Research Article Details
Article ID: | A16774 |
PMID: | 28185715 |
Source: | Clin Ther |
Title: | Effects of Oral Antidiabetic Drugs on Changes in the Liver-to-Spleen Ratio on Computed Tomography and Inflammatory Biomarkers in Patients With Type 2 Diabetes and Nonalcoholic Fatty Liver Disease. |
Abstract: | PURPOSE: Oral antidiabetic drugs (OADs) such as pioglitazone and metformin have beneficial effects in patients with nonalcoholic steatohepatitis. We prospectively assessed the effects of OADs on nonalcoholic fatty liver disease (NAFLD) in 886 men with type 2 diabetes mellitus and in a murine model of NAFLD. METHODS: Patients were randomized to receive pioglitazone, metformin, sitagliptin, or a non-OAD (control) for 6 months. All the patients received dietary and exercise guidance once a month during this study. Changes in the liver-to-spleen ratio on computed tomography (CT) and NAFLD-related parameters were measured from baseline to the end of treatment. FINDINGS: The liver/spleen ratio improved significantly in the pioglitazone and metformin groups compared with the control group (both P < 0.01), but not in the sitagliptin group (P = 0.73). The mean changes from baseline were -3.464 ± 10.156%, 19.236 ± 9.896%, 4.783 ± 1.467%, and 1.328 ± 0.802% in the control, pioglitazone, metformin, and sitagliptin groups, respectively. Multivariable analysis showed that the liver/spleen ratio was strongly correlated with high-sensitivity C-reactive protein concentration in the pioglitazone group (F = 9.973; P < 0.01) and abdominal visceral fat volume in the metformin group (F = 6.049; P < 0.05). CONCLUSIONS: Pioglitazone elicited the greatest improvements in features of NAFLD in type 2 diabetes mellitus. (Trial Registration: www.isrctn.org/, ISRCTN33414972, http://www.isrctn.org/). |
DOI: | 10.1016/j.clinthera.2017.01.015 |

Strategy ID | Therapy Strategy | Synonyms | Therapy Targets | Therapy Drugs | |
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S08 | Lifestyle measures | Lifestyle intervention; weight loss; diet adaptation; dietary interventions; lifestyle modifications; Exercise | -- | -- | Details |
S05 | Anti-inflammatory | inflammatory | Bile acid; TNF-a inhibitor; Dual PPAR-α and -δ agonists; Toll-Like Receptor; (TLR)-4 antagonist; Caspase inhibitor; ASK-1 inhibitor | Ursodeoxycholic Acid; Pentoxifylline; Elafibranor; JKB-121; Emricasan; Selonsertib; | Details |
Target ID | Target Name | GENE | Action | Class | UniProtKB ID | Entry Name |
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Diseases ID | DO ID | Disease Name | Definition | Class | |
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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 | |
---|---|---|---|---|---|---|---|
D225 | Metformin | Chemical drug | DB00331 | PRKAB1 inducer activator; ETEDH inhibitor; GPD1 inhibitor | Improve insulin resistance | Under clinical trials | Details |
D366 | Thiazolidinediones | Chemical drug | DB11898 | -- | -- | Under clinical trials | Details |
D080 | Citrulline | Chemical drug | DB00155 | -- | -- | Under clinical trials | Details |
D338 | Sitagliptin | Chemical drug | DB01261 | DPP4 inhibitor | Antidiabetic drug | Under clinical trials | Details |
D275 | Pioglitazone | Chemical drug | DB01132 | PPARG agonist | Improve insulin resistance | Advanced in clinical trials | Details |
D157 | Glucophage | Chemical drug | DB00331 | -- | -- | 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 |