Research Article Details
| Article ID: | A03354 |
| PMID: | 34031327 |
| Source: | Med J Malaysia |
| Title: | Liver fibrosis associated with adipose tissue and liver inflammation in an obesity model. |
| Abstract: | INTRODUCTION: Obesity, the main risk factor for type 2 diabetes mellitus (T2DM), affects the secretion of various hormones that lead to change in metabolism. Visceral adipose tissue accumulation may contribute to Non-alcoholic Fatty Liver Disease (NAFLD) and induce liver injury. This study was aimed to investigate the association between adipose tissue inflammation and liver fibrosis. MATERIALS AND METHODS: Wistar male rats (3 months old, 160- 230 grams) were divided into 4 groups that consisted of six rats in each group. The obesity model was induced through the administration of high-fat diet for a month (OB1), two months (OB2), and four months (OB4). Standard chow was provided for the control group for four months. After the specified date the rats were euthanized and the liver and retroperitoneal white adipose tissue (RWAT) were harvested. We performed RT-PCR to assess the mRNA expressions involved in proinflammatory mediators, fibrosis and antifibrosis signaling. Sirius red staining was performed to assess liver fibrosis. Data were analyzed with SPSS 23 for Windows with significance set as p<0.05. RESULTS: Obesity-induced high-fat diet stimulated an increase of body mass index (BMI) in the OB groups (p<0.05) compared to the control group. Increased BMI was followed by upregulation of proinflammatory mediators (MCP-1, CD68, TLR4, and NFκB) of the RWAT and liver in the obese groups (p<0.05), which promoted hepatic fibrosis in triad portal areas and upregulation of TGFβ (p<0.05) mRNA expression as well as downregulation of HGF and c-Met (p<0.05). In addition, hepatic ppET1 and EDNRB mRNA level expressions (p<0.05) were obviously upregulated in the obese groups followed by downregulation of eNOS (p<0.05) mRNA expressions. CONCLUSION: Obesity enhanced inflammation in RWAT and was associated with inflammation and fibrosis of liver. |
| DOI: |
| Strategy ID | Therapy Strategy | Synonyms | Therapy Targets | Therapy Drugs | |
|---|---|---|---|---|---|
| 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 |
| 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 |
| 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 |
| I14 | 9970 | Obesity | An overnutrition that is characterized by excess body fat, traditionally defined as an elevated ratio of weight to height (specifically 30 kilograms per meter squared), has_material_basis_in a multifactorial etiology related to excess nutrition intake, decreased caloric utilization, and genetic susceptibility, and possibly medications and certain disorders of metabolism, endocrine function, and mental illness. https://en.wikipedia.org/wiki/Obesity | disease of metabolism/acquired metabolic disease/ nutrition disease/overnutrition | Details |