High‐fat, high‐sucrose, and combined high‐fat/high‐sucrose diets effects in oxidative stress and inflammation in male rats under presence or absence of obesity

Kobi, Jéssika Butcovsky Botto Sarter; Matias, Amanda Martins; Gasparini, P.; Torezani-Sales, Suellem; Madureira, Amanda Rangel; Silva, Daniel Sesana da; Corrêa, Camila Renata; Garcia, Jéssica Leite; Haese, Douglas; Nogueira, Breno Valentim; Assis, Arícia Leone Evangelista Monteiro de; Lima-Leopoldo, Ana Paula; Leopoldo, André Soares

doi:10.14814/phy2.15635

Cited by 11 publications

(4 citation statements)

References 63 publications

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“…This result is consistent with a previous study using similar formulations of HF diet to induce nonobese nonalcoholic fatty liver disease in mice (Tu et al, 2017). The lower food intake due to HF or higher caloric diet consumption was also similarly observed in other studies (Hambly et al, 2005;Jayaprakasam et al, 2006;Kobi et al, 2023;Li et al, 2020;Townsend et al, 2008). Treatment with LLA caused lower BW growth rate and lowest food intake as compared to VCO and MCT.…”

Section: Discussionsupporting

confidence: 92%

Reduction of lauric acid content in virgin coconut oil improved plasma lipid profile in high‐fat diet‐induced hypercholesterolemic mice

Chatturong,

Palang,

To‐on

et al. 2023

Journal of Food Science

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Virgin coconut oil (VCO) is claimed to have various health benefits, but favorable effects of its major component (∼50%), lauric acid, are controversial. Therefore, we aimed to reduce lauric acid content (∼30%) in VCO and evaluate its effect compared to VCO and medium‐chain triglycerides (MCT), on food intake, bodyweight (BW), lipid profiles, and hepatic histology. Female C57BL/6 mice were treated with different diets for 3 months: control (normal diet), high‐fat diet (HF), HF + VCO, HF + MCT, HF + low lauric acid VCO (LLA), and normal diet + LLA (C + LLA). LLA was prepared by enzymatic interesterification of VCO with methyl octanoate (methyl caprylate) and methyl decanoate (methyl caprate). Plasma and liver lipids, including total cholesterol (TC), high‐density lipoprotein (HDL), and triglyceride, were measured by colorimetric assay, and hepatic fat accumulation was examined by oil‐red‐O staining. HF mice exhibited high plasma and liver TC and low‐density lipoprotein (LDL). VCO or MCT treatment lowered liver TC and LDL, whereas LLA increased plasma HDL and markedly improved TC:HDL ratio. The HF‐induced hepatic fat accumulation was attenuated by all treatments, of which VCO was the most effective. Control mice administered with LLA demonstrated lower liver TC and LDL, but higher plasma TC and HDL compared to controls. Lowest BW gain and food intake were found in mice treated with LLA. In conclusion, VCO, MCT, and LLA ameliorated hepatic histopathology caused by HF. VCO and MCT improved liver lipid profiles, whereas LLA has more beneficial effect on plasma lipids via a better TC:HDL ratio and showed promise for BW control.

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Section: Discussionsupporting

confidence: 92%

Reduction of lauric acid content in virgin coconut oil improved plasma lipid profile in high‐fat diet‐induced hypercholesterolemic mice

Chatturong,

Palang,

To‐on

et al. 2023

Journal of Food Science

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“…Given that HFHS diet is known to induce lipid peroxidation and RCS formation in the heart, particularly in GPx4 +/− mice, ( Méndez et al, 2014 ; Kobi et al, 2023 ), we next sought to the evaluate the effect of carnosine on protein carbonylation in myocardium from these mice. HFHS diet did indeed increase myocardial protein carbonyls, particularly in GPx4 +/− mice, while carnosine treatment effectively blunted protein carbonylation in both genotypes ( Figures 1D,E ).…”

Section: Resultsmentioning

confidence: 99%

Iron scavenging and suppression of collagen cross-linking underlie antifibrotic effects of carnosine in the heart with obesity

Berdaweel,

Monroe,

Alowaisi

et al. 2024

Front. Pharmacol.

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Oral consumption of histidyl dipeptides such as l-carnosine has been suggested to promote cardiometabolic health, although therapeutic mechanisms remain incompletely understood. We recently reported that oral consumption of a carnosine analog suppressed markers of fibrosis in liver of obese mice, but whether antifibrotic effects of carnosine extend to the heart is not known, nor are the mechanisms by which carnosine is acting. Here, we investigated whether oral carnosine was able to mitigate the adverse cardiac remodeling associated with diet induced obesity in a mouse model of enhanced lipid peroxidation (i.e., glutathione peroxidase 4 deficient mice, GPx4+/−), a model which mimics many of the pathophysiological aspects of metabolic syndrome and T2 diabetes in humans. Wild-type (WT) and GPx4+/−male mice were randomly fed a standard (CNTL) or high fat high sucrose diet (HFHS) for 16 weeks. Seven weeks after starting the diet, a subset of the HFHS mice received carnosine (80 mM) in their drinking water for duration of the study. Carnosine treatment led to a moderate improvement in glycemic control in WT and GPx4+/−mice on HFHS diet, although insulin sensitivity was not significantly affected. Interestingly, while our transcriptomic analysis revealed that carnosine therapy had only modest impact on global gene expression in the heart, carnosine substantially upregulated cardiac GPx4 expression in both WT and GPx4+/−mice on HFHS diet. Carnosine also significantly reduced protein carbonyls and iron levels in myocardial tissue from both genotypes on HFHS diet. Importantly, we observed a robust antifibrotic effect of carnosine therapy in hearts from mice on HFHS diet, which further in vitro experiments suggest is due to carnosine’s ability to suppress collagen-cross-linking. Collectively, this study reveals antifibrotic potential of carnosine in the heart with obesity and illustrates key mechanisms by which it may be acting.

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“…The response to HFHSD was sex-specific implying that females may develop skeletal muscle insulin resistance, while males may develop hepatic insulin resistance prediabetes is a reversible condition, so we see a small difference between STD and HFHSD. Decompensation in glucose tolerance occurs somewhere between 12 and 18 weeks after prolonged feeding with HFHSD (20). Diminished glucose tolerance as a sign of b-cell loss was considerably higher in females than in males, and it supported earlier onset of diabetes in females compared to males.…”

Section: Aging Was the Primary Metabolic Culprit In The Dm2 Pathology...mentioning

confidence: 90%

“…Chronic low-grade systemic inflammation, underlying both aging and obesity, may be the culprit behind many age-related conditions, including insulin resistance (16). Despite this, most HFHSD rodent studies were conducted on young adult animals (14,15,(17)(18)(19)(20). Furthermore, females and males differ in body composition, adipose tissue metabolism, weight gain susceptibility, as well as cardiometabolic and dysglycemic risks (21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

Elderly rats fed with a high-fat high-sucrose diet developed sex-dependent metabolic syndrome regardless of long-term metformin and liraglutide treatment

Ivić,

Zjalić,

Blažetić

et al. 2023

Front. Endocrinol.

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Aim/IntroductionThe study aimed to determine the effectiveness of early antidiabetic therapy in reversing metabolic changes caused by high-fat and high-sucrose diet (HFHSD) in both sexes.MethodsElderly Sprague–Dawley rats, 45 weeks old, were randomized into four groups: a control group fed on the standard diet (STD), one group fed the HFHSD, and two groups fed the HFHSD along with long-term treatment of either metformin (HFHSD+M) or liraglutide (HFHSD+L). Antidiabetic treatment started 5 weeks after the introduction of the diet and lasted 13 weeks until the animals were 64 weeks old.ResultsUnexpectedly, HFHSD-fed animals did not gain weight but underwent significant metabolic changes. Both antidiabetic treatments produced sex-specific effects, but neither prevented the onset of prediabetes nor diabetes.ConclusionLiraglutide vested benefits to liver and skeletal muscle tissue in males but induced signs of insulin resistance in females.

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High‐fat, high‐sucrose, and combined high‐fat/high‐sucrose diets effects in oxidative stress and inflammation in male rats under presence or absence of obesity

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 11 publications

References 63 publications

Reduction of lauric acid content in virgin coconut oil improved plasma lipid profile in high‐fat diet‐induced hypercholesterolemic mice

Reduction of lauric acid content in virgin coconut oil improved plasma lipid profile in high‐fat diet‐induced hypercholesterolemic mice

Iron scavenging and suppression of collagen cross-linking underlie antifibrotic effects of carnosine in the heart with obesity

Elderly rats fed with a high-fat high-sucrose diet developed sex-dependent metabolic syndrome regardless of long-term metformin and liraglutide treatment

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