Abstract
Since the incidence of the metabolic syndrome is on the rise in the western world, its coherence to cancer is becoming more apparent. In this review we discuss the different potential factors involved in the increase of cancer in the metabolic syndrome including obesity, dyslipidemia and Type 2 Diabetes Mellitus (T2DM) as well as inflammation and hypoxia. We especially focus on the insulin and IGF systems with their intracellular signaling cascades mediated by different receptor subtypes, and suggest that they may play major roles in this process. Understanding the mechanisms involved will be helpful in developing potential therapeutics.
Keywords:
cancer; metabolic syndrome.
MeSH terms
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Dyslipidemias / complications
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Dyslipidemias / metabolism
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Incidence
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Insulin / metabolism
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Insulin-Like Growth Factor Binding Proteins / metabolism
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Insulin-Like Growth Factor Binding Proteins / physiology
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Insulin-Like Growth Factor I / metabolism
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Insulin-Like Growth Factor I / physiology
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Metabolic Syndrome / complications*
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Metabolic Syndrome / metabolism
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Models, Biological
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Neoplasms / complications*
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Neoplasms / metabolism
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Obesity / complications
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Obesity / metabolism
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Receptor, Insulin / metabolism
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Receptor, Insulin / physiology
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Risk Factors
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Signal Transduction
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TOR Serine-Threonine Kinases / metabolism
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TOR Serine-Threonine Kinases / physiology
Substances
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Insulin
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Insulin-Like Growth Factor Binding Proteins
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Insulin-Like Growth Factor I
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MTOR protein, human
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Receptor, Insulin
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TOR Serine-Threonine Kinases