Apolipoprotein A-I Modulates Processes Associated with Diet-Induced Nonalcoholic Fatty Liver Disease in Mice

Karavia, Eleni A.; Papachristou, Dionysios J.; Liopeta, Kassiani; Triantaphyllidou, Irene-Eva; Dimitrakopoulos, Odyssefs; Kypreos, Kyriakos E.

doi:10.2119/molmed.2012.00113

Cited by 50 publications

(58 citation statements)

References 46 publications

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“…Determination of post-prandial TG kinetics was performed by oral administration (gavage) of 300μl of extra virgin olive oil, as described previously (Karavia et al, 2012). Values were expressed in mg/dl ± S.E.M.…”

Section: Western Blot Analysismentioning

confidence: 99%

“…Page 10 of 38 Conventional hematoxylin and eosing (H&E) and reticulin histological staining of hepatic sections were performed as described previously (Karavia et al, 2013;Karavia et al, 2012). From each section three different areas were photographed using a Nikon Eclipse 80i microscope with a Nikon DXM 1200C digital camera (original magnification 20X) and histomorphometric analysis was performed as described previously (Karavia et al, 2013;Karavia et al, 2012).…”

Section: Histological Analysis Of Tissue Samplesmentioning

confidence: 99%

“…From each section three different areas were photographed using a Nikon Eclipse 80i microscope with a Nikon DXM 1200C digital camera (original magnification 20X) and histomorphometric analysis was performed as described previously (Karavia et al, 2013;Karavia et al, 2012).…”

Section: Histological Analysis Of Tissue Samplesmentioning

confidence: 99%

“…Recently we reported that in addition to its role in plasma cholesterol homeostasis, apolipoprotein A-I (ApoA-I) (Zannis et al, 2004), the main protein component of HDL, in an important modulator of processes associated with glucose intolerance and diet-induced NAFLD development in mice (Karavia et al, 2012). Our studies in ApoA-I-deficient (apoa1 -/ ) mice raised the interesting possibility that expression of therapeutic forms of ApoA-I, such as ApoA-I Milano , by gene therapy approaches may have beneficial effects on NAFLD (Karavia et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

“…Our studies in ApoA-I-deficient (apoa1 -/ ) mice raised the interesting possibility that expression of therapeutic forms of ApoA-I, such as ApoA-I Milano , by gene therapy approaches may have beneficial effects on NAFLD (Karavia et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Deficiency in apolipoprotein A-I ablates the pharmacological effects of metformin on plasma glucose homeostasis and hepatic lipid deposition

Karavia

Hatziri

Kalogeropoulou

et al. 2015

European Journal of Pharmacology

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Section: Western Blot Analysismentioning

confidence: 99%

Section: Histological Analysis Of Tissue Samplesmentioning

confidence: 99%

Section: Histological Analysis Of Tissue Samplesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Deficiency in apolipoprotein A-I ablates the pharmacological effects of metformin on plasma glucose homeostasis and hepatic lipid deposition

Karavia

Hatziri

Kalogeropoulou

et al. 2015

European Journal of Pharmacology

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Folate Deficiency and/or the Genetic Variant Mthfr^{677C >T} Can Drive Hepatic Fibrosis or Steatosis in Mice, in a Sex‐Specific Manner

Leclerc,

Christensen,

Reagan

et al. 2024

Molecular Nutrition Food Res

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ScopeDisturbances in one‐carbon metabolism contribute to nonalcoholic fatty liver disease (NAFLD) which encompasses steatosis, steatohepatitis, fibrosis, and cirrhosis. The goal is to examine impact of folate deficiency and the Mthfr677C >T variant on NAFLD.Methods and resultsThis study uses the new Mthfr677C >T mouse model for the human MTHFR677C >T variant. Mthfr677CC and Mthfr677TT mice were fed control diet (CD) or folate‐deficient (FD) diets for 4 months. FD and Mthfr677TT alter choline/methyl metabolites in liver and/or plasma (decreased S‐adenosylmethionine (SAM):S‐adenosylhomocysteine (SAH) ratio, methyltetrahydrofolate, and betaine; increased homocysteine [Hcy]). FD, with contribution from Mthfr677TT, provokes fibrosis in males. Studies of normal livers reveal alterations in plasma markers and gene expression that suggest an underlying predisposition to fibrosis induced by FD and/or Mthfr677TT in males. These changes are absent or reverse in females, consistent with the sex disparity of fibrosis. Sex‐based differences in methylation potential, betaine, sphingomyelin, and trimethylamine‐N‐oxide (TMAO) levels may prevent fibrogenesis in females. In contrast, Mthfr677TT alters choline metabolism, dysregulates expression of lipid metabolism genes, and promotes steatosis in females.ConclusionThis study suggests that folate deficiency predisposes males to fibrosis, which is exacerbated by Mthfr677TT, whereas Mthfr677TT predisposes females to steatosis, and reveal novel contributory mechanisms for these NAFLD‐related disorders.

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Açaí (Euterpe oleracea Martius) supplementation in the diet during gestation and lactation attenuates liver steatosis in dams and protects offspring

et al. 2019

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Purpose Maternal high-fat diet affects offspring and can induce metabolic disorders such as non-alcoholic fatty liver disease (NAFLD). New therapeutic strategies are being investigated as way to prevent or attenuate this condition. The objective of this study was to evaluate the effect of açaí supplementation in the maternal high-fat diet on dams and offspring lipid metabolism. Methods Female Fisher rats were divided in four groups and fed a control diet (C), a high-fat diet (HF), an açaí supplemented diet (CA) and a high-fat diet supplemented with açaí (HFA) 2 weeks before mating, during gestation and lactation. The effects of açaí were evaluated in the male offspring after birth (P1) and weaning (P21). Results HFA reduced relative liver weight, fat and cholesterol liver content in dams and improved liver steatosis as confirmed by histological analyses. HFA increased serum cholesterol and expression of Srebpf1 and Fasn genes. In offspring, HFA decreased relative liver weight, and serum cholesterol only in P21. An increase in the Sirt1, Srebpf1 and Fasn genes expression was observed in P21. Conclusions These results suggest that açaí supplementation may attenuate NAFLD in dams and protect offspring from the detrimental effects of lipid excess from a maternal high-fat diet.

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Apolipoprotein A-I Modulates Processes Associated with Diet-Induced Nonalcoholic Fatty Liver Disease in Mice

Cited by 50 publications

References 46 publications

Deficiency in apolipoprotein A-I ablates the pharmacological effects of metformin on plasma glucose homeostasis and hepatic lipid deposition

Deficiency in apolipoprotein A-I ablates the pharmacological effects of metformin on plasma glucose homeostasis and hepatic lipid deposition

Folate Deficiency and/or the Genetic Variant Mthfr^{677C >T} Can Drive Hepatic Fibrosis or Steatosis in Mice, in a Sex‐Specific Manner

Açaí (Euterpe oleracea Martius) supplementation in the diet during gestation and lactation attenuates liver steatosis in dams and protects offspring

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Apolipoprotein A-I Modulates Processes Associated with Diet-Induced Nonalcoholic Fatty Liver Disease in Mice

Cited by 50 publications

References 46 publications

Deficiency in apolipoprotein A-I ablates the pharmacological effects of metformin on plasma glucose homeostasis and hepatic lipid deposition

Deficiency in apolipoprotein A-I ablates the pharmacological effects of metformin on plasma glucose homeostasis and hepatic lipid deposition

Folate Deficiency and/or the Genetic Variant Mthfr677C >T Can Drive Hepatic Fibrosis or Steatosis in Mice, in a Sex‐Specific Manner

Açaí (Euterpe oleracea Martius) supplementation in the diet during gestation and lactation attenuates liver steatosis in dams and protects offspring

Contact Info

Product

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Folate Deficiency and/or the Genetic Variant Mthfr^{677C >T} Can Drive Hepatic Fibrosis or Steatosis in Mice, in a Sex‐Specific Manner