Glycerokinase in mammalian adipose tissue: stimulation by lipogenic substances

Persico, Paola; Cerchio, M; Jeffay, Henry

doi:10.1152/ajplegacy.1975.228.6.1868

Cited by 31 publications

(13 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Indeed, PEPCK-C expression is stimulated by ␤-agonists and in the fasting state (21), whereas GyK expression is not (7,22), arguing for GNG as the major physiological pathway involved in the control of FA output from human SCAT. This greater implication of GNG is in agreement with what Chen et al (23) recently observed in vivo in young mice fed a low carbohydrate diet in which GNG was by far the predominant pathway leading to G3P synthesis for TG accumulation in fat.…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone Controls Fatty Acid Cycling in Human Adipose Tissue by Means of Glyceroneogenesis and Glycerol Phosphorylation

Leroyer

Tordjman

Chauvet

et al. 2006

Journal of Biological Chemistry

View full text Add to dashboard Cite

Control of fatty acid homeostasis is crucial to prevent insulin resistance. During fasting, the plasma fatty acid level depends on triglyceride lipolysis and fatty acid re-esterification within fat cells. In rodents, Rosiglitazone controls fatty acid homeostasis by stimulating two pathways in the adipocytes, glyceroneogenesis and glycerol phosphorylation, that provide the glycerol 3-phosphate necessary for fatty acid re-esterification. Here, we analyzed the functionality of both pathways for controlling fatty acid release in subcutaneous adipose tissue samples from lean and overweight women before and after Rosiglitazone ex vivo treatment. In controls, pyruvate, used as a substrate of glyceroneogenesis, could contribute to the re-esterification of up to 65% of the fatty acids released after basal lipolysis, whereas glycerol phosphorylation accounted for only 14 ؎ 9%. However, the efficiency of glyceroneogenesis diminished as body mass index (BMI) of women increased. After Rosiglitazone treatment, increase of either pyruvate-or glyceroldependent fatty acid re-esterification was strictly correlated to that of phosphoenolpyruvate carboxykinase and glycerol kinase, the key enzymes of each pathway, but depended on BMI of the women. Whereas the Rosiglitazone responsiveness of glyceroneogenesis was rather constant according to the BMI of the women, glycerol phosphorylation was mostly enhanced in lean women (BMI < 27). Overall, these data indicate that, whereas glyceroneogenesis is more utilized than glycerol phosphorylation for fatty acid re-esterification in human subcutaneous adipose tissue in the physiological situation, both are solicited in response to Rosiglitazone but with lower efficiency when BMI is increased.

show abstract

Section: Discussionmentioning

confidence: 99%

Rosiglitazone Controls Fatty Acid Cycling in Human Adipose Tissue by Means of Glyceroneogenesis and Glycerol Phosphorylation

Leroyer

Tordjman

Chauvet

et al. 2006

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…In contrast to adipocyte-specific genes such as aP2, glycerol kinase (GyK) is normally expressed at low levels in white adipose tissue (Wieland and Suyter 1957;Treble and Mayer 1963;Persico et al 1975;Sargent et al 1994), but is markedly up-regulated by TZD treatment of adipocytes (Guan et al 2002;Tordjman et al 2003;Patsouris et al 2004). GyK catalyzes the phosphorylation of glycerol to produce glycerol-3-phosphate, the backbone for esterification of FFAs in the production of triglycerides (TGs).…”

mentioning

confidence: 99%

Corepressors selectively control the transcriptional activity of PPARγ in adipocytes

Guan¹,

Ishizuka²,

Chui³

et al. 2005

Genes Dev.

266

194

View full text Add to dashboard Cite

Peroxisome proliferator-activated receptor ␥ (PPAR␥) is the master regulator of adipogenesis as well as the target of thiazolidinedione (TZD) antidiabetic drugs. Many PPAR␥ target genes are induced during adipogenesis, but others, such as glycerol kinase (GyK), are expressed at low levels in adipocytes and dramatically up-regulated by TZDs. Here, we have explored the mechanism whereby an exogenous PPAR␥ ligand is selectively required for adipocyte gene expression. The GyK gene contains a functional PPAR␥-response element to which endogenous PPAR␥ is recruited in adipocytes. However, unlike the classic PPAR␥-target gene aP2, which is constitutively associated with coactivators, the GyK gene is targeted by nuclear receptor corepressors in adipocytes. TZDs trigger the dismissal of corepressor histone deacetylase (HDAC) complexes and the recruitment of coactivators to the GyK gene. TZDs also induce PPAR␥-Coactivator 1␣ (PGC-1␣), whose recruitment to the GyK gene is sufficient to release the corepressors. Thus, selective modulation of adipocyte PPAR␥ target genes by TZDs involves the dissociation of corepressors by direct and indirect mechanisms.

show abstract

“…Brown adipose tissue from the newborn rabbit [10] like white adipose tissue [20] from adult animals has low glycerol kinase activi ty. When glycerol kinase is absent the glyc erol released by hydrolysis of triglyceride is not metabolized in the cell, and passes into the bloodstream.…”

Section: Discussionmentioning

confidence: 99%

Metabolic and Hormonal Response to Endotoxin Fever in Fed and Starved One-Week Rabbits

Molnár¹,

Milner²

1983

Neonatology

View full text Add to dashboard Cite

The metabolic and hormonal effect of Escherichia coli endotoxin injected intraperitoneally was studied in fed and starved rabbits aged 6–9 days. Fed rabbits responded to endotoxin with fever, starved animals became hypothermic. Endotoxin caused a transient rise in blood glucose in both groups which was associated with a rise in plasma insulin concentration. Blood glycerol levels fell only in starved rabbits, and hydroxybutyrate concentration in both groups following endotoxin treatment. No change in blood pyruvate, lactate, alanine, or acetoacetate level was observed in either group.

show abstract

Glycerokinase in mammalian adipose tissue: stimulation by lipogenic substances

Cited by 31 publications

References 0 publications

Rosiglitazone Controls Fatty Acid Cycling in Human Adipose Tissue by Means of Glyceroneogenesis and Glycerol Phosphorylation

Rosiglitazone Controls Fatty Acid Cycling in Human Adipose Tissue by Means of Glyceroneogenesis and Glycerol Phosphorylation

Corepressors selectively control the transcriptional activity of PPARγ in adipocytes

Metabolic and Hormonal Response to Endotoxin Fever in Fed and Starved One-Week Rabbits

Contact Info

Product

Resources

About