Effects of HRT on liver enzyme levels in women with type 2 diabetes: a randomized placebo‐controlled trial

McKenzie, Joyce; Fisher, BM; Jaap, Alan J.; Stanley, Adrian J.; Paterson, Ken; Sattar, Naveed

doi:10.1111/j.1365-2265.2006.02543.x

Cited by 125 publications

(93 citation statements)

References 25 publications

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“…These results may suggest a possible relation of HRT in a less liver injury, and they are in agreement with a study performed in Scotland, which suggested that HRT improved the results of liver-enzyme levels in women with type 2 diabetes (16) . However, in both studies was not performed liver biopsy, that remains the gold standard for diagnosis and staging of hepatic fibrosis (24) .…”

Section: Discussionsupporting

confidence: 81%

Nonalcoholic Fatty Liver Disease in Menopausal Women

Florentino

Cotrim

Vilar

et al. 2013

Arq. Gastroenterol.

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-Context -Nonalcoholic Fatty Liver Disease (NAFLD) is common in postmenopausal women. It is associated with metabolic syndrome. However, the influence of hormone replacement therapy in NAFLD development in these women needs to be investigated. This study aimed to describe the clinical characteristics of NAFLD in postmenopausal women, and the relationship between hormone replacement therapy and this disease. (79/198) without hormone replacement therapy. Gamma-glutamyl transpeptidase (P = 0.001), alanine transaminase (P<0.01), ferritin (P<0.001) and insulin resistance (homeostatic model assessment of insulin resistance ≥3) (P<0.001) were higher in the group of women with NAFLD diagnosis who did not referred the use of hormone replacement therapy. Metabolic syndrome was also more frequent in women with NAFLD, who did not refer hormone replacement therapy. Conclusion -In conclusion this data suggests elevated prevalence of NAFLD in postmenopausal women; negative association of hormone replacement therapy and NAFLD. HEADINGS -Fatty Liver. Hormone replacement therapy.

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Section: Discussionsupporting

confidence: 81%

Nonalcoholic Fatty Liver Disease in Menopausal Women

Florentino

Cotrim

Vilar

et al. 2013

Arq. Gastroenterol.

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“…We saw that a short 2 month course without HRT lead to elevation of liver enzymes, readily suppressible by standard HRT, as also documented previously (3)(4)(5). Recently, the same response to HRT, albeit less pronounced, has also been found among postmenopausal women (27). Thus, lack of estrogens in some way seems to affect the liver.…”

Section: Discussionsupporting

confidence: 59%

Quantitative liver functions in Turner syndrome with and without hormone replacement therapy

et al. 2007

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Background: Studies have documented elevated levels of liver enzymes in many females with Turner syndrome (TS). Histology has shown a range of changes. Treatment with female hormone replacement therapy (HRT) reduces liver enzymes. Aim: To study quantitative liver functions in TS in detail with and without HRT. Design: Randomized crossover study with active treatment (HRT in TS and P-pill in controls) or no treatment. Subjects: Women with TS (nZ8, age 29.7G5.6 (meanGS.D.) years), verified by karyotype, and agematched controls (C; nZ8, age 27.3G4.9 years). Methods: We determined liver enzymes in blood, used the galactose elimination capacity to assess hepatocyte cytosol activity, plasma clearance of indocyanine green to assess excretory function, antipyrine clearance to estimate microsomal activity, and the functional hepatic nitrogen clearance (FHNC) to assess mitochondrial-cytosolic metabolic capacity for conversion of amino-nitrogen. Results: Liver enzymes were elevated in untreated TS and reduced by HRT. The hepatic capacities for conversion of galactose, indocyanine green, and antipyrine were normal and did not change by HRT.

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“…Furthermore, in an OVX SpragueDawley rat model, 17b-estradiol treatment decreased fatty acid synthesis in a hepatic zone 3-specific manner through increasing the phosphorylation of acetyl coenzyme-A carboxylase via an estrogen receptor-a-mediated pathway (Zhang et al 2013). Menopausal women have been shown to exhibit hepatic steatosis which is ameliorated by estrogen replacement therapy, although the results are inconsistent (Florentino et al 2013;McKenzie et al 2006). Thus, the activation of estrogen receptors in the liver may prevent hepatic steatosis by increasing b-oxidation of fatty acids and decreasing lipogenesis.…”

Section: Discussionmentioning

confidence: 99%

Cyanidin and malvidin in aqueous extracts of black carrots fermented with Aspergillus oryzae prevent the impairment of energy, lipid and glucose metabolism in estrogen-deficient rats by AMPK activation

Park

Kang²,

Jeong³

et al. 2015

Genes Nutr

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Black carrots (Daucus carota L.) are rich in anthocyanins which contribute many health benefits, but are limited by bioavailability and instability when exposed to oxygen, heat and light. Fermenting black carrots may improve the stability, absorption and bioactivity of its anthocyanins. Here, we examined whether and by what mechanisms the long-term consumption of unfermented black carrot extract (BC) and its extracts fermented with Lactobacillus plantarum (BCLP) or Aspergillus oryzae (BCAO) might prevent menopausal symptoms including impaired energy, glucose and lipid metabolism in estrogen-deficient animals with diet-induced obesity. Ovariectomized (OVX) rats were fed four different high-fat diets containing 2 % dextrin (OVX-control), 2 % BC, 2 % BCLP, or 2 % BCAO for 12 weeks. Sham rats were fed high-fat diets containing 2 % dextrin. The contents of total anthocyanins increased in BCAO compared to BC and BCLP, whereas the contents of cyanidin-3-rutinosides, malvidin-3,5-diglycosides and delphine-3-glucoside were lower and cyanidin and malvidin were much higher in BCLP and BCAO than BC. Fat mass and weight gain were lower in descending order of OVX-control [ BC and BCLP [ BCAO due to increased energy expenditure and fat oxidation. However, BC, BCLP and especially BCAO all normalized HOMA-IR, an indicator of insulin resistance and glucose intolerance, in OVX rats. OVX increased serum total and LDL cholesterol and triglycerides, but BC, BCLP and BCAO significantly prevented the increases. BCAO markedly decreased hepatic triglyceride levels by increasing gene expressions of CPT-1 and PPAR-a, which are involved in fatty acid oxidation, and decreasing mRNA expressions of FAS and SREBP-1c, which are associated with fatty acid synthesis. This was related to increased pAMPK ? pACC signaling and improved hepatic insulin signaling (pAkt ? pFOXO-1). Cyanidin and malvidin markedly decreased fat accumulation in 3T3-L1 adipocytes by increasing CPT-1 and decreasing FAS and SREBP-1c expression in comparison with cyanidin-3-rutinoside and malvidin-3,5-diglycosides. In conclusion, with increasing cyanidin and malvidin, BCAO prevented the exacerbation of lipid and glucose metabolism by activating hepatic insulin signaling and AMPK activation by in OVX rats.

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Effects of HRT on liver enzyme levels in women with type 2 diabetes: a randomized placebo‐controlled trial

Cited by 125 publications

References 25 publications

Nonalcoholic Fatty Liver Disease in Menopausal Women

Nonalcoholic Fatty Liver Disease in Menopausal Women

Quantitative liver functions in Turner syndrome with and without hormone replacement therapy

Cyanidin and malvidin in aqueous extracts of black carrots fermented with Aspergillus oryzae prevent the impairment of energy, lipid and glucose metabolism in estrogen-deficient rats by AMPK activation

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