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. 2011:2011:490650.
doi: 10.1155/2011/490650. Epub 2011 Feb 15.

Different adipose depots: their role in the development of metabolic syndrome and mitochondrial response to hypolipidemic agents

Bodil Bjørndal  1 , Lena Burri, Vidar Staalesen, Jon Skorve, Rolf K Berge
Affiliations

Different adipose depots: their role in the development of metabolic syndrome and mitochondrial response to hypolipidemic agents

Bodil Bjørndal et al. J Obes. 2011.

Abstract

Adipose tissue metabolism is closely linked to insulin resistance, and differential fat distributions are associated with disorders like hypertension, diabetes, and cardiovascular disease. Adipose tissues vary in their impact on metabolic risk due to diverse gene expression profiles, leading to differences in lipolysis and in the production and release of adipokines and cytokines, thereby affecting the function of other tissues. In this paper, the roles of the various adipose tissues in obesity are summarized, with particular focus on mitochondrial function. In addition, we discuss how a functionally mitochondrial-targeted compound, the modified fatty acid tetradecylthioacetic acid (TTA), can influence mitochondrial function and decrease the size of specific fat depots.

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Figures

Figure 1
Figure 1
(A) The main white adipose tissues (WATs) are abdominal subcutaneous adipose tissue (SAT, (a)), and visceral adipose tissue (VAT). VAT surrounds the inner organs and can be divided in omental (b), mesenteric (c), retroperitoneal ((d): surrounding the kidney), gonadal ((e): attached to the uterus and ovaries in females and epididymis and testis in men), and pericardial (f). The omental depot stars near the stomach and spleen and can expand into the ventral abdomen, while the deeper mesenteric depot is attached in a web-form to the intestine. The gluteofemoral adipose tissue (g) is the SAT located to the lower-body parts and is measured by hip, thigh, and leg circumference. WAT can also be found intramuscularly (h). Brown adipose tissue is found above the clavicle ((i): supraclavicular) and in the subscapular region (j). Although the mentioned subcutaneous and visceral adipose tissues are found in humans, depots (d) and (e) are mostly studied in rodents. (B) The adipose tissue depots that have been linked to risk of developing obesity-related diseases are indicated in red. The best-documented link to risk is found for the omental and mesenteric VAT.
Figure 2
Figure 2
(A) The role of white adipose tissue (WAT) is to store excess dietary fat in the form of triglycerides (TGs) and to release free fatty acids (FFAs) in times of starvation or energy demand. In addition WAT releases several important factors that regulate energy homeostasis. Lipolysis takes place in the cytosol and is also dependent on processes in the mitochondria. The resulting FFA can be released to the blood or directly used as an energy source by β-oxidation in the mitochondria. In lipogenesis, glycerol and acyl-CoA produced in the mitochondria are used to generate TG for storage in the adipocytes. (B) In brown adipose tissue (BAT) the FFAs are β-oxidized, and the resulting acetyl-CoA enters the Krebs cycle. The reduction potential is used to form a mitochondrial proton gradient that instead of producing ATP is released by uncoupling protein 1 (UCP1), a process that generates heat.
Figure 3
Figure 3
(A) During obesity, the adipocytes will have reduced lipid storage capacity, leading to increased lipolysis and release of free fatty acids (FFAs), inflammatory agents, and disturbed adipokine release. The FFAs will be repackaged to triglycerides (TGs) in the liver where they are released as very low-density lipoprotein particles (VLDL). Together this has secondary effects on organs such as skeletal muscle and pancreas, as well as liver, and can result in hyperlipidemia, tissue lipid deposition, mitochondrial malfunction, insulin resistance, increased insulin production, and pancreatic β-cell disruption. (B) The effect of tetradecylthioacetic acid-(TTA-) treatment on metabolic syndrome. In the liver, TTA treatment will increase the degradation of FFA, by the induction of both mitochondrial and peroxisomal genes involved in β-oxidation. The excess FFA released from adipose tissue during metabolic syndrome (hyperlipidemia) is drained from the blood, thereby reducing TG, cholesterol, and FFA levels. In addition the TTA-induced increase in uncoupling protein 3 (UCP3) could increase energy expenditure, as well as function as a protection from the excess ROS production observed with obesity and high levels of FA degradation. The effect of TTA on liver is probably due to PPARα-mediated mechanisms, while the effect on adipose tissue may arrive from PPARγ as well as PPARα activation. In adipose tissue, the main effect of TTA is an increase in the brown adipose tissue marker Ucp1 in visceral adipose tissue (VAT) indicating higher energy expenditure and heat production. The higher metabolic activity of VAT compared to SAT will cause it to be the major source of FFA during increased hepatic β-oxidation. Together, this may explain the specific reduction of these risk-linked adipose depots with TTA-treatment.
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