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Isomer-specific mechanisms by which ...

Brown, J. Mark.

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Isomer-specific mechanisms by which conjugated linoleic acid opposes human adipogenesis.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Isomer-specific mechanisms by which conjugated linoleic acid opposes human adipogenesis./
作者:	Brown, J. Mark.
面頁冊數:	148 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1254.
Contained By:	Dissertation Abstracts International65-03B.
標題:	Health Sciences, Nutrition. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3126769
ISBN:	0496740474

Isomer-specific mechanisms by which conjugated linoleic acid opposes human adipogenesis.
Brown, J. Mark.

Isomer-specific mechanisms by which conjugated linoleic acid opposes human adipogenesis. - 148 p.

Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1254.

Thesis (Ph.D.)--The University of North Carolina at Greensboro, 2004.

Obesity has reached epidemic proportions in United States. This has prompted many health organizations to advocate low-fat diets that are low in animal products to help reduce the incidence of obesity. However, certain animal products contain isomers of CLA. Traditionally fatty acids have been thought to promote obesity, yet CLA has been shown to have potential antiobesity actions. This research addresses potential mechanisms by which a specific isomer of CLA reduces adipogenesis using a human cell culture model. The studies included in this body of work are significant because they provide novel insight into the mechanism(s) by which trans-10, cis-12 CLA reduces human adipocyte triglyceride (TG) content.

ISBN: 0496740474Subjects--Topical Terms:

1017801
Health Sciences, Nutrition.

Isomer-specific mechanisms by which conjugated linoleic acid opposes human adipogenesis.
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245 1 0 $a Isomer-specific mechanisms by which conjugated linoleic acid opposes human adipogenesis.
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500 $a Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1254.
500 $a Director: Michael K. McIntosh.
502 $a Thesis (Ph.D.)--The University of North Carolina at Greensboro, 2004.
520 $a Obesity has reached epidemic proportions in United States. This has prompted many health organizations to advocate low-fat diets that are low in animal products to help reduce the incidence of obesity. However, certain animal products contain isomers of CLA. Traditionally fatty acids have been thought to promote obesity, yet CLA has been shown to have potential antiobesity actions. This research addresses potential mechanisms by which a specific isomer of CLA reduces adipogenesis using a human cell culture model. The studies included in this body of work are significant because they provide novel insight into the mechanism(s) by which trans-10, cis-12 CLA reduces human adipocyte triglyceride (TG) content.
520 $a Conjugated linoleic acid (CLA) isomers, a group of positional and geometric isomers of the essential fatty acid linoleic acid [18:2(n-6)], have been extensively studied due to their ability to modulate cancer, atherosclerosis, obesity, immune function, and diabetes in a variety of experimental models. It has been clearly demonstrated that specific CLA isomers or a crude mixture of CLA isomers prevent the development of obesity in certain rodent and pig models. This has been attributed mainly to trans-10, cis-12 CLA, both in vivo and in vitro. However, CLA's ability to modulate human obesity remains controversial, because data from clinical trials using mixed isomers are conflicting. The purpose of these studies was to examine CLA's isomer-specific regulation of adiposity and insulin sensitivity in cultures of human adipocytes.
520 $a The data resulting from this body of work collectively support the previously demonstrated notion that CLA isomers can act as an antiadipogenic nutrient when fed to animals. Furthermore, my data provide the first insight into isomer-specific mechanisms by which CLA prevents human adipocyte differentiation and induces delipidation of mature human adipocytes through paracrine signaling networks. This is important because isomer-specific mechanistic insight into CLA's antiadipogenic actions has been elusive for over 15 years. The knowledge we have gained from the studies should provide an exciting platform for future studies examining the role of paracrine inflammatory signaling between the multiple cell types present in adipose tissue. The relatively new area of paracrine signaling in adipose tissue will no doubt be an exciting potential avenue for future anti-obesity therapeutics.
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