“…Adenosine, prostaglandin E2 (PGE2) and NPY are examples of molecules that inhibit lipolysis in this manner. Stimulation of the A1-adenosine receptor, NPY-Y1 receptor and EP3 receptor results in the inhibition of lipolysis while antagonists to these receptors enhance lipolysis suggesting that they may have a role in fine tuning the lipolytic response [104-106]. In addition, PGE2 has been implicated as an important regulator of lipolysis in vivo.…”
The trafficking of fatty acids into and out of adipocytes is regulated by a complex series of proteins and enzymes and is under control by a variety of hormonal and metabolic factors. The biochemical basis of fatty acid influx, despite its widespread appreciation, remains enigmatic with regard to the biophysical and biochemical properties that facilitate long chain fatty acid uptake. Fatty acid efflux is initiated by hormonally controlled lipolysis of the droplet stores and produces fatty acids that must transit from their site of production to the plasma membrane and subsequently out of the cells. This review will focus on the "in's and out's" of fatty acid trafficking and summarize the current concepts in the field.
“…Adenosine, prostaglandin E2 (PGE2) and NPY are examples of molecules that inhibit lipolysis in this manner. Stimulation of the A1-adenosine receptor, NPY-Y1 receptor and EP3 receptor results in the inhibition of lipolysis while antagonists to these receptors enhance lipolysis suggesting that they may have a role in fine tuning the lipolytic response [104-106]. In addition, PGE2 has been implicated as an important regulator of lipolysis in vivo.…”
The trafficking of fatty acids into and out of adipocytes is regulated by a complex series of proteins and enzymes and is under control by a variety of hormonal and metabolic factors. The biochemical basis of fatty acid influx, despite its widespread appreciation, remains enigmatic with regard to the biophysical and biochemical properties that facilitate long chain fatty acid uptake. Fatty acid efflux is initiated by hormonally controlled lipolysis of the droplet stores and produces fatty acids that must transit from their site of production to the plasma membrane and subsequently out of the cells. This review will focus on the "in's and out's" of fatty acid trafficking and summarize the current concepts in the field.
“…The reason for this is not clear, but it is thought to reflect the expanded body fat mass.83'84 At the level of the adipocyte the basal lipolysis is elevated both when expressed in relation to cell concentration and cell surface area. 85 The mechanisms behind the increased basal lipolysis in fat cells from obese are also unkown, but it might be due to an imbalance of adipose tissue in sensitivity to the dual effects of the sympathetic nervous system (which stimulates lipolysis through beta receptors and inhibits lipolysis through alpha-2 receptorss6). Studies of the antilipolytic actions of adenosine and prostaglandin E2 have revealed decreased sensitivity in adipocytes from the ~b e s e .~~, '~ These findings may offer a tentative explanation for the increase in lipolysis provided the fat tissue concentrations of these compounds in vivo are within the normal range.…”
Section: Free Fatty Acids: a Possible Biochemical Link Between Amentioning
“…Receptors for other antilipolytic compounds (R, and R, in Fig. 28.3), such as adenosine (745,750,508) and prostaglandin E (682,684), exert their effects by inactivating or antagonizing the activation of AC. Coupling of receptors for lipolytic and antilipolytic agents to AC is accomplished by the stimulatory and inhibitory heterotrimeric guanine nucleotidebinding proteins (G-proteins) abbreviated as Gs or Gi.…”
Section: Adipose Tissuementioning
confidence: 99%
“…No longer is it possible to assume that the medium bathing in vitro or cultured preparations contains only those chemicals that were added by the investigator. Endogenous antilipolytic factors such as adenosine (750) and prostaglandin E (559,(682)(683)(684) are released from adipocytes and modify responses to exogenous agonists. With this in mind, it may be possible to rationalize some of the conflicting findings mentioned above because species and even subtle experimental differences may affect the production, degradation, or response to autocrine and paracrine influences.…”
A Endocrinology 109: 990-992, 1981. 485. LeRoith, D., V. A. Blakesley, and H. Werner. Molecular mechanism of IGF-I receptor function: implications for normal physiology and pathological states.
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