Lipolysis and the integrated physiology of lipid energy metabolism

Wang, Shupei; Soni, Krishnakant G.; Semache, Meriem; Casavant, Stéphanie; Fortier, Mélanie; Pan, Linge; Mitchell, Grant A.

doi:10.1016/j.ymgme.2008.06.012

Cited by 145 publications

(114 citation statements)

References 120 publications

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“…Sulfonylureas stimulate insulin secretion, and DPP-4 inhibitors augment glucose-induced insulin secretion as well as inhibit glucagon release. Lipolysis is controlled by β-adrenergic stimulation and suppression by insulin, both of which affect the cytoplasmic cyclic AMP levels [28,29]. However, ketogenesis is subject to bihormonal control through the relative blood concentrations of insulin and glucagon [30].…”

Section: Acknowledgementsmentioning

confidence: 99%

Age-related changes in the diurnal variation of ketogenesis in patients with type 2 diabetes and relevance to hypoglycemic medications

et al. 2015

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Section: Acknowledgementsmentioning

confidence: 99%

Age-related changes in the diurnal variation of ketogenesis in patients with type 2 diabetes and relevance to hypoglycemic medications

et al. 2015

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“…21 It supplies FAs for energy during fasting and stress, and influences the level of FA storage in WAT as TG. The traditional view that a single lipase mediates all cytoplasmic TG degradation has been replaced by a more accurate but much more elaborate picture.…”

Section: Adipocyte Lipolysismentioning

confidence: 99%

“…31 HSL also functions in several extra-adipose sites. 21,32 The normal fasting lipolysis present in HSL deficiency 33 and even in mice in which all b-adrenergic receptors are absent, 34 illustrates the importance of HSL-and catecholamine-independent pathways of lipolysis.…”

Section: Hormone-sensitive Lipasementioning

confidence: 99%

“…21 Continual recycling occurs. In rats, 50% of FA cleaved from TGs reincorporate to TGs rather than exit the cell.…”

Section: Recyclingmentioning

confidence: 99%

“…Furthermore, each step of TG synthesis can be mediated by any of up to six isozymes. 21,71 The reason for this high redundancy is unclear, although it provides material for tissue specificity and refined, specific responses to given physiological conditions.…”

Section: Recyclingmentioning

confidence: 99%

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Genetics, physiology and perinatal influences in childhood obesity: view from the Chair

Mitchell

2009

Int J Obes

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The current epidemic of childhood obesity will be a serious threat to population health for at least the next several decades. The biology of childhood obesity was the theme of an international symposium held in November 2007. Speakers discussed monogenic causes of obesity, prenatal epigenetic programing, neurobehavioral aspects of obesity, and hormonal and neuroendocrine abnormalities, and the insights provided by non-murine models for understanding the biology of early-onset obesity. Several new developments have been reported in white and brown adipose tissue biology. They are summarized briefly in this review and include observations about cell lineage of adipocytes, the renewal of adipocytes throughout life and the numerous factors that influence adipocyte fatty acid release. The biological underpinnings of childhood obesity are multiple and complex.

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Deficiency of liver adipose triglyceride lipase in mice causes progressive hepatic steatosis

Wang

Álvarez³

et al. 2011

Hepatology

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Accumulation of cytoplasmic triacylglycerol (TG) underlies hepatic steatosis, a major cause of cirrhosis. The pathways of cytoplasmic TG metabolism are not well known in hepatocytes, but evidence suggests an important role in lipolysis for adipose triglyceride lipase (ATGL). We created mice with liver-specific inactivation of Pnpla2, the ATGL gene. These ATGLLKO mice had severe progressive periportal macrovesicular and pericentral microvesicular hepatic steatosis (73, 150, and 226 lmol TG/g liver at 4, 8, and 12 months, respectively). However, plasma levels of glucose, TG, and cholesterol were similar to those of controls. Fasting 3-hydroxybutyrate level was normal, but in thin sections of liver, beta oxidation of palmitate was decreased by one-third in ATGLLKO mice compared with controls. Tests of very low-density lipoprotein production, glucose, and insulin tolerance and gluconeogenesis from pyruvate were normal. Plasma alanine aminotransferase levels were elevated in ATGLLKO mice, but histological estimates of inflammation and fibrosis and messenger RNA (mRNA) levels of tumor necrosis factor-a and interleukin-6 were similar to or lower than those in controls. ATGLLKO cholangiocytes also showed cytoplasmic lipid droplets, demonstrating that ATGL is also a major lipase in cholangiocytes. There was a 50-fold reduction of hepatic diacylglycerol acyltransferase 2 mRNA level and a 2.7-fold increase of lipolysosomes in hepatocytes (P < 0.001), suggesting reduced TG synthesis and increased lysosomal degradation of TG as potential compensatory mechanisms. Conclusion: Compared with the hepatic steatosis of obesity and diabetes, steatosis in ATGL deficiency is well tolerated metabolically. ATGLLKO mice will be useful for studying the pathophysiology of hepatic steatosis. (HEPATOLOGY 2011;54:122-132)

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Lipolysis and the integrated physiology of lipid energy metabolism

Cited by 145 publications

References 120 publications

Age-related changes in the diurnal variation of ketogenesis in patients with type 2 diabetes and relevance to hypoglycemic medications

Age-related changes in the diurnal variation of ketogenesis in patients with type 2 diabetes and relevance to hypoglycemic medications

Genetics, physiology and perinatal influences in childhood obesity: view from the Chair

Deficiency of liver adipose triglyceride lipase in mice causes progressive hepatic steatosis

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