Role of Estrogens in the Regulation of Liver Lipid Metabolism

Palmisano, Brian T.; Zhu, Lin; Stafford, John M.

doi:10.1007/978-3-319-70178-3_12

Cited by 296 publications

(185 citation statements)

References 173 publications

(249 reference statements)

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“…Upon completion of the lactation period (postnatal day 23), the pups were separated from their mothers, and the sex of each offspring was determined. Only male offspring were included in the study since they have been repeatedly shown as prone to metabolic deregulation under high fructose diets [17,18]. Two or three male rats were randomly selected from each litter.…”

Section: Experimental Designmentioning

confidence: 99%

Metabolic Response of Adult Male Offspring Rats to Prenatal Caffeine Exposure

Mastroleon

Κορού

Pergialiotis

et al. 2020

Cureus

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Caffeine is the most widely consumed psychoactive substance, with recommendations from health associations and regulatory bodies for limiting caffeine consumption during pregnancy being increasingly common. Prenatal exposure to caffeine has been shown to increase the risk of developing abnormalities in lipid metabolism in adult life. We further investigated the effect of prenatal caffeine exposure (PCE) (20 mg/kg of body weight) on the metabolic "reserve" of male Sprague Dawley offspring fed on a high fructose diet in adult life. Male adult PCE offspring were assigned to four groups; Nw and Nf: offspring of control mothers (N group of mothers), having received tap water or high fructose water respectively; Cw and Cf: offspring exposed to caffeine during gestation (C group of mothers) and receiving tap water or a high fructose water solution, respectively. Cf rats presented increased serum triglyceride level, as well as raised systolic and diastolic blood pressure levels, together with extensive renal tissue oedema in adulthood, compared to the other groups (p<0.05 for all comparisons). These findings show further evidence for potential detrimental metabolic effects of prenatal caffeine exposure during adulthood in this animal model.

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Section: Experimental Designmentioning

confidence: 99%

Metabolic Response of Adult Male Offspring Rats to Prenatal Caffeine Exposure

Mastroleon

Κορού

Pergialiotis

et al. 2020

Cureus

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“…Sexual dimorphism concerns both NAFLD and cardiovascular comorbidities, 38,39 and hormonal modulation is a key element to understand variations in risk by age and sex. 40,41 Premenopausal women seem to be protected from developing high levels of NAFLD, while ovarian senescence appears to be associated with severe steatosis and fibrosing NASH. Due to an age >40 yo in the COPD population, we could expect more or equal risk of steatosis in women than men.…”

Section: Discussionmentioning

confidence: 99%

<p>Low Liver Density Is Linked to Cardiovascular Comorbidity in COPD: An ECLIPSE Cohort Analysis</p>

Viglino¹,

Martin²,

Alméras³

et al. 2020

COPD

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These authors contributed equally to this workPurpose: Fatty liver disease is associated with cardiometabolic disorders and represents a potential key comorbidity in Chronic Obstructive Pulmonary Disease (COPD). Some intermediary mechanisms of fatty liver disease (including its histological component steatosis) include tissue hypoxia, low-grade inflammation and oxidative stress that are key features of COPD. Despite these shared physiological pathways, the effect of COPD on the prevalence of hepatic steatosis, and the association between hepatic steatosis and comorbidities in this population remain unclear. Liver density measured by computed tomography (CT)-scan is a non-invasive surrogate of fat infiltration, with lower liver densities reflecting more fat infiltration and a liver density of 40 Hounsfield Units (HU) corresponding to a severe 30% fat infiltration. Patients and Methods: We took advantage of the international cohort ECLIPSE in which non-enhanced chest CT-scans were obtained in 1554 patients with COPD and 387 healthy controls to analyse the liver density at T12-L1. Results: The distribution of liver density was similar and the prevalence of severe steatosis (density<40 HU) was not different (4.7% vs 5.2%, p=0.7) between COPD and controls. In patients with COPD, the lowest liver density quartile was associated, after age and sex adjustment, with coronary artery disease (OR a =1.59, 95% CI 1.12 to 2.24) and stroke (OR a =2.20, 95% CI 1.07 to 4.50), in comparison with the highest liver density quartile. Conclusion: The present data indicate that a low liver density emerged as a predictor of cardiovascular comorbidities in the COPD population. However, the distribution of liver density and the prevalence of severe steatosis were similar in patients with COPD and control subjects.

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“…Previous studies suggest that sexual dimorphism in NAFLD prevalence may be explained by differences in de novo lipogenesis 26 . Oestrogens, binding their nuclear receptor ERα, downregulate the expression of genes involved in de novo lipogenesis, thus preventing the intracellular accumulation of FFAs in hepatocytes and the consequent lipotoxicity 27 . Sexual differences in de novo lipogenesis are not only quantitative, but also qualitative.…”

Section: Metabolic Pro‐inflammatory Signals: Potential Triggers Of Nafldmentioning

confidence: 99%

Macrophages in the pathophysiology of NAFLD: The role of sex differences

Ministrini

Montecucco

Sahebkar

et al. 2020

Eur J Clin Investigation

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Nonalcoholic fatty liver disease (NAFLD) is a multifactorial pathological condition, which recognizes a certain sexual dimorphism. Experimental and clinical studies provided evidence for a critical role of macrophages in NAFLD development and progression. Especially, liver-resident macrophages (also known as Kupffer cells) are likely the common final pathway of several pro-steatosic signals. A huge amount of danger-associated molecular patterns recognized by Kupffer cells is provided within the liver by lipid and glucose toxicity. Other pro-inflammatory signals come from surrounding tissues into the portal vein, directly to the liver: they come from dysfunctional adipocytes, adipose tissue macrophages and gut dysbiosis. These complex crosstalks are differently represented across sexes, as sexual hormones control many of these processes. Sexual dimorphism then modulates metabolic and inflammatory cascades driving the liver from a simple steatosis to NAFLD and beyond.Here, metabolic and inflammatory mechanisms underlying NALFD pathophysiology will be updated. A special attention will be paid to describe sex-related differences that could provide insights for patient stratification and more tailored therapeutic approaches. K E Y W O R D Sinflammation, Kupffer cells, macrophages, microbiome, nonalcoholic fatty live disease 2 of 9 | MINISTRINI eT al.

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Role of Estrogens in the Regulation of Liver Lipid Metabolism

Cited by 296 publications

References 173 publications

Metabolic Response of Adult Male Offspring Rats to Prenatal Caffeine Exposure

Metabolic Response of Adult Male Offspring Rats to Prenatal Caffeine Exposure

<p>Low Liver Density Is Linked to Cardiovascular Comorbidity in COPD: An ECLIPSE Cohort Analysis</p>

Macrophages in the pathophysiology of NAFLD: The role of sex differences

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