Dataset for "Hepatic inflammation precedes steatosis and is mediated by visceral fat accumulation"

Published: 26-01-2021| Version 1 | DOI: 10.17632/g2wk65v7v9.1
Breno Picin Casagrande,


This dataset refers to the article "Hepatic inflammation precedes steatosis and is mediated by visceral fat accumulation" published in 2020 at the Journal of Endocrinology (DOI:10.1530/JOE-20-0073). Abstract (DOI:10.1530/JOE-20-0073): The negative aspects of unhealthy eating on obesity and hepatic health are well described. The axis between the adipose tissue and the liver participates in most of the damage caused to this tissue regarding obesogenic diets (OD). At the same time that the effects of consuming simple carbohydrates and saturated fatty acids are known, the effects of the cessation of its intake are scarce. Withdrawing from OD is thought to improve health; despite some studies had shown improvement in hepatic conditions in the long-term, short-term studies were not found. Therefore, we aimed to determine how OD intake and withdrawal would influence visceral and hepatic fat accumulation and inflammation. To this end, male 60-days-old Wistar rats received standard chow (n = 16) or a high-sugar/ high-fat diet (HSHF) for 30 days (n = 32), a cohort of the HSHF-fed animals was then kept 48 h on standard chow (n = 16). In opposition to the generally reported, the results indicate that hepatic inflammation preceded hepatic steatosis. Additionally, inflammatory markers on the liver positively correlated visceral adipokines and visceral fat accumulation mediated them in a deposit-dependent manner. At the same time, a 48-h withdrawal was capable of reverting most of the risen inflammatory mediators, although MyD88 and TNFα persisted and serum non-HDL cholesterol was higher than control levels. It contains the .csv file with the data used in the publication.


Steps to reproduce

Male Wistar rats (60 days old, n=30, 210g to 260g) were habituated to the bioterium for seven days and were randomly assigned into three groups (n=10 per group). Animals were held in cages (40cm x 35cm x 15cm) of 3-4 individuals in a 12h/12h light-dark cycle, at 22±2ºC. They received water and chow ad libitum. The control group, Ct, n=10 received the standard chow for 30 days; the high-sugar and high-fat diet fed (HSHF-fed) group, Hd, n=10 received the modified diet for 30 days; and the HSHF-fed + withdrawal group, Hw, n=10 received the modified diet for 30 days and the standard chow for two days. The standard chow was Nuvilab CR1 (Quimtia, Brazil) and the HSHF diet consisted of grounded standard Nuvilab CR1 added of sweetened condensed milk (Nestle, São Paulo, Brazil), lard (Sadia, Brazil), casein (Labsynth, Brazil), soybean oil (Bunge, Brazil), vitamins (RHOSTER, Brazil), and minerals (RHOSTER, Brazil). After the protocol, the animals were anesthetized with isoflurane and euthanized by decapitation. An additional cohort (Ct, n=6; Hd, n=6; Hw, n=6) was carried out and euthanized by perfusion with 0.9% sodium chloride in water (Labsynth, Diadema, Brazil) and 4% paraformaldehyde in phosphate buffer, 0.1M, pH 7.4 (fixing solution) (Labsynth, Diadema, Brazil). The livers were removed and kept in fixing solution for 48h and then transferred to a 70% alcohol solution. Serum lipids were determined by an enzymatic method using commercial colorimetric kits (Labtest, Brazil). Hepatic lipids were determined using Folch's method followed by an analysis with the above-mentioned colorimetric kits (Labtest, Brazil). Hepatic and adipose tissue (mesenteric, retroperitoneal, and epididymal) cytokines were quantified using ELISA kits (R&D System, USA). Hepatic levels of pNFkBp65 and MyD88 were quantified by western blotting. Hepatic histological features were observed on H&E staining.