Influence of Morbid Obesity and Insulin Resistance on Gene Expression Levels of AQP7 in Visceral Adipose Tissue and AQP9 in Liver

Catalán, Victoria; Gómez-Ambrosi, Javier; Pastor, Carlos; Rotellar, Fernando; Silva, Camilo; Rodríguez, Amaia; Gil, Marı́a J.; Cienfuegos, Javier A.; Salvador, Javier; Vendrell, Joan; Frühbeck, Gema

doi:10.1007/s11695-008-9453-7

Cited by 68 publications

(65 citation statements)

References 36 publications

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“…The decrease in AQP7 might reflect an overall decreased lipolytic capacity, thereby promoting the maintenance of lipid stores and a progressive adipocyte hypertrophy. 52,53 On the other hand, de novo synthesis of the FFA or lipogenesis produced in adipocytes further contributes to fat accumulation. SREBP1 (originally named ADD1, adipocyte determination and differentiation dependent factor 1) is a transcription factor that regulates the expression of lipogenic genes.…”

Section: Discussionmentioning

confidence: 99%

Acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes

et al. 2009

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Objectives: The orexigenic hormone ghrelin circulates mainly in two forms, acylated and desacyl ghrelin. We evaluated the impact of obesity and obesity-associated type 2 diabetes (T2D) on ghrelin forms and the potential role of acylated and desacyl ghrelin in the control of adipogenesis in humans. Methods: Plasma concentrations of the different ghrelin forms were measured in 80 subjects. The expression of the ghrelin receptor (growth hormone secretagogue receptor, GHS-R) was analyzed in omental adipose tissue using western blot and immunohistochemistry, and the effect of acylated ghrelin and desacyl ghrelin (0.1-1000 pmol l À1 ) on adipogenesis was determined in vitro in omental adipocytes. Results: Circulating concentrations of acylated ghrelin were increased, whereas desacyl ghrelin levels were decreased, in obesity and obesity-associated T2D. Body mass index, waist circumference, insulin and HOMA (homeostasis model assessment) index were positively correlated with acylated ghrelin levels. Obese individuals showed a lower protein expression of GHS-R in omental adipose tissue. In differentiating omental adipocytes, incubation with both acylated and desacyl ghrelin significantly increased PPARg (peroxisome proliferator-activated receptor g) and SREBP1 (sterol-regulatory element binding protein-1) mRNA levels, as well as several fat storage-related proteins, including acetyl-CoA carboxylase, fatty acid synthase, lipoprotein lipase and perilipin. Consequently, both the ghrelin forms stimulated intracytoplasmatic lipid accumulation. Conclusions: Both acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes. Given the lipogenic effect of acylated ghrelin on visceral adipocytes, the herein-reported elevation of its circulating concentrations in obese individuals may play a role in excessive fat accumulation in obesity.

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Section: Discussionmentioning

confidence: 99%

Acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes

et al. 2009

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“…Most of the studies evaluating the AQP7 mRNA expression in association with T2D did not find significant changes in the expression in SAT or VAT (Ceperuelo-Mallafre et al , Catalan et al 2008, Miranda et al 2009, Lebeck et al 2012a, but an increased AQP7 abundance in VAT (Miranda et al 2010, Rodriguez et al 2011 has also been reported. These studies were performed in mixed gender cohorts, except for two studies (Catalan et al 2008, Lebeck et al 2012a.…”

Section: Figurementioning

confidence: 99%

“…The relative expression of AQP9 in the liver has been investigated in obese individuals with T2D and obese with no impairment of their glucose tolerance. This has given variable results with some reporting a reduced expression of AQP9 in T2D (Catalan et al 2008, Rodriguez et al 2011 and others finding no significant changes (Miranda et al 2009). These findings contrast the increased expression of AQP9 found in male rodent models of diabetes , Carbrey et al 2003.…”

Section: Human Studies On Aqp9 Expressed In Livermentioning

confidence: 99%

Metabolic impact of the glycerol channels AQP7 and AQP9 in adipose tissue and liver

Lebeck

2014

Journal of Molecular Endocrinology

106

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Obesity and secondary development of type 2 diabetes (T2D) are major health care problems throughout the developed world. Accumulating evidence suggest that glycerol metabolism contributes to the pathophysiology of obesity and T2D. Glycerol is a small molecule that serves as an important intermediate between carbohydrate and lipid metabolism. It is stored primarily in adipose tissue as the backbone of triglyceride (TG) and during states of metabolic stress, such as fasting and diabetes, it is released for metabolism in other tissues. In the liver, glycerol serves as a gluconeogenic precursor and it is used for the esterification of free fatty acid into TGs. Aquaporin 7 (AQP7) in adipose tissue and AQP9 in the liver are transmembrane proteins that belong to the subset of AQPs called aquaglyceroporins. AQP7 facilitates the efflux of glycerol from adipose tissue and AQP7 deficiency has been linked to TG accumulation in adipose tissue and adult onset obesity. On the other hand, AQP9 expressed in liver facilitates the hepatic uptake of glycerol and thereby the availability of glycerol for de novo synthesis of glucose and TG that both are involved in the pathophysiology of diabetes. The aim of this review was to summarize the current knowledge on the role of the two glycerol channels in controlling glycerol metabolism in adipose tissue and liver. Glycerol metabolismThe metabolic switching between feeding and fasting is central to everyday life and involves tight hormonal control with effects on muscle, adipose tissue, and liver that maintains an adequate handling of metabolic precursors to support energy demands. One of the molecules affected by metabolic switching is glycerol, which is a small 3-carbon alcohol that in the fed state is stored as the backbone of triglyceride (TG) mainly in adipose tissue.In the fed state, after ingestion of dietary fats (w90% TG), !30% of TG is fully hydrolyzed into free fatty acids (FFA) and glycerol. Glycerol rapidly enters the enterocytes of the small intestine and thereafter the circulation through the portal vein and is primarily metabolized by the liver (Lin 1977). In adipose tissue, the activity of glycerol kinase (GlyK), that catalyzes the initial phosphorylation of glycerol into glycerol-3-phosphate (G3P), is negligible and therefore glycerol is not normally utilized in adipose tissue. Instead G3P used for the synthesis of TG in the fed state is derived from glycolysis.During states of increased energy demand, such as fasting and exercise, adipocyte lipolysis is increased by activation of adipose TG lipase and hormone-sensitive

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“…In humans, AQP7 expression levels were found to be significantly decreased in severely obese women compared with lean and nonseverely obese subjects [24]. However, other investigators have reported a different result, namely that AQP7 transcript levels tended to be increased in women with nonsevere obesity compared with lean women [25]. In terms of the PCOS, our present study showed that AQP7 expression, at both the mRNA and protein levels, is significantly higher in PCOS individuals (p < 0.05) compared to controls.…”

Section: Discussionmentioning

confidence: 99%

Aquaglyceroporin-7 Overexpression in Women with the Polycystic Ovary Syndrome

Seow¹,

Lin

Wang

et al. 2012

Gynecol Obstet Invest

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Background: Aquaglyceroporin-7 (AQP7) is an adipose glycerol channel protein that has been suggested to be involved in whole-body glucose homeostasis and insulin sensitivity. The aim of this study was to investigate the expression of AQP7 in visceral adipose tissues from women with the polycystic ovary syndrome (PCOS). Methods:AQP7 mRNA and protein levels were measured in omental adipose tissue from 5 women with the PCOS and 4 healthy controls matched for body mass index and age; this was done by the real-time polymerase chain reaction (PCR) and Western blotting. -Results: The women with the PCOS had significantly higher homeostasis model insulin resistance indices (HOMA_IR) and their quantitative insulin sensitivity check indices were significantly lower compared to the controls (p < 0.05). No significant difference was noted between the two groups for the plasma glycerol concentration. AQP7 mRNA expression and protein levels in omental adipose tissue from women with the PCOS were significantly higher than those of the controls (p = 0.007). AQP7 expression showed a positive correlation with fasting insulin levels, insulin levels at 2 h after glucose loading and HOMA_IR in women with the PCOS. Conclusion:AQP7 overexpression may be related to insulin sensitivity and glucose homeostasis in women with the PCOS.

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Influence of Morbid Obesity and Insulin Resistance on Gene Expression Levels of AQP7 in Visceral Adipose Tissue and AQP9 in Liver

Cited by 68 publications

References 36 publications

Acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes

Acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes

Metabolic impact of the glycerol channels AQP7 and AQP9 in adipose tissue and liver

Aquaglyceroporin-7 Overexpression in Women with the Polycystic Ovary Syndrome

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