Research Article Details
| Article ID: | A22865 |
| PMID: | 24267865 |
| Source: | Liver Int |
| Title: | Coffee consumption in NAFLD patients with lower insulin resistance is associated with lower risk of severe fibrosis. |
| Abstract: | BACKGROUND & AIMS: Coffee has inverse relationships with both type 2 diabetes and hepatic fibrosis in patients with nonalcoholic fatty liver disease (NAFLD). Relationships were explored between coffee intake and insulin resistance (IR) with respect to NAFLD histologic severity. METHODS: We analyzed data from 782 adults (≥18 years) in the Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN) from 2004 to 2008. IR was assessed using the HOMA-IR. We modeled associations between coffee intake and NAFLD histologic severity using multiple logistic regression; and interactions between coffee and IR on NAFLD histology were explored. RESULTS: Among 782 participants, 38% (n = 295) were men, 12% (n = 97) were Latino, mean age (± standard deviation) was 48 ± 12 years. Median BMI was 33.5 kg/m(2) [interquartile range, 29.7-38.3] and median HOMA-IR was 4.3 [2.7-7.2]. Diabetes was present in 24% (n = 189). NASH was present in 79% (n = 616), and 25% (n = 199) had advanced fibrosis. The frequency of coffee intake (cups/day, cpd) was as follows: 0 cpd, n = 230 (29%); <1 cpd, n = 219 (28%); 1 to <2 cpd, n = 116 (15%); ≥2 cpd, n = 217 (28%). The effect of coffee on fibrosis varied with degree of IR (interaction P = 0.001). Coffee consumers with less IR, defined as HOMA-IR<4.3, had a lower odds of advanced fibrosis [OR = 0.64; 95% CI, (0.46-0.88), P = 0.001]. There was no protective effect of coffee on advanced fibrosis among individuals with higher HOMA-IR [OR = 1.06, 95% CI (0.87-1.28), P = 0.6]. CONCLUSIONS: Coffee intake is inversely associated with advanced fibrosis among NAFLD patients with lower HOMA-IR. Our findings warrant further investigation given the worldwide ubiquity of coffee intake. |
| DOI: | 10.1111/liv.12379 |
| 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 |
| S03 | Anti-fibrosis | fibrosis | Angiotensin Receptor Blocker (ARB); CCR2/CCR5 antagonist; Thyroid receptor β agonist; PEGylated human FGF21 analogue; Monoclonal antibody to lysyl oxidase-like 2 (LOXL2); Galectin-3 inhibitor; FGF19 variant | Losartan; Cenicriviroc; VK-2809; MGL-3196; Pegbelfermin; Simtuzumab; GR-MD-02; NGM282 | Details |
| Diseases ID | DO ID | Disease Name | Definition | Class | |
|---|---|---|---|---|---|
| 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 | |
|---|---|---|---|---|---|---|---|
| D579 | Emfilermin | Miscellany | -- | adipocytes | Enhance lipid metabolism | Under investigation | Details |
| D182 | Insulin | Biological drug | DB00030 | INSR agonist; CPE modulator&product of | -- | 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 |