The relationship between aquaglyceroporin expression and development of fatty liver in diet-induced obesity and ob/ob mice

Hirako, Satoshi; Wakayama, Yoshihiro; Kim, Hyounju; Iizuka, Yuzuru; Matsumoto, Akiyo; Wada, Nobuhiro; Kimura, Ai; Okabe, Mai; Sato, Junichi; Suzuki, Mamiko; Takenoya, Fumiko; Shioda, Seiji

doi:10.1016/j.orcp.2015.12.001

Cited by 17 publications

(11 citation statements)

References 35 publications

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“…), as well as in diet‐induced obese mice (Hirako et al. ). In the present study, amnion AQP3 and AQP9 mRNA levels in HFD resistant macaques were not different from that in control animals.…”

Section: Discussionmentioning

confidence: 99%

High-fat diet effects on amniotic fluid volume and amnion aquaporin expression in non-human primates

et al. 2018

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Western style, high‐fat diet (HFD) and associated high lipid levels have deleterious effects on fetal and placental development independent of maternal obesity and/or diabetes. Our objectives were to determine whether HFD without development of obesity would alter amniotic fluid volume (AFV) and amnion aquaporin (AQP) expression in a non‐human primate model. Japanese macaques were fed either a control diet or HFD before and during pregnancy. The four quadrant amniotic fluid index (AFI) was used as an ultrasonic estimate of AFV at 120 days gestation. Amnion samples were collected at 130 days gestation by cesarean section and AQP mRNA levels were determined by quantitative RT‐PCR. Similar to that in human, AQP1, AQP3, AQP8, AQP9, and AQP11 were expressed in the macaque amnion with significant differences in levels among AQPs. In macaque, neither individual AQPs nor expression profiles of the five AQPs differed between control and non‐obese HFD animals. There were regional differences in AQP expression in that, AQP1 mRNA levels were highest and AQP8 lowest in reflected amnion while AQP3, AQP9, and AQP11 were not different among amnion regions. When subdivided into control and HFD groups, AQP1 mRNA levels remain highest in the reflected amnion of both groups. The HFD did not significantly affect the AFI, but AFI was positively correlated with AQP11 mRNA levels independent of diet. Collectively, these data suggest that HFD in pregnant non‐obese individuals may have at most modest effects on AFV as the AFI and amnion AQP expression are not substantially altered.

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Section: Discussionmentioning

confidence: 99%

High-fat diet effects on amniotic fluid volume and amnion aquaporin expression in non-human primates

et al. 2018

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“…The mRNA expression levels of fatty acid and TG synthesis-related genes and fatty acid β-oxidation-related genes in the liver were increased in this mouse model, suggesting that TG synthesis in this organ results in glycerol release from adipocytes. Furthermore, adipose AQP7 and AQP9 gene expressions were increased in DIO mice [100].…”

Section: New and Alternative Mechanismsmentioning

confidence: 92%

Nonalcoholic Fatty Liver Disease: A Challenge from Mechanisms to Therapy

Tarantino

Citro

Capone

2019

JCM

114

110

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Focusing on previously published mechanisms of non-alcoholic fatty liver disease (NAFLD), their uncertainty does not always permit a clear elucidation of the grassroot alterations that are at the basis of the wide-spread illness, and thus curing it is still a challenge. There is somehow exceptional progress, but many controversies persist in NAFLD research and clinical investigation. It is likely that hidden mechanisms will be brought to light in the near future. Hereby, the authors present, with some criticism, classical mechanisms that stand at the basis of NAFLD, and consider contextually different emerging processes. Without ascertaining these complex interactions, investigators have a long way left ahead before finding an effective therapy for NAFLD beyond diet and exercise. few are conclusively accepted by experts. We try to provide evidence of the complexity, and for some aspects the contradictions, of the main lines of basic and clinical research addressing this topic. The Role of Reactive Oxygen Species (ROS) OverproductionMalnutrition splits in two directions; undernutrition and overnutrition; both of them leading to severe health complications: Famine and overweight/obesity are the result of calorie deficit or excess, and both of them are major health problems. Constantly eating excess calories leads body fat stores to expand. One of the most active and productive hypotheses about the mechanisms inducing or worsening obesity and consequently NAFLD is the over-production of reactive oxygen species (ROS). Oxidative stress accompanying obesity is reckoned to be a key factor in the development of insulin resistance (IR), [4]. In fact, obese mice treated with NADPH oxidase inhibitors (reducing ROS) have clearly demonstrated the involvement of ROS in the genesis of IR, hepatic steatosis, and T2DM [5]. Mitochondria are clearly considered to be main contributors to oxidative stress in obesity induced by chronic over-nutrition, with subsequent reduced insulin sensitivity or IR [6]. The trigger that causes the oxidative stress in obesity is the energy surplus that eventually generates reducing equivalents. These exceed the rate of ATP utilization, giving space to the over-production of O 2 , and consequently reducing the redox-buffering capacity [7]. The aforementioned pathway has been fully highlighted in mice, characterized by deletion of manganese superoxide dismutase at the adipocyte level through enhanced mitochondrial biogenesis, mediated by uncoupling protein 1 [8].

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“…In different mouse models of obesity, a coordinated upregulation of AQP7 and AQP9 mRNA has been reported in male mice (3,10). However, further studies are needed to confirm that the coordinated upregulation of AQP7 and AQP9 in relation to obesity also occurs at the protein level.…”

Section: Introductionmentioning

confidence: 97%

Sex-Specific Effect of High-Fat Diet on Glycerol Metabolism in Murine Adipose Tissue and Liver

et al. 2020

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Obesity is associated with increased plasma glycerol levels. The coordinated regulation of glycerol channels in adipose tissue (AQP7) and the liver (AQP9) has been suggested as an important contributor to the pathophysiology of type-2-diabetes mellitus, as it would provide glycerol for hepatic synthesis of glucose and triglycerides. The regulation of AQP7 and AQP9 is influenced by sex. This study investigates the effect of a high-fat diet (HFD) on glycerol metabolism in mice and the influence of sex and GLP-1-receptor agonist treatment. Female and male C57BL/6JRj mice were fed either a control diet or a HFD for 12 or 24 weeks. Liraglutide was administered (1 mg/kg/day) to a subset of female mice. After 12 weeks of HFD, females had gained less weight than males. In adipose tissue, only females demonstrated an increased abundance of AQP7, whereas only males demonstrated a significant increase in glycerol kinase abundance and adipocyte size. 24 weeks of HFD resulted in a more comparable effect on weight gain and adipose tissue in females and males. HFD resulted in marked hepatic steatosis in males only and had no significant effect on the hepatic abundance of AQP9. Liraglutide treatment generally attenuated the effects of HFD on glycerol metabolism. In conclusion, no coordinated upregulation of glycerol channels in adipose tissue and liver was observed in response to HFD. The effect of HFD on glycerol metabolism is sex-specific in mice, and we propose that the increased AQP7 abundance in female adipose tissue could contribute to their less severe response to HFD.

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The relationship between aquaglyceroporin expression and development of fatty liver in diet-induced obesity and ob/ob mice

Cited by 17 publications

References 35 publications

High-fat diet effects on amniotic fluid volume and amnion aquaporin expression in non-human primates

High-fat diet effects on amniotic fluid volume and amnion aquaporin expression in non-human primates

Nonalcoholic Fatty Liver Disease: A Challenge from Mechanisms to Therapy

Sex-Specific Effect of High-Fat Diet on Glycerol Metabolism in Murine Adipose Tissue and Liver

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