Age-dependent hepatic alterations induced by a high-fat high-fructose diet

Casagrande, Breno Picin; Gomes, Moisés Felipe Pereira; Moura, Eliane; Santos, Albert; Kubota, Melina Chiemi; Ribeiro, Daniel Araki; Pisani, Luciana Pellegrini; Medeiros, Alessandra; Estadella, Débora

doi:10.1007/s00011-019-01223-1

Cited by 13 publications

(9 citation statements)

References 46 publications

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“…The start date for a rodent diet can be arbitrary, ranging from birth (uncommon), weaning (3 weeks old) and up to 12 weeks old. When comparing Wistar rats started on a high-fat/high-fructose diet at 6 versus 12 weeks old, animals started at a younger age have higher levels of hepatic triglycerides, more weight gain, and increased IL-6 and IL-10 after 13 weeks [ 84 ]. Mice started at an older age show only increases in TNF-α.…”

Section: How Long Do I Need To Feed Mice To Promote Nash?mentioning

confidence: 99%

“…Mice started at an older age show only increases in TNF-α. Both age groups exhibit similar increases in serum triglycerides and adiposity [ 84 ]. Collectively these results indicate that an obesogenic diet can promote NASH development after 16 weeks in mice, but for progression to NASH and cancer, it likely requires much longer diet regimes, upwards of 36 weeks.…”

Section: How Long Do I Need To Feed Mice To Promote Nash?mentioning

confidence: 99%

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Diet-Induced Models of Non-Alcoholic Fatty Liver Disease: Food for Thought on Sugar, Fat, and Cholesterol

Eng

Estall

2021

Cells

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Non-alcoholic fatty liver disease (NAFLD) affects approximately 1 in 4 people worldwide and is a major burden to health care systems. A major concern in NAFLD research is lack of confidence in pre-clinical animal models, raising questions regarding translation to humans. Recently, there has been renewed interest in creating dietary models of NAFLD with higher similarity to human diets in hopes to better recapitulate disease pathology. This review summarizes recent research comparing individual roles of major dietary components to NAFLD and addresses common misconceptions surrounding frequently used diet-based NAFLD models. We discuss the effects of glucose, fructose, and sucrose on the liver, and how solid vs. liquid sugar differ in promoting disease. We consider studies on dosages of fat and cholesterol needed to promote NAFLD versus NASH, and discuss important considerations when choosing control diets, mouse strains, and diet duration. Lastly, we provide our recommendations on amount and type of sugar, fat, and cholesterol to include when modelling diet-induced NAFLD/NASH in mice.

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Section: How Long Do I Need To Feed Mice To Promote Nash?mentioning

confidence: 99%

Section: How Long Do I Need To Feed Mice To Promote Nash?mentioning

confidence: 99%

Diet-Induced Models of Non-Alcoholic Fatty Liver Disease: Food for Thought on Sugar, Fat, and Cholesterol

Eng

Estall

2021

Cells

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“…The consumption of an obesogenic diet is known to increase body mass, VAT, and to promote hepatic inflammation and hepatic steatosis (Lozano et al 2016, Casagrande et al 2019. Still, there is not much information regarding these parameters when terminating the intake of OD.…”

Section: Discussionmentioning

confidence: 99%

“…Hepatic inflammation occurred despite hepatic TAG accumulation following HSHF intake and is related to visceral fat accumulation and inflammation. We have recently shown that chronic OD intake, 13 weeks of a high-fat and high-fructose diet, can drive VAT accumulation and hepatic inflammation despite no significant hepatic TAG increase (Casagrande et al 2019).…”

Section: Journal Of Endocrinologymentioning

confidence: 99%

“…The negative aspects of obesogenic diets (OD) on adipose tissue accumulation, hepatic fat accumulation (steatosis), and inflammation are well described (Van Herck et al 2017, Bortolin et al 2018, Casagrande et al 2019. Obesity and non-alcoholic fatty liver disease (NAFLD) are two parts of the same role, respectively, as causation and consequence of the metabolic syndrome (Kanwar & Kowdley 2016).…”

Section: Introductionmentioning

confidence: 99%

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Hepatic inflammation precedes steatosis and is mediated by visceral fat accumulation

Casagrande

Souza

Ribeiro

et al. 2020

Journal of Endocrinology

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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.

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AMPK in the gut-liver-brain axis and its influence on OP rats in an HSHF intake and WTD rat model

Casagrande

Pisani

Estadella

2021

Pflugers Arch - Eur J Physiol

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Age-dependent hepatic alterations induced by a high-fat high-fructose diet

Cited by 13 publications

References 46 publications

Diet-Induced Models of Non-Alcoholic Fatty Liver Disease: Food for Thought on Sugar, Fat, and Cholesterol

Diet-Induced Models of Non-Alcoholic Fatty Liver Disease: Food for Thought on Sugar, Fat, and Cholesterol

Hepatic inflammation precedes steatosis and is mediated by visceral fat accumulation

AMPK in the gut-liver-brain axis and its influence on OP rats in an HSHF intake and WTD rat model

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