Research Article Details
| Article ID: | A47796 |
| PMID: | 31735070 |
| Source: | Curr Eye Res |
| Title: | Diet Mimicking "Fast Food" Causes Structural Changes to the Retina Relevant to Age-Related Macular Degeneration. |
| Abstract: | Introduction: Metabolic syndrome is a disorder characterized by a constellation of findings including truncal obesity, elevated blood pressure, abnormal cholesterol levels, and high blood glucose. Recent evidence suggests that metabolic syndrome may be associated with increased risk of age-related macular degeneration (AMD) and other eye diseases. Recently, C57BL/6J wild-type mice fed with a "fast food" diet consisting of high fat, cholesterol, and fructose-supplemented water showed unique systemic pathology consistent with metabolic syndrome and nonalcoholic steatohepatitis. Additionally, these mice showed higher levels of fibrosis, inflammation, endoplasmic reticulum stress, and mitochondrial dysfunction compared to mice fed with only a high-fat diet alone. Since similar pathways are activated in AMD, we sought to determine whether mice fed a "fast food" diet exhibited retinal changes.Methods: 3-month-old wild-type mice were randomized to a standard chow (n = 11) or a "fast food" (n = 18) diet and fed for 9 months. At 1 year of age, tissues were collected and retinas were analyzed using transmission electron microscopy. Quantitative measures of Bruch's membrane thickness and retinal pigment epithelium (RPE) cell counts were performed.Results: "Fast food" fed mice showed ocular pathology relevant to various stages of AMD including basal laminar deposits, focal thickening of Bruch's membrane, and a significant loss of RPE cells.Discussion/conclusion: A wild-type mouse model of metabolic syndrome fed a "fast food" diet developed changes to the retina similar to some of the pathologic features seen in AMD. Further investigations into this and similar animal models as well as further epidemiological studies are needed to more clearly define the association between metabolic syndrome and AMD. |
| DOI: | 10.1080/02713683.2019.1694156 |
| 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 |
| Diseases ID | DO ID | Disease Name | Definition | Class | |
|---|---|---|---|---|---|
| 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 |
| Drug ID | Drug Name | Type | DrugBank ID | Targets | Category | Latest Progress | |
|---|---|---|---|---|---|---|---|
| D142 | Fructose | Chemical drug | DB04173 | -- | Intravenous nutrition drug | Under clinical trials | Details |
| D018 | Aspirin | Chemical drug | DB00945 | AKR1C1 inhibitor; PCNA downregulator | Enhance lipid metabolism | Under clinical trials | Details |
| D248 | Obeticholic Acid | Chemical drug | DB05990 | NR1H4 activator; NR1H4 agonist; FXR agonist | Enhance lipid metabolism | Approval rejected | Details |
| D094 | Cysteamine | Chemical drug | DB00847 | GSS stimulant | Renal drug | Under clinical trials | Details |
| D095 | Cysteamine bitartrate | Chemical drug | DB00847 | -- | -- | Under clinical trials | Details |