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The Subtle Balance between Lipolysis and Lipogenesis: A Critical Point in Metabolic Homeostasis.

Saponaro C, Gaggini M, Carli F, Gastaldelli A - Nutrients (2015)

Bottom Line: Excessive accumulation of lipids can lead to lipotoxicity, cell dysfunction and alteration in metabolic pathways, both in adipose tissue and peripheral organs, like liver, heart, pancreas and muscle.This is now a recognized risk factor for the development of metabolic disorders, such as obesity, diabetes, fatty liver disease (NAFLD), cardiovascular diseases (CVD) and hepatocellular carcinoma (HCC).The causes for lipotoxicity are not only a high fat diet but also excessive lipolysis, adipogenesis and adipose tissue insulin resistance.

View Article: PubMed Central - PubMed

Affiliation: Cardiometabolic Risk Unit, Institute of Clinical Physiology, CNR, via Moruzzi, 1 56124 Pisa, Italy. chiara.saponaro@gmail.com.

ABSTRACT
Excessive accumulation of lipids can lead to lipotoxicity, cell dysfunction and alteration in metabolic pathways, both in adipose tissue and peripheral organs, like liver, heart, pancreas and muscle. This is now a recognized risk factor for the development of metabolic disorders, such as obesity, diabetes, fatty liver disease (NAFLD), cardiovascular diseases (CVD) and hepatocellular carcinoma (HCC). The causes for lipotoxicity are not only a high fat diet but also excessive lipolysis, adipogenesis and adipose tissue insulin resistance. The aims of this review are to investigate the subtle balances that underlie lipolytic, lipogenic and oxidative pathways, to evaluate critical points and the complexities of these processes and to better understand which are the metabolic derangements resulting from their imbalance, such as type 2 diabetes and non alcoholic fatty liver disease.

No MeSH data available.


Related in: MedlinePlus

Imbalance in lipid metabolism causes increased efflux of FFA to adipose tissue. Reduced free fatty acids (FFA) utilization and β-oxidation and increased lipogenic and lipolytic pathways lead to overflow of FFA in the circulation. Adipose tissue activates adipogenesis and increases the number of adipocytes becoming hyperplastic or enlarges adipocyte size becoming hypertrophic. Hyperplastic adipose tissue is normally metabolically healthy while hypertrophic adipose tissue is characterized by dysfunctional adipocytes, insulin resistance, hypoxia and inflammation.
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nutrients-07-05475-f004: Imbalance in lipid metabolism causes increased efflux of FFA to adipose tissue. Reduced free fatty acids (FFA) utilization and β-oxidation and increased lipogenic and lipolytic pathways lead to overflow of FFA in the circulation. Adipose tissue activates adipogenesis and increases the number of adipocytes becoming hyperplastic or enlarges adipocyte size becoming hypertrophic. Hyperplastic adipose tissue is normally metabolically healthy while hypertrophic adipose tissue is characterized by dysfunctional adipocytes, insulin resistance, hypoxia and inflammation.

Mentions: During adipose tissue expansion adipocytes become either hyperplastic, when their number increases through adipogenesis, or hypertrophic, when their size increases via lipogenesis [77] (Figure 4). Adipocytes act both as energy storage and as endocrine organ, being able to produce and release hormones, such as leptin, that is involved in the regulation of appetite; adiponectin, implicated in fatty acid oxidation and insulin action; cytokines like IL6 and tumor necrosis factor-α (TNF-α) that are involved in the regulation of lipolysis and can activate the complement system and vascular homeostasis [78,79,80] (Figure 4). Adipocyte cell size correlates positively with secretion of proinflammatory adipocytokines, e.g., leptin, inteleukin 6 and 8 (IL-6, IL-8), and monocyte chemoattractant protein-1 (MCP-1), as shown by data from cultured adipocytes [81]. In humans, visceral adipocyte size correlates directly with leptin [45] and inversely with adiponectin [82]. Adipose tissue expansion is regulated by storage-related genes like DGAT2, SREBP1c and cell death activator (CIDEA). A hypercaloric diet upregulates lipogenic genes in the adipose tissue [71]. Interestingly it has been shown that when the regulation of these genes in subcutaneous tissue is defective, the subjects tend to accumulate more visceral and ectopic fat [83].


The Subtle Balance between Lipolysis and Lipogenesis: A Critical Point in Metabolic Homeostasis.

Saponaro C, Gaggini M, Carli F, Gastaldelli A - Nutrients (2015)

Imbalance in lipid metabolism causes increased efflux of FFA to adipose tissue. Reduced free fatty acids (FFA) utilization and β-oxidation and increased lipogenic and lipolytic pathways lead to overflow of FFA in the circulation. Adipose tissue activates adipogenesis and increases the number of adipocytes becoming hyperplastic or enlarges adipocyte size becoming hypertrophic. Hyperplastic adipose tissue is normally metabolically healthy while hypertrophic adipose tissue is characterized by dysfunctional adipocytes, insulin resistance, hypoxia and inflammation.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4663603&req=5

nutrients-07-05475-f004: Imbalance in lipid metabolism causes increased efflux of FFA to adipose tissue. Reduced free fatty acids (FFA) utilization and β-oxidation and increased lipogenic and lipolytic pathways lead to overflow of FFA in the circulation. Adipose tissue activates adipogenesis and increases the number of adipocytes becoming hyperplastic or enlarges adipocyte size becoming hypertrophic. Hyperplastic adipose tissue is normally metabolically healthy while hypertrophic adipose tissue is characterized by dysfunctional adipocytes, insulin resistance, hypoxia and inflammation.
Mentions: During adipose tissue expansion adipocytes become either hyperplastic, when their number increases through adipogenesis, or hypertrophic, when their size increases via lipogenesis [77] (Figure 4). Adipocytes act both as energy storage and as endocrine organ, being able to produce and release hormones, such as leptin, that is involved in the regulation of appetite; adiponectin, implicated in fatty acid oxidation and insulin action; cytokines like IL6 and tumor necrosis factor-α (TNF-α) that are involved in the regulation of lipolysis and can activate the complement system and vascular homeostasis [78,79,80] (Figure 4). Adipocyte cell size correlates positively with secretion of proinflammatory adipocytokines, e.g., leptin, inteleukin 6 and 8 (IL-6, IL-8), and monocyte chemoattractant protein-1 (MCP-1), as shown by data from cultured adipocytes [81]. In humans, visceral adipocyte size correlates directly with leptin [45] and inversely with adiponectin [82]. Adipose tissue expansion is regulated by storage-related genes like DGAT2, SREBP1c and cell death activator (CIDEA). A hypercaloric diet upregulates lipogenic genes in the adipose tissue [71]. Interestingly it has been shown that when the regulation of these genes in subcutaneous tissue is defective, the subjects tend to accumulate more visceral and ectopic fat [83].

Bottom Line: Excessive accumulation of lipids can lead to lipotoxicity, cell dysfunction and alteration in metabolic pathways, both in adipose tissue and peripheral organs, like liver, heart, pancreas and muscle.This is now a recognized risk factor for the development of metabolic disorders, such as obesity, diabetes, fatty liver disease (NAFLD), cardiovascular diseases (CVD) and hepatocellular carcinoma (HCC).The causes for lipotoxicity are not only a high fat diet but also excessive lipolysis, adipogenesis and adipose tissue insulin resistance.

View Article: PubMed Central - PubMed

Affiliation: Cardiometabolic Risk Unit, Institute of Clinical Physiology, CNR, via Moruzzi, 1 56124 Pisa, Italy. chiara.saponaro@gmail.com.

ABSTRACT
Excessive accumulation of lipids can lead to lipotoxicity, cell dysfunction and alteration in metabolic pathways, both in adipose tissue and peripheral organs, like liver, heart, pancreas and muscle. This is now a recognized risk factor for the development of metabolic disorders, such as obesity, diabetes, fatty liver disease (NAFLD), cardiovascular diseases (CVD) and hepatocellular carcinoma (HCC). The causes for lipotoxicity are not only a high fat diet but also excessive lipolysis, adipogenesis and adipose tissue insulin resistance. The aims of this review are to investigate the subtle balances that underlie lipolytic, lipogenic and oxidative pathways, to evaluate critical points and the complexities of these processes and to better understand which are the metabolic derangements resulting from their imbalance, such as type 2 diabetes and non alcoholic fatty liver disease.

No MeSH data available.


Related in: MedlinePlus