Research Article Details
| Article ID: | A25538 |
| PMID: | 21735081 |
| Source: | Dig Dis Sci |
| Title: | Nonalcoholic fatty liver disease markers are associated with insulin resistance in type 1 diabetes. |
| Abstract: | BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) has been associated with the insulin resistance. AIMS: To explore the relationship between markers of NAFLD, namely concentrations of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALK), γ-glutamyltransferase (GGT), ferritin and bilirubin and insulin resistance in type 1 diabetes. METHODS: Our study included 353 patients with type 1 diabetes. Insulin sensitivity was measured with estimated glucose disposal rate calculated using the equation: eGDR = 24.31 - (12.22 × WHR) - (3.29 × HT) - (0.57 × HbA1c); WHR = waist to hip ratio, HT = hypertension. Correlations and multiple logistic regressions analysis were performed to identify the relationships between NAFLD associated markers and eGDR, individual components of insulin resistance and risk of insulin resistance. RESULTS: AST, ALT, AST-to-ALT ratio, ALK and ferritin significantly correlated with insulin resistance measured by eGDR (r = -0.13, -0.14, 0.13, -0.18, and -0.24, respectively; all P < 0.05), and with individual components of insulin resistance, most notably WHR. In a multiple logistic regression model adjusted according to age, sex, duration of diabetes and BMI, increased levels of AST, ALT and ALK resulted in an increased risk for the development of insulin resistance in our subjects (OR = 1.03, 1.02, and 1.01, respectively; all P < 0.05). CONCLUSIONS: These findings indicate that higher levels of ALT, AST and ALK are additional markers of insulin resistance in type 1 diabetes and suggest that those subjects must be considered as potentially affected not only by a hepatic but also by a multisystemic disease through altered insulin sensitivity. |
| DOI: | 10.1007/s10620-011-1807-7 |
| Strategy ID | Therapy Strategy | Synonyms | Therapy Targets | Therapy Drugs | |
|---|---|---|---|---|---|
| S01 | Improve insulin resistance | insulin sensitizer; insulin resistance; glucose tolerance | Biguanide: increases 5-AMP activated protein kinase signaling; SGLT-2 inhibitor; Thiazalidinedione: selective PPAR-γ agonists; GLP-1 agonist | Metformin; Empagliflozin; Canagliflozin; Rosiglitazone; Pioglitazone; Liraglutide | Details |
| Diseases ID | DO ID | Disease Name | Definition | Class | |
|---|---|---|---|---|---|
| I12 | 10763 | Hypertension | An artery disease characterized by chronic elevated blood pressure in the arteries. https://en.wikipedia.org/wiki/Hypertension, https://www.ncbi.nlm.nih.gov/pubmed/24352797 | disease of anatomical entity/ cardiovascular system disease/vascular disease/ artery disease | Details |
| I05 | 9352 | Type 2 diabetes mellitus | A diabetes that is characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both. A diabetes mellitus that is characterized by high blood sugar, insulin resistance, and relative lack of insulin. http://en.wikipedia.org/wiki/Diabetes, http://en.wikipedia.org/wiki/Diabetes_mellitus_type_2 | disease of metabolism/inherited metabolic disorder/ carbohydrate metabolic disorder/glucose metabolism disease/diabetes/ diabetes mellitus | Details |
| Drug ID | Drug Name | Type | DrugBank ID | Targets | Category | Latest Progress | |
|---|---|---|---|---|---|---|---|
| D199 | L-alanine | Chemical drug | DB00160 | KYNU | -- | Failed in clinical trials | Details |
| D182 | Insulin | Biological drug | DB00030 | INSR agonist; CPE modulator&product of | -- | Under clinical trials | Details |
| D316 | S-adenosyl-L-methionine | Chemical drug | DB00118 | GNMT cofactor | Antiviral | Under clinical trials | Details |
| D094 | Cysteamine | Chemical drug | DB00847 | GSS stimulant | Renal drug | Under clinical trials | Details |
| D095 | Cysteamine bitartrate | Chemical drug | DB00847 | -- | -- | Under clinical trials | Details |