Sexual Dimorphism of Adipose and Hepatic Aquaglyceroporins in Health and Metabolic Disorders

Rodrı́guez, Amaia; Marinelli, Raúl A.; Tesse, Angela; Frühbeck, Gema; Calamita, Giuseppe

doi:10.3389/fendo.2015.00171

Cited by 46 publications

(48 citation statements)

References 62 publications

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“…The expression of AQPs also appears to be location-specific. Visceral adipocytes exhibit a higher expression level of AQP3 and AQP7, which may result in the overall rise in the lipolytic rate and glycerol release from VAT ( Miranda et al, 2010 ; Rodríguez et al, 2015a ). In contrast, subcutaneous fat with a lower AQP7 level may help promote glycerol accumulation and thus adipocyte hypertrophy ( Rodríguez et al, 2015a ).…”

Section: Genders Aquaglyceroporins and Hccmentioning

confidence: 99%

“…Visceral adipocytes exhibit a higher expression level of AQP3 and AQP7, which may result in the overall rise in the lipolytic rate and glycerol release from VAT ( Miranda et al, 2010 ; Rodríguez et al, 2015a ). In contrast, subcutaneous fat with a lower AQP7 level may help promote glycerol accumulation and thus adipocyte hypertrophy ( Rodríguez et al, 2015a ). AQP regulation in adipocytes is crucial in maintain the fat and glucose homeostasis, i.e., a deregulation will lead to obesity and insulin resistance ( Kuriyama et al, 2002 ; Hibuse et al, 2005 ).…”

Section: Genders Aquaglyceroporins and Hccmentioning

confidence: 99%

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Gender Differences in Adipocyte Metabolism and Liver Cancer Progression

Cheung

Cheng

2016

Front. Genet.

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Liver cancer is the third most common cancer type and the second leading cause of deaths in men. Large population studies have demonstrated remarkable gender disparities in the incidence and the cumulative risk of liver cancer. A number of emerging risk factors regarding metabolic alterations associated with obesity, diabetes and dyslipidemia have been ascribed to the progression of non-alcoholic fatty liver diseases (NAFLD) and ultimately liver cancer. The deregulation of fat metabolism derived from excessive insulin, glucose, and lipid promotes cancer-causing inflammatory signaling and oxidative stress, which eventually triggers the uncontrolled hepatocellular proliferation. This review presents the current standing on the gender differences in body fat compositions and their mechanistic linkage with the development of NAFLD-related liver cancer, with an emphasis on genetic, epigenetic and microRNA control. The potential roles of sex hormones in instructing adipocyte metabolic programs may help unravel the mechanisms underlying gender dimorphism in liver cancer and identify the metabolic targets for disease management.

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Section: Genders Aquaglyceroporins and Hccmentioning

confidence: 99%

Section: Genders Aquaglyceroporins and Hccmentioning

confidence: 99%

Gender Differences in Adipocyte Metabolism and Liver Cancer Progression

Cheung

Cheng

2016

Front. Genet.

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“…Expression of AQP9 is influenced by gender and disease state. In human, despite exhibiting similar hepatic AQP9 protein, women manifest lower hepatocyte glycerol permeability compared to men [16]. In obese subjects with Non-Alcoholic Fatty Liver Disease (NAFLD), the hepatic expression of AQP9 was decreased [16].…”

Section: Citation: Zeng L Mei L Tan H Li H Lv W Et Al (2017) a mentioning

confidence: 99%

“…In human, despite exhibiting similar hepatic AQP9 protein, women manifest lower hepatocyte glycerol permeability compared to men [16]. In obese subjects with Non-Alcoholic Fatty Liver Disease (NAFLD), the hepatic expression of AQP9 was decreased [16]. In the rodent, female rats have lower levels of hepatic AQP9 protein compared with males in both fed and fasting conditions.…”

Section: Analysis Of Gk Expression By Real-time Quantitative Pcrmentioning

confidence: 99%

“…In the rodent, female rats have lower levels of hepatic AQP9 protein compared with males in both fed and fasting conditions. The mice model of NAFLD, demonstrated decreased hepatocyte AQP9 and glycerol permeability correlated with increased plasma glycerol [16], andAQP9 -/-mice exhibited a marked increase in plasma glycerol and triglyceride levels compared with AQP9 +/-mice, revealing a deficient glycerol metabolism [17]. Therefore, in addition to the GK mutation that causes a high serum triglyceride, the possible role of AQP9 needs to be emphasized, but this still needs to be further studied in GKD patients.…”

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confidence: 99%

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A Novel Splice-Site Mutation of the Gk Gene in a Chinese Patient with Isolate Glycerol Kinase Deficiency

Wu¹

2015

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What is already known on this topic?Glycerol Kinase Deficiency (GKD) [OMIM 307030] is a rare X-linked recessive metabolic disorder, which is characterized biochemically by hyperglycerolaemia and glyceroluria. Mutations in the GK gene are the major causes of isolate GKD. What this study adds?We report a novel splice-site mutation (c.1340 -2A>G) identified at GK gene analysis. IntroductionGlycerol Kinase Deficiency (GKD) [OMIM 307030] is a rare X-linked recessive metabolic disorder, which is characterized biochemically by hyperglycerolemia and glyceroluria [1]. The clinical spectrum varies from asymptomatic and Central Nervous System (CNS) deterioration to severe developmental delay, and is found to be related with GK gene mutation. The gene (GK) is located on Xp21 and encodes a key enzyme in regulation of glycerol uptake and metabolism that catalyzes the phosphorylation of glycerol [2].GKD can be categorized into three types: Infantile GKD, Juvenile GKD and Adult GKD. The Infantile GKD, also called the complex GKD or Xp21 contiguous gene deletion syndrome, is the most common type of GK mutation, which is caused by a deletion of GK gene or the neighboring genes, the clinical manifestations depends on the deletion of the genes [3]. The juvenile GKD is called symptomatic GKD, with symptoms like episodic vomiting, acidemia and Central Nervous System (CNS) deterioration. The adult GKD is called asymptomatic GKD, which detected incidentally with pseudohypertriglyceridemia. The juvenile and adult GKD are also called isolated GKD, which mainly caused by point mutations in GK gene.In this case report, a Chinese patient clinically diagnosed with isolated glycerol kinase deficiency is detected to have a novel splice-site mutation in the GK gene, which leads to a skip of exon 17. Case Report General information and clinical manifestationsA 3-month-old male term infant was referred to hospital due to no weight gain for three months. He was born with uterine-incision delivery route due to malpresentation after a first pregnancy of a 27-year-old mother at 38 weeks of uncomplicated gestation. His Apgar score was 9 points at 5min, with birth weight 3250g and head circumference 32cm. The parents were nonconsanguineous. Laboratory testsThe infant's serum triglyceride was 11.17mmol/l (normal range: 0.52-1.56mmol/l), and his urine analysis revealed increased urine glycerol. His serum cortisol level was 1.00μg/dl (normal range: 3.7-19.4μg/dl (8 am); 2.9-17.3μg/dl (4 pm)), testosterone was 1.02ng/ml (normal range:1.42-9.23ng/ml), lactate dehydrogenase was 275.5U/l (normal range: 109-245U/l), and creatine kinase was 77.0U/l (normal range: 24-190U/l). Molecular studiesThe clinical and laboratory findings were consistent with the clinical diagnosis of isolated glycerol kinase deficiency. The proband and his mother were recruited at the Hunan Jiahui genetics hospital. The study was approved by the Ethics Committee of the State Key AbstractGlycerol Kinase Deficiency (GKD) is a rare X-linked recessive metabolic disorder. Mutations in the G...

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Aquaporins in Obesity

Silva

Soveral

2017

Advances in Experimental Medicine and Biology

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Obesity is one of the most important metabolic disorders of this century and is associated with a cluster of the most dangerous cardiovascular disease risk factors, such as insulin resistance and diabetes , dyslipidemia and hypertension , collectively named Metabolic Syndrome. The role of aquaporins in glycerol metabolism facilitating glycerol release from the adipose tissue and distribution to various tissues and organs, unveils these membrane channels as important players in lipid balance and energy homeostasis and points to their involvement in a variety of pathophysiological mechanisms including insulin resistance, obesity and diabetes.This review summarizes the physiologic role of aquaglyceroporins in glycerol metabolism and lipid homeostasis, describing their specific tissue distribution, their involvement in glycerol balance and their implication in obesity and fat-related metabolic complications. The development of specify pharmacologic modulators able to regulate aquaglyceroporins expression and function , in particular AQP7 in adipose tissue, might constitute a novel approach for controlling obesity and other metabolic disorders.

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Sexual Dimorphism of Adipose and Hepatic Aquaglyceroporins in Health and Metabolic Disorders

Cited by 46 publications

References 62 publications

Gender Differences in Adipocyte Metabolism and Liver Cancer Progression

Gender Differences in Adipocyte Metabolism and Liver Cancer Progression

A Novel Splice-Site Mutation of the Gk Gene in a Chinese Patient with Isolate Glycerol Kinase Deficiency

Aquaporins in Obesity

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