![\"\"](\"https:\/\/meddists.com\/learn\/wp-content\/uploads\/2021\/11\/Lipid31.png\")
<\/a>Adiponectin<\/h2>\n<\/span>\n\n\nAdiponectin is known as an adipose tissue-specific protein (Figure 1). <\/p>\n\n\n\n
The most important biological actions of adiponectin are improved insulin sensitivity and fatty acid oxidation<\/strong>. <\/p>\n\n\n\nAdiponectin action is inhibited by adrenergic stimulation and glucocorticoids. <\/strong><\/p>\n\n\n\nExpression and release of adiponectin are triggered by insulin and suppressed by TNF-\u03b1<\/strong>.<\/p>\n\n\n\nUnlike leptin, amounts of adiponectin are lowered in obese and type 2 diabetic patients<\/strong> and elevated in patients with anorexia nervosa<\/strong>.<\/p>\n\n\n<\/span>\nResistin<\/h2>\n<\/span>\n\n\nThe name of resistin comes from the initial observation that the protein caused insulin resistance in mice. <\/em><\/p>\n\n\n\n![\"\"](\"https:\/\/meddists.com\/learn\/wp-content\/uploads\/2021\/11\/Lipid33-1024x764.png\")
<\/a>Figure 2. Resistin roles<\/strong><\/figcaption><\/figure><\/div>\n\n\n\nIn mice, the expression of resistin increases during adipocyte differentiation and amounts of resistin increase in diet-induced obesity.<\/p>\n\n\n\n
Local secretion of resistin from adipocytes\/macrophages can induce the release of endothelin-1, vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and monocyte chemoattractant proteins 1 (MCP-1) by vascular endothelial cells, affecting the endothelial function and vascular smooth muscle cell migration.<\/p>\n\n\n\n
A decrease in resistin levels is associated with increased AMPK activity within the liver, which results in the diminished expression of gluconeogenic enzymes and an accompanying reduction in hepatic glucose production.<\/p>\n\n\n\n
On the other hand, elevation in resistin<\/strong> levels is associated with elevated hepatic glucose synthesis<\/strong> and glucose intolerance<\/strong>. In other aspects, resistin increases the production of LDL in human liver cells and also decreases LDL receptors in the liver<\/strong>. As a result, the liver will be less capable to clean up the ‘bad’ cholesterol from the body. Resistin accelerates the accumulation of LDL in arteries<\/strong>, thus increasing the risk of heart disease.<\/p>\n\n\n<\/span>\nLeptin<\/h2>\n<\/span>\n\n\n![\"\"](\"https:\/\/meddists.com\/learn\/wp-content\/uploads\/2021\/11\/Lipid34-1024x567.png\")
<\/a>Figure 3. Leptin roles<\/strong><\/figcaption><\/figure><\/div>\n\n\n\nCells maintain an equilibrium of\u00a0transport of fatty acids into mitochondria and their subsequent oxidation and storage as triglycerides in the cytoplasm. This equilibrium is mainly controlled by\u00a0malonyl-CoA<\/strong> (Transport of Fatty Acids<\/a>).<\/p>\n\n\n\nLeptin brings about the phosphorylation of AMP-activated protein kinase (AMPK), which in turn phosphorylates ACC (Synthesis of Malonyl-CoA<\/a>), inactivating it.<\/p>\n\n\n\nLeptin,<\/strong>\u00a0therefore, suppresses malonyl-CoA<\/strong> synthesis, resulting in increased mitochondrial import<\/strong> and \u03b2-oxidation of fatty acids<\/strong>. <\/p>\n\n\n\n<\/p>\n\n\n\n
<\/p>\n\n\n\n
<\/p>\n\n\n<\/span>\nAppetite regulation<\/h2>\n<\/span>\n\n\nThe level of leptin is equal to the amount of adipose tissue<\/strong>. <\/p>\n\n\n\n
Adiponectin action is inhibited by adrenergic stimulation and glucocorticoids. <\/strong><\/p>\n\n\n\n Expression and release of adiponectin are triggered by insulin and suppressed by TNF-\u03b1<\/strong>.<\/p>\n\n\n\n Unlike leptin, amounts of adiponectin are lowered in obese and type 2 diabetic patients<\/strong> and elevated in patients with anorexia nervosa<\/strong>.<\/p>\n\n\n<\/span>\n The name of resistin comes from the initial observation that the protein caused insulin resistance in mice. <\/em><\/p>\n\n\n\n In mice, the expression of resistin increases during adipocyte differentiation and amounts of resistin increase in diet-induced obesity.<\/p>\n\n\n\n Local secretion of resistin from adipocytes\/macrophages can induce the release of endothelin-1, vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and monocyte chemoattractant proteins 1 (MCP-1) by vascular endothelial cells, affecting the endothelial function and vascular smooth muscle cell migration.<\/p>\n\n\n\n A decrease in resistin levels is associated with increased AMPK activity within the liver, which results in the diminished expression of gluconeogenic enzymes and an accompanying reduction in hepatic glucose production.<\/p>\n\n\n\n On the other hand, elevation in resistin<\/strong> levels is associated with elevated hepatic glucose synthesis<\/strong> and glucose intolerance<\/strong>. In other aspects, resistin increases the production of LDL in human liver cells and also decreases LDL receptors in the liver<\/strong>. As a result, the liver will be less capable to clean up the ‘bad’ cholesterol from the body. Resistin accelerates the accumulation of LDL in arteries<\/strong>, thus increasing the risk of heart disease.<\/p>\n\n\n<\/span>\n Cells maintain an equilibrium of\u00a0transport of fatty acids into mitochondria and their subsequent oxidation and storage as triglycerides in the cytoplasm. This equilibrium is mainly controlled by\u00a0malonyl-CoA<\/strong> (Transport of Fatty Acids<\/a>).<\/p>\n\n\n\n Leptin brings about the phosphorylation of AMP-activated protein kinase (AMPK), which in turn phosphorylates ACC (Synthesis of Malonyl-CoA<\/a>), inactivating it.<\/p>\n\n\n\n Leptin,<\/strong>\u00a0therefore, suppresses malonyl-CoA<\/strong> synthesis, resulting in increased mitochondrial import<\/strong> and \u03b2-oxidation of fatty acids<\/strong>. <\/p>\n\n\n\n <\/p>\n\n\n\n <\/p>\n\n\n\n <\/p>\n\n\n<\/span>\n The level of leptin is equal to the amount of adipose tissue<\/strong>. <\/p>\n\n\n\nResistin<\/h2>\n<\/span>\n\n\n
<\/a>Leptin<\/h2>\n<\/span>\n\n\n
<\/a>Appetite regulation<\/h2>\n<\/span>\n\n\n