Cd36 gene expression in adipose and hepatic tissue mediates the lipids accumulation in liver of obese rats with sucrose-induced hepatic steatosis

Quintana‐Castro, Rodolfo; Aguirre-Maldonado, Isaac; Soto-Rodríguez, Ida; Deschamps-Lago, Rosa A.; Gruber-Pagola, Peter; Larrea, Yolanda K. Urbina de; Juárez-Rivera, Victoria E.; Ramos-Manuel, Luis E.; Alexander‐Aguilera, Alfonso

doi:10.1016/j.prostaglandins.2019.106404

Cited by 10 publications

(10 citation statements)

References 56 publications

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“…CD36 is a multifunctional, transmembrane, glycoprotein scavenger receptor belonging to the class B family receptors originally found in platelets [11,25]. CD36 is encoded on chromosome 7 in humans and consists of a single peptide chain of 472 amino acids with a molecular weight of 88 kDa [26,27]. Structurally, CD36 has two intracellular domains, a large extracellular domain, and two transmembrane domains [28].…”

Section: Scd36 Receptormentioning

confidence: 99%

Soluble Receptors Affecting Stroke Outcomes: Potential Biomarkers and Therapeutic Tools

Bhattacharya

Ashouri

Fangman

et al. 2021

IJMS

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Soluble receptors are widely understood to be freestanding moieties formed via cleavage from their membrane-bound counterparts. They have unique structures, are found among various receptor families, and have intriguing mechanisms of generation and release. Soluble receptors’ ability to exhibit pleiotropic action by receptor modulation or by exhibiting a dual role in cytoprotection and neuroinflammation is concentration dependent and has continually mystified researchers. Here, we have compiled findings from preclinical and clinical studies to provide insights into the role of soluble/decoy receptors, focusing on the soluble cluster of differentiation 36, the soluble cluster of differentiation 163, and soluble lipoprotein-related protein 1 (sCD36, sCD163, and sLRP1, respectively) and the functions they could likely serve in the management of stroke, as they would notably regulate the bioavailability of the hemoglobin and heme after red blood cell lysis. The key roles that these soluble receptors play in inflammation, oxidative stress, and the related pharmacotherapeutic potential in improving stroke outcomes are described. The precise pleiotropic physiological functions of soluble receptors remain unclear, and further scientific investigation/validation is required to establish their respective role in diagnosis and therapy.

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Section: Scd36 Receptormentioning

confidence: 99%

Soluble Receptors Affecting Stroke Outcomes: Potential Biomarkers and Therapeutic Tools

Bhattacharya

Ashouri

Fangman

et al. 2021

IJMS

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“…However, CD36 can be highly upregulated in a response to the elevated plasma FFA level to contribute to lipid accumulation and activation of inflammation [ 7 , 29 ]. Prolonged sucrose consumption [ 116 , 117 ] and hyperinsulinemia [ 30 ] also cause CD36 upregulation in the liver. CD36 overexpression is induced by liver X receptor (LXR), pregnane X receptor (PXR), and PPAR-γ [ 30 , 118 ].…”

Section: The Role Of Cd36 In the Pathogenesis Of Dmmentioning

confidence: 99%

The Multifunctionality of CD36 in Diabetes Mellitus and Its Complications—Update in Pathogenesis, Treatment and Monitoring

Puchałowicz

Rać

2020

Cells

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CD36 is a multiligand receptor contributing to glucose and lipid metabolism, immune response, inflammation, thrombosis, and fibrosis. A wide range of tissue expression includes cells sensitive to metabolic abnormalities associated with metabolic syndrome and diabetes mellitus (DM), such as monocytes and macrophages, epithelial cells, adipocytes, hepatocytes, skeletal and cardiac myocytes, pancreatic β-cells, kidney glomeruli and tubules cells, pericytes and pigment epithelium cells of the retina, and Schwann cells. These features make CD36 an important component of the pathogenesis of DM and its complications, but also a promising target in the treatment of these disorders. The detrimental effects of CD36 signaling are mediated by the uptake of fatty acids and modified lipoproteins, deposition of lipids and their lipotoxicity, alterations in insulin response and the utilization of energy substrates, oxidative stress, inflammation, apoptosis, and fibrosis leading to the progressive, often irreversible organ dysfunction. This review summarizes the extensive knowledge of the contribution of CD36 to DM and its complications, including nephropathy, retinopathy, peripheral neuropathy, and cardiomyopathy.

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“…From the result section, sucrose is one of the obesity inducers, as aldose reductase expression in the liver converts glucose into sorbitol by the polyol path and contributes to fatty liver development. 8 Sugars' metabolic effects can differ from starch due to the fructose component of sucrose, which causes many liver-related diseases. 30 Based on Table 3 findings, we find that HSD has many effects experimented on in animals, especially rats.…”

Section: Discussionmentioning

confidence: 99%

“…Obesity commonly occurs when there is no balance between energy intake and demand in our diets 8 and is also known as NAFLD risk promoter in children. 15 Obesity will increase body weight and fat, 8 associated with increased glucose serum levels in blood and liver.…”

Section: Discussionmentioning

confidence: 99%

The Effect and Mechanism of Sucrose Consumption to Liver Disease – A Systematic Literature Review

Sigma

2022

BHSJ

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Introduction: One liver disease caused by excessive fat in the liver, called non-alcoholic liver disease (NAFLD), commonly occurs with obesity, diabetes, and other disorders. NAFLD is also associated with hepatic insulin resistance, steatosis, non-alcoholic steatohepatitis (NASH), and cirrhosis. Sucrose consumption has increased recently, and known can promotes NAFLD and will accelerate NAFLD development. This study aimed to discuss the effect and mechanism of sucrose intake on liver disease using a systematic literature review. Methods: The author identified the articles from 6 online search engines, including PubMed, Science Direct, Sinta, Garuda, Google Scholar, and EBSCOHost. A total of 2271 retrieved articles were obtained from combined search strings in Indonesian and English from the search through online search engines. Excluded articles include title not relevant, duplicate articles, not open access, secondary study or review articles, research objective not appropriate, abstract not suitable, and the results/findings not relevant to the aims of this paper. Results: A final of twenty-three articles were retrieved using the Mendeley reference manager. Studies included were published studies, types of experimental and observational studies, and their specific findings of sucrose effects on liver disease. Results reveal that most research was primarily conducted experimentally and in case-control study types on male rats. Conclusion: The most common disease related to sucrose is NAFLD, fibrosis/cirrhosis with the indication of NASH, obesity, insulin resistance (IR), triglycerides (TG), hepatic steatosis, hepatocyte ballooning, and weight gain, which we will discuss further in this review.

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Cd36 gene expression in adipose and hepatic tissue mediates the lipids accumulation in liver of obese rats with sucrose-induced hepatic steatosis

Cited by 10 publications

References 56 publications

Soluble Receptors Affecting Stroke Outcomes: Potential Biomarkers and Therapeutic Tools

Soluble Receptors Affecting Stroke Outcomes: Potential Biomarkers and Therapeutic Tools

The Multifunctionality of CD36 in Diabetes Mellitus and Its Complications—Update in Pathogenesis, Treatment and Monitoring

The Effect and Mechanism of Sucrose Consumption to Liver Disease – A Systematic Literature Review

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