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Cycling our way to fit fat

View Article: PubMed Central - PubMed

ABSTRACT

Adipose tissue is increasingly being recognized as a key regulator of whole body carbohydrate and lipid metabolism. In conditions of obesity and insulin resistance mitochondrial content in this tissue is reduced, while treatment with insulin sensitizing drugs such as thiazolidinediones (TZDs) increase mitochondrial content. It has been known for decades that exercise increases mitochondrial content in skeletal muscle and now several laboratories have shown similar effects in adipose tissue. To date the specific mechanisms mediating this effect have not been fully identified. In this review we highlight recent work suggesting that increases in lipolysis and subsequently fatty acid re‐esterification trigger the activation of 5' AMP‐activated protein kinase (AMP) activated protein kinase and ultimately the induction of mitochondrial biogenesis. It is our current view that this pathway could be a unifying mechanism linking numerous systemic factors (catecholamines, interleukin‐6, meteorin‐like) to induction of mitochondrial biogenesis following exercise.

No MeSH data available.


Exercise stimulates secretion of catecholamines, interleukin‐6, and meteorin‐like (metrl). Catecholamines bind to β‐adrenergic receptors on the adipocyte to stimulate lipolysis through a PKA‐mediated pathway. IL‐6 stimulates lipolysis, though speculation remains regarding the precise mechanisms. Metrl indirectly drives lipolysis by modulating the secretion of catecholamines from adipose tissue macrophages. These factors activate lipolysis and consequently re‐esterification. This increases AMP‐activated protein kinase activity, the expression of PGC‐1ɑ and mitochondrial biogenesis. Figure clipart provided by Servier Medical Art (www.servier.com).
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phy213247-fig-0003: Exercise stimulates secretion of catecholamines, interleukin‐6, and meteorin‐like (metrl). Catecholamines bind to β‐adrenergic receptors on the adipocyte to stimulate lipolysis through a PKA‐mediated pathway. IL‐6 stimulates lipolysis, though speculation remains regarding the precise mechanisms. Metrl indirectly drives lipolysis by modulating the secretion of catecholamines from adipose tissue macrophages. These factors activate lipolysis and consequently re‐esterification. This increases AMP‐activated protein kinase activity, the expression of PGC‐1ɑ and mitochondrial biogenesis. Figure clipart provided by Servier Medical Art (www.servier.com).

Mentions: The obesity epidemic has ushered in a growing appreciation for AT as a central control point in the regulation of systemic carbohydrate and lipid metabolism. Unfortunately, as opposed to the mechanisms regulating skeletal muscle mitochondrial biogenesis, relatively little is known about AT. Here, we have proposed a potential mechanism whereby re‐esterification is activated in response to exercise, driving the activation of AMPK that enhances the expression of PGC‐1α, a chief regulator of mitochondrial biogenesis. This process is primarily activated by catecholamines but additional factors, such as the myokines IL‐6 and meteorin‐like, are emerging as important contributors (Fig. 3). More work into these ideas will ultimately provide a greater understanding of the pathologies to which AT directly contributes, including type 2 diabetes, and potentially lead to new therapeutic targets.


Cycling our way to fit fat
Exercise stimulates secretion of catecholamines, interleukin‐6, and meteorin‐like (metrl). Catecholamines bind to β‐adrenergic receptors on the adipocyte to stimulate lipolysis through a PKA‐mediated pathway. IL‐6 stimulates lipolysis, though speculation remains regarding the precise mechanisms. Metrl indirectly drives lipolysis by modulating the secretion of catecholamines from adipose tissue macrophages. These factors activate lipolysis and consequently re‐esterification. This increases AMP‐activated protein kinase activity, the expression of PGC‐1ɑ and mitochondrial biogenesis. Figure clipart provided by Servier Medical Art (www.servier.com).
© Copyright Policy - creativeCommonsBy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5392531&req=5

phy213247-fig-0003: Exercise stimulates secretion of catecholamines, interleukin‐6, and meteorin‐like (metrl). Catecholamines bind to β‐adrenergic receptors on the adipocyte to stimulate lipolysis through a PKA‐mediated pathway. IL‐6 stimulates lipolysis, though speculation remains regarding the precise mechanisms. Metrl indirectly drives lipolysis by modulating the secretion of catecholamines from adipose tissue macrophages. These factors activate lipolysis and consequently re‐esterification. This increases AMP‐activated protein kinase activity, the expression of PGC‐1ɑ and mitochondrial biogenesis. Figure clipart provided by Servier Medical Art (www.servier.com).
Mentions: The obesity epidemic has ushered in a growing appreciation for AT as a central control point in the regulation of systemic carbohydrate and lipid metabolism. Unfortunately, as opposed to the mechanisms regulating skeletal muscle mitochondrial biogenesis, relatively little is known about AT. Here, we have proposed a potential mechanism whereby re‐esterification is activated in response to exercise, driving the activation of AMPK that enhances the expression of PGC‐1α, a chief regulator of mitochondrial biogenesis. This process is primarily activated by catecholamines but additional factors, such as the myokines IL‐6 and meteorin‐like, are emerging as important contributors (Fig. 3). More work into these ideas will ultimately provide a greater understanding of the pathologies to which AT directly contributes, including type 2 diabetes, and potentially lead to new therapeutic targets.

View Article: PubMed Central - PubMed

ABSTRACT

Adipose tissue is increasingly being recognized as a key regulator of whole body carbohydrate and lipid metabolism. In conditions of obesity and insulin resistance mitochondrial content in this tissue is reduced, while treatment with insulin sensitizing drugs such as thiazolidinediones (TZDs) increase mitochondrial content. It has been known for decades that exercise increases mitochondrial content in skeletal muscle and now several laboratories have shown similar effects in adipose tissue. To date the specific mechanisms mediating this effect have not been fully identified. In this review we highlight recent work suggesting that increases in lipolysis and subsequently fatty acid re‐esterification trigger the activation of 5' AMP‐activated protein kinase (AMP) activated protein kinase and ultimately the induction of mitochondrial biogenesis. It is our current view that this pathway could be a unifying mechanism linking numerous systemic factors (catecholamines, interleukin‐6, meteorin‐like) to induction of mitochondrial biogenesis following exercise.

No MeSH data available.