Prolactin improves hepatic steatosis via CD36 pathway

Zhang, Pengzi; Ge, Zhijuan; Wang, Hongdong; Feng, Wenhuan; Sun, Xu; Chu, Xuehui; Jiang, Can; Wang, Yan; Zhu, Dalong; Bi, Yan

doi:10.1016/j.jhep.2018.01.035

Cited by 80 publications

(79 citation statements)

References 37 publications

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“…11), but future investigations will be required to determine whether these drugs also increase the activity of this translocase. Enhanced FAT/CD36 expression and activity plays a major role in higher hepatic fatty acid uptake and fatty liver in different pathophysiological situations (He et al 2011;Zhang et al 2018). Previous studies also suggested that steatosis induced by RIF, tetracycline, and valproic acid could be, at least in part, secondary to increased FAT/CD36 expression or activity (Benet et al 2014;Choi et al 2015;Huang et al 2016), although this effect was not observed with RIF in our study ( Supplementary Fig.…”

Section: Discussioncontrasting

confidence: 51%

Drug-induced hepatic steatosis in absence of severe mitochondrial dysfunction in HepaRG cells: proof of multiple mechanism-based toxicity

et al. 2020

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Steatosis is a liver lesion reported with numerous pharmaceuticals. Prior studies showed that severe impairment of mitochondrial fatty acid oxidation (mtFAO) constantly leads to lipid accretion in liver. However, much less is known about the mechanism(s) of drug-induced steatosis in the absence of severe mitochondrial dysfunction, although previous studies suggested the involvement of mild-to-moderate inhibition of mtFAO, increased de novo lipogenesis (DNL), and impairment of very low-density lipoprotein (VLDL)

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Section: Discussioncontrasting

confidence: 51%

Drug-induced hepatic steatosis in absence of severe mitochondrial dysfunction in HepaRG cells: proof of multiple mechanism-based toxicity

et al. 2020

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“…145 Several favourable, and some unfavourable, actions have been ascribed to the sexually dimorphic liver Prlr expression. In rodents and humans, prolactin protects the liver from NAFLD 148,149 and this finding is in line with results from in vitro approaches. 149 Furthermore, protective actions of prolactin in hepatocarcinoma (HCC) development 150 and liver inflammation have been described.…”

Section: Prol Ac Tin and The Liversupporting

confidence: 83%

Metabolic functions of prolactin: Physiological and pathological aspects

Lopez‐Vicchi

Winne

Brie

et al. 2020

J Neuroendocrinology

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Prolactin is a pleiotropic hormone that is named after its major role in lactation in mammals. Alongside this role in milk production, prolactin has been implicated in a wide range of functions, including regulating aspects of the immune system, the reproductive system and metabolism. The wide scope of functions for prolactin is considered to converge during pregnancy and lactation, when prolactin concentrations are high, and it is hypothesised that prolactin has a role not only in milk production, but also as a signal to many of the systems in the body driving maternal adaptations to meet the demands of these physiologically challenging states. 1 Although high prolactin concentrations are appropriate during pregnancy and lactation, 1-3 there are many pathological conditions of hyperprolactinaemia, such as prolactin-secreting tumours and dopamine receptor antagonising drug treatments, 4 and these pathologically high prolactin concentrations are likely to impact on many different aspects of physiology and lead to metabolic dysfunction. The focus of this review is to examine the effects of prolactin on metabolism and energy homeostasis in both the physiological and pathological states of hyperprolactinaemia. Prolactin is secreted by lactotroph cells and, unlike other hormones secreted by the anterior pituitary, its secretion is regulated

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“…In our study, serum IL‐6 levels decreased significantly (liraglutide group) or had a decreasing trend (sitagliptin group), and positive correlation was found between ΔIL‐6 and ΔMRI‐PDFF. It was reported very recently by Bi et al that PRL could improve hepatic steatosis through the CD36 pathway . CD36 was one of the receptors for free fatty acids (FFAs) that facilitated FFA uptake.…”

Section: Discussionmentioning

confidence: 99%

Liraglutide, Sitagliptin, and Insulin Glargine Added to Metformin: The Effect on Body Weight and Intrahepatic Lipid in Patients With Type 2 Diabetes Mellitus and Nonalcoholic Fatty Liver Disease

et al. 2019

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To investigate the effect of antidiabetic agents on nonalcoholic fatty liver disease (NAFLD) in patients with type 2 diabetes mellitus (T2DM), 75 patients with T2DM and NAFLD under inadequate glycemic control by metformin were randomized (1:1:1) to receive add‐on liraglutide, sitagliptin, or insulin glargine in this 26‐week trial. The primary endpoint was the change in intrahepatic lipid (IHL) from baseline to week 26 as quantified by magnetic resonance imaging–estimated proton density fat fraction (MRI‐PDFF). Secondary endpoints included changes in abdominal adiposity (subcutaneous adipose tissue [SAT] and visceral adipose tissue [VAT]), glycated hemoglobin, and body weight from baseline to week 26. We analysed data from intent‐to‐treat population. MRI‐PDFF, VAT, and weight decreased significantly with liraglutide (15.4% ± 5.6% to 12.5% ± 6.4%, P < 0.001; 171.4 ± 27.8 to 150.5 ± 30.8, P = 0.003; 86.6 ± 12.9 kg to 82.9 ± 11.1 kg, P = 0.005, respectively) and sitagliptin (15.5% ± 5.6% to 11.7% ± 5.0%, P = 0.001; 153.4 ± 31.5 to 139.8 ± 27.3, P = 0.027; 88.2 ± 13.6 kg to 86.5 ± 13.2 kg, P = 0.005, respectively). No significant change in MRI‐PDFF, VAT, or body weight was observed with insulin glargine. SAT decreased significantly in the liraglutide group (239.9 ± 69.0 to 211.3 ± 76.1; P = 0.020) but not in the sitagliptin and insulin glargine groups. Changes from baseline in MRI‐PDFF, VAT, and body weight were significantly greater with liraglutide than insulin glargine but did not differ significantly between liraglutide and sitagliptin. Conclusion: Combined with metformin, both liraglutide and sitagliptin, but not insulin glargine, reduced body weight, IHL, and VAT in addition to improving glycemic control in patients with T2DM and NAFLD.

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Prolactin improves hepatic steatosis via CD36 pathway

Cited by 80 publications

References 37 publications

Drug-induced hepatic steatosis in absence of severe mitochondrial dysfunction in HepaRG cells: proof of multiple mechanism-based toxicity

Drug-induced hepatic steatosis in absence of severe mitochondrial dysfunction in HepaRG cells: proof of multiple mechanism-based toxicity

Metabolic functions of prolactin: Physiological and pathological aspects

Liraglutide, Sitagliptin, and Insulin Glargine Added to Metformin: The Effect on Body Weight and Intrahepatic Lipid in Patients With Type 2 Diabetes Mellitus and Nonalcoholic Fatty Liver Disease

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