage renal disease (ESRD) and cardiovascular disease (CVD). ESRD or CVD develop in a substantial proportion of patients with CKD receiving standard-of-care therapy, and mortality in CKD remains unchanged. These data suggest that key pathogenetic mechanisms underlying CKD progression go unaffected by current treatments. Growing evidence suggests that nonalcoholic fatty liver disease (NAFLD) and CKD share common pathogenetic mechanisms and potential therapeutic targets. Common nutritional conditions predisposing to both NAFLD and CKD include excessive fructose intake and vitamin D deficiency. Modulation of nuclear transcription factors regulating key pathways of lipid metabolism, inflammation, and fibrosis, including peroxisome proliferator–activated receptors and farnesoid X receptor, is advancing to stage III clinical development. The relevance of epigenetic regulation in the pathogenesis of NAFLD and CKD is also emerging, and modulation of microRNA21 is a promising therapeutic target. Although single antioxidant supplementation has yielded variable results, modulation of key effectors of redox regulation and molecular sensors of intracellular energy, nutrient, or oxygen status show promising preclinical results. Other emerging therapeutic approaches target key mediators of inflammation, such as chemokines; fibrogenesis, such as galectin-3; or gut dysfunction through gut microbiota manipulation and incretin-based therapies. Furthermore, NAFLD per se affects CKD through lipoprotein metabolism and hepatokine secretion, and conversely, targeting the renal tubule by sodium–glucose cotransporter 2 inhibitors can improve both CKD and NAFLD. Implications for the treatment of NAFLD and CKD are discussed in light of this new therapeutic armamentarium.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc15-1182
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2016
    detail.hit.zdb_id: 1490520-6
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