Visceral adipokines, inflammation and insulin action in dysmetabolic states

PCOS is the commonest endocrine disorder amongst women associated with insulin resistance and adverse metabolic outcomes e.g. T2DM, dyslipidemia. TlDM, another metabolic disorder, on the other hand, results from auto immune destruction of insulin- producing pancreatic ~-cells, leading to hyperglycem...

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Main Author: Tan, Bee Kang
Published: University of East Anglia 2012
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Online Access:http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.577569
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spelling ndltd-bl.uk-oai-ethos.bl.uk-5775692015-03-20T04:55:29ZVisceral adipokines, inflammation and insulin action in dysmetabolic statesTan, Bee Kang2012PCOS is the commonest endocrine disorder amongst women associated with insulin resistance and adverse metabolic outcomes e.g. T2DM, dyslipidemia. TlDM, another metabolic disorder, on the other hand, results from auto immune destruction of insulin- producing pancreatic ~-cells, leading to hyperglycemia and its deleterious effects. The metabolic syndrome is associated with accumulation of visceral AT, which produces cytokines termed 'adipokines' implicated in the pathogenesis of diabetes and atherosclerosis. Circulating and AT omentin-l, an insulin sensitizing adipokine, were decreased in women with PCOS; metformin treatment (6 months) increased circulating omentin-l levels. Insulin and glucose decreased omentin-l production in AT; insulin also decreased circulating omentin-l in vivo. Furthermore, in vitro migration and angiogenesis were increased by serum from PCOS women compared to controls; these effects were attenuated by metformin treatment plausibly through the regulation of omentin-l levels via NF-KB (a pro-inflammatory nuclear transcription factor) and Akt pathways. CRP and VEGF induced in vitro migration and angiogenesis was decreased by omentin-l. In another study, there was a decrease in circulating omentin-l together with an increase in circulating adiponectin (fasting and postprandial), in TlDM subjects. Also, circulating and AT ASAA, a pro-inflammatory adipokine, which antagonizes insulin action, were increased in women with PCOS; metformin treatment (6 months) decreased circulating ASAA levels. Glucose increased ASAA production in AT. ASAA production by macrophages may account for these observations. Finally, circulating HMW and total adiponectin, an anti-inflammatory and insulin sensitizing adipokine, were higher in the morning and lower at night; corresponding NF-KB activities in serum treated endothelial cells were lower in the morning and higher at night. Hyperinsulinemic induction decreased HMW and total adiponectin levels but increased NF-N B activity in serum treated endothelial cells. These studies provide novel insights into the biology of adipokines, inflammation and insulin action pertinent to dysmetabolic states such as PCOS and diabetes.616.716University of East Angliahttp://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.577569Electronic Thesis or Dissertation
collection NDLTD
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topic 616.716
spellingShingle 616.716
Tan, Bee Kang
Visceral adipokines, inflammation and insulin action in dysmetabolic states
description PCOS is the commonest endocrine disorder amongst women associated with insulin resistance and adverse metabolic outcomes e.g. T2DM, dyslipidemia. TlDM, another metabolic disorder, on the other hand, results from auto immune destruction of insulin- producing pancreatic ~-cells, leading to hyperglycemia and its deleterious effects. The metabolic syndrome is associated with accumulation of visceral AT, which produces cytokines termed 'adipokines' implicated in the pathogenesis of diabetes and atherosclerosis. Circulating and AT omentin-l, an insulin sensitizing adipokine, were decreased in women with PCOS; metformin treatment (6 months) increased circulating omentin-l levels. Insulin and glucose decreased omentin-l production in AT; insulin also decreased circulating omentin-l in vivo. Furthermore, in vitro migration and angiogenesis were increased by serum from PCOS women compared to controls; these effects were attenuated by metformin treatment plausibly through the regulation of omentin-l levels via NF-KB (a pro-inflammatory nuclear transcription factor) and Akt pathways. CRP and VEGF induced in vitro migration and angiogenesis was decreased by omentin-l. In another study, there was a decrease in circulating omentin-l together with an increase in circulating adiponectin (fasting and postprandial), in TlDM subjects. Also, circulating and AT ASAA, a pro-inflammatory adipokine, which antagonizes insulin action, were increased in women with PCOS; metformin treatment (6 months) decreased circulating ASAA levels. Glucose increased ASAA production in AT. ASAA production by macrophages may account for these observations. Finally, circulating HMW and total adiponectin, an anti-inflammatory and insulin sensitizing adipokine, were higher in the morning and lower at night; corresponding NF-KB activities in serum treated endothelial cells were lower in the morning and higher at night. Hyperinsulinemic induction decreased HMW and total adiponectin levels but increased NF-N B activity in serum treated endothelial cells. These studies provide novel insights into the biology of adipokines, inflammation and insulin action pertinent to dysmetabolic states such as PCOS and diabetes.
author Tan, Bee Kang
author_facet Tan, Bee Kang
author_sort Tan, Bee Kang
title Visceral adipokines, inflammation and insulin action in dysmetabolic states
title_short Visceral adipokines, inflammation and insulin action in dysmetabolic states
title_full Visceral adipokines, inflammation and insulin action in dysmetabolic states
title_fullStr Visceral adipokines, inflammation and insulin action in dysmetabolic states
title_full_unstemmed Visceral adipokines, inflammation and insulin action in dysmetabolic states
title_sort visceral adipokines, inflammation and insulin action in dysmetabolic states
publisher University of East Anglia
publishDate 2012
url http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.577569
work_keys_str_mv AT tanbeekang visceraladipokinesinflammationandinsulinactionindysmetabolicstates
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