Glycerolkinase Activity in White Adipose Tissue of Obese-hyperglycæmic Mice

Treble, D.H.; Mayer, Jean

doi:10.1038/200363a0

Cited by 118 publications

(11 citation statements)

References 5 publications

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“…In obese hyperglycemic animals, release of free fatty acids by adipose tissue, unlike such release in normal animals or in regulatory obesities, is independent of the nature of dietary fats and insensitive to the effect of epinephrine or of the fatmobilizing substance (FMS) isolated from human urine (45, 46). It may well be that the basic disorder in these animals is the presence of glycerokinase activity in the adipose tissue, a possibility suggesting that the absence of the repressor to the enzyme, normally present in this tissue, is the genetic abnormality primary to all others (glycerokinase activity is found in other tissues and, hence, is coded in the nucleic acid, but is normally repressed in adipose tissue) (52). Normally, in the absence of glycerokinase activity, adipose tissue cannot reutilize glycerol released by lipolysis and must depend upon glycerophosphate provided by glucose catabolism to resynthesize fat.…”

Section: However Comparisons Between Different Types Of Obesity In Mmentioning

confidence: 99%

Regulation of Food Intake and Obesity

Mayer

Thomas

1967

Science

Self Cite

296

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This is not the place to consider the medical significance of obesity in terms of conditions such as heart disease and hypertension, diabetes, and arthritis. These very complex interrelationships have been dealt with elsewhere (69). We hope that enough evidence has been presented to demonstrate that energy balance is normally maintained by a precise and reliable physiologic mechanism, and that the energy surplus represented by obesity may reflect direct failure of this mechanism or some combination from a variety of neurological, endocrine, enzymatic, and psychological disorders. Environmental conditions as well as genetic and traumatic factors may contribute to the development of obesity. If increasing mechanization brings tus below the level of energy expenditure at which food intake is properly regulated, appropriate habits of exercise will have to be established and maintained.

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Section: However Comparisons Between Different Types Of Obesity In Mmentioning

confidence: 99%

Regulation of Food Intake and Obesity

Mayer

Thomas

1967

Science

Self Cite

296

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“…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

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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.

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“…Thus in the present study of a type of experimental obesity different from those previously described, glycerol production, considered a better indicator of lipolysis [4,20] than FFA release, was determined in addition to measuring FFA changes. Recent reports, however, have appeared in the literature describing the presence of glycerol kinase in adipose tissue capable of activating free glycerol that can then be incorporated into lipids [15,18]. Adipose tissue of weanling rats, both VMN and control, was also found to be capable of incorporating glycerol-U-14C into tissue lipids [unpublished data].…”

Section: Discussionmentioning

confidence: 99%

Fat Mobilization in Adipose Tissue of Weanling Rats with Hypothalamic Obesity

Kasemsri¹,

Bernardis²,

Schnatz³

1972

Horm Res Paediatr

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In vitro lipolysis (glycerol release), hormone-sensitive lipolytic activity and free fatty acid (FFA) release as well as the response of these parameters to adrenaline, were studied inadipose tissue of obese weanling rats with electrolytic lesions in the hypothalamic ventromedial nuclei (VMN). In the absence of adrenaline, adipose tissue from weanling VMN rats showed neither depressed lipolysis nor diminished lipolytic activity per mg of tissue protein, and esterification appeared to be equal to lipolysis since there was no FFA release. Adrenaline augmented lipolysis and hormone-sensitive lipolytic activity to the same extent in VMN as in control tissue, but produced an overall release of FFA which was significantly less in VMN than control. The lesser FFA release in the VMN tissue compared to control may be a result of greater utilization of FFA, by oxidation or for esterification, by that tissue when stimulated by adrenaline.

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Glycerolkinase Activity in White Adipose Tissue of Obese-hyperglycæmic Mice

Cited by 118 publications

References 5 publications

Regulation of Food Intake and Obesity

Regulation of Food Intake and Obesity

Corepressors selectively control the transcriptional activity of PPARγ in adipocytes

Fat Mobilization in Adipose Tissue of Weanling Rats with Hypothalamic Obesity

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