Loading…

obesity pandemic: Where have we been and where are we going?

Obesity, a new pandemic, is associated with an increased risk of death, morbidity, and accelerated aging. The multiple therapeutic modalities used to promote weight loss are outlined with caution, especially for patients who are very young or old. Except for very rare single gene defects, the inheri...

Full description

Saved in:
Bibliographic Details
Published in:Obesity (Silver Spring, Md.) Md.), 2004-11, Vol.12 (90002), p.88S-101S
Main Authors: Roth, J, Qiang, X, Marban, S.L, Redelt, H, Lowell, B.C
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c5435-4c6c3327cd132c63558acbe639b09f06af81b5d620b2c8c3ba3ec0ede9dcd88c3
cites cdi_FETCH-LOGICAL-c5435-4c6c3327cd132c63558acbe639b09f06af81b5d620b2c8c3ba3ec0ede9dcd88c3
container_end_page 101S
container_issue 90002
container_start_page 88S
container_title Obesity (Silver Spring, Md.)
container_volume 12
creator Roth, J
Qiang, X
Marban, S.L
Redelt, H
Lowell, B.C
description Obesity, a new pandemic, is associated with an increased risk of death, morbidity, and accelerated aging. The multiple therapeutic modalities used to promote weight loss are outlined with caution, especially for patients who are very young or old. Except for very rare single gene defects, the inheritance of obesity is complex and still poorly understood, despite active investigations. Recent advances that have shed light on the pathophysiology of obesity are the recognition that 1) excess fat is deposited in liver, muscle, and pancreatic islets; 2) fat tissue secretes a large number of active signaling molecules including leptin, adiponectin, and resistin, as well as free fatty acids; and 3) activated macrophages colonize the adipose tissue. Other candidates for key roles in the causes and consequences of obesity include 1) metabolic programming, where food acts as a developmental regulator; 2) the constellation of defects known as the “metabolic syndrome;” 3) cortisol overproduction in the adipose tissue; and especially, 4) insulin resistance. The possible etiologies of insulin resistance include cytokine excess, elevated free fatty acids, and hyperinsulinemia itself, as with transgenic overproduction of insulin in mice.
doi_str_mv 10.1038/oby.2004.273
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67184319</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>17803223</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5435-4c6c3327cd132c63558acbe639b09f06af81b5d620b2c8c3ba3ec0ede9dcd88c3</originalsourceid><addsrcrecordid>eNqF0N-L1DAQB_AgineevvmsBcEnu85kmjQVQfTwFxzcgx7iU0jS6V6P3XZNti7735u9Lgo-6FPC5DMz5CvEY4QFApmXo98vJEC1kDXdEaeoFJRGSXM336HGsiZJJ-JBSjcAqCuD98UJKg3YKH0qXo-eU7_dFxs3tLzuw6vi2zVHLq7dTy52XHjmochvxe627OJtdTn2w_LNQ3Gvc6vEj47nmbj68P7r-afy4vLj5_O3F2VQFamyCjoQyTq0SDJoUsq44FlT46HpQLvOoFetluBlMIG8Iw7ALTdtaE0unInn89xNHH9MnLZ23afAq5UbeJyS1TWairD5L8TaAElJGT77C96MUxzyJ2wOFWqjsdJZvZhViGNKkTu7if3axX1GB2dsDt8ewrc5_MyfHIdOfs3tH3xMOwOcwa5f8f6fw-zlu--IWuWeYu4Z3HaK_Lsp44Od9z6dSedG65axT_bqiwQkgMagAUO_AFStoOI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1030786146</pqid></control><display><type>article</type><title>obesity pandemic: Where have we been and where are we going?</title><source>Wiley</source><creator>Roth, J ; Qiang, X ; Marban, S.L ; Redelt, H ; Lowell, B.C</creator><creatorcontrib>Roth, J ; Qiang, X ; Marban, S.L ; Redelt, H ; Lowell, B.C</creatorcontrib><description>Obesity, a new pandemic, is associated with an increased risk of death, morbidity, and accelerated aging. The multiple therapeutic modalities used to promote weight loss are outlined with caution, especially for patients who are very young or old. Except for very rare single gene defects, the inheritance of obesity is complex and still poorly understood, despite active investigations. Recent advances that have shed light on the pathophysiology of obesity are the recognition that 1) excess fat is deposited in liver, muscle, and pancreatic islets; 2) fat tissue secretes a large number of active signaling molecules including leptin, adiponectin, and resistin, as well as free fatty acids; and 3) activated macrophages colonize the adipose tissue. Other candidates for key roles in the causes and consequences of obesity include 1) metabolic programming, where food acts as a developmental regulator; 2) the constellation of defects known as the “metabolic syndrome;” 3) cortisol overproduction in the adipose tissue; and especially, 4) insulin resistance. The possible etiologies of insulin resistance include cytokine excess, elevated free fatty acids, and hyperinsulinemia itself, as with transgenic overproduction of insulin in mice.</description><identifier>ISSN: 1071-7323</identifier><identifier>ISSN: 1930-7381</identifier><identifier>EISSN: 1550-8528</identifier><identifier>EISSN: 1930-739X</identifier><identifier>DOI: 10.1038/oby.2004.273</identifier><identifier>PMID: 15601956</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adipose Tissue - pathology ; Adipose Tissue - secretion ; adiposity ; Aging ; Body Composition ; Humans ; Hydrocortisone - biosynthesis ; Insulin Resistance ; Islets of Langerhans ; Liver ; Macrophages - pathology ; Metabolic Syndrome ; Muscles ; Obesity - epidemiology ; Obesity - genetics ; Obesity - physiopathology ; Obesity - therapy ; pandemic ; Signal Transduction ; Weight Loss</subject><ispartof>Obesity (Silver Spring, Md.), 2004-11, Vol.12 (90002), p.88S-101S</ispartof><rights>2004 North American Association for the Study of Obesity (NAASO)</rights><rights>Copyright Nature Publishing Group Nov 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5435-4c6c3327cd132c63558acbe639b09f06af81b5d620b2c8c3ba3ec0ede9dcd88c3</citedby><cites>FETCH-LOGICAL-c5435-4c6c3327cd132c63558acbe639b09f06af81b5d620b2c8c3ba3ec0ede9dcd88c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15601956$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Roth, J</creatorcontrib><creatorcontrib>Qiang, X</creatorcontrib><creatorcontrib>Marban, S.L</creatorcontrib><creatorcontrib>Redelt, H</creatorcontrib><creatorcontrib>Lowell, B.C</creatorcontrib><title>obesity pandemic: Where have we been and where are we going?</title><title>Obesity (Silver Spring, Md.)</title><addtitle>Obes Res</addtitle><description>Obesity, a new pandemic, is associated with an increased risk of death, morbidity, and accelerated aging. The multiple therapeutic modalities used to promote weight loss are outlined with caution, especially for patients who are very young or old. Except for very rare single gene defects, the inheritance of obesity is complex and still poorly understood, despite active investigations. Recent advances that have shed light on the pathophysiology of obesity are the recognition that 1) excess fat is deposited in liver, muscle, and pancreatic islets; 2) fat tissue secretes a large number of active signaling molecules including leptin, adiponectin, and resistin, as well as free fatty acids; and 3) activated macrophages colonize the adipose tissue. Other candidates for key roles in the causes and consequences of obesity include 1) metabolic programming, where food acts as a developmental regulator; 2) the constellation of defects known as the “metabolic syndrome;” 3) cortisol overproduction in the adipose tissue; and especially, 4) insulin resistance. The possible etiologies of insulin resistance include cytokine excess, elevated free fatty acids, and hyperinsulinemia itself, as with transgenic overproduction of insulin in mice.</description><subject>Adipose Tissue - pathology</subject><subject>Adipose Tissue - secretion</subject><subject>adiposity</subject><subject>Aging</subject><subject>Body Composition</subject><subject>Humans</subject><subject>Hydrocortisone - biosynthesis</subject><subject>Insulin Resistance</subject><subject>Islets of Langerhans</subject><subject>Liver</subject><subject>Macrophages - pathology</subject><subject>Metabolic Syndrome</subject><subject>Muscles</subject><subject>Obesity - epidemiology</subject><subject>Obesity - genetics</subject><subject>Obesity - physiopathology</subject><subject>Obesity - therapy</subject><subject>pandemic</subject><subject>Signal Transduction</subject><subject>Weight Loss</subject><issn>1071-7323</issn><issn>1930-7381</issn><issn>1550-8528</issn><issn>1930-739X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNqF0N-L1DAQB_AgineevvmsBcEnu85kmjQVQfTwFxzcgx7iU0jS6V6P3XZNti7735u9Lgo-6FPC5DMz5CvEY4QFApmXo98vJEC1kDXdEaeoFJRGSXM336HGsiZJJ-JBSjcAqCuD98UJKg3YKH0qXo-eU7_dFxs3tLzuw6vi2zVHLq7dTy52XHjmochvxe627OJtdTn2w_LNQ3Gvc6vEj47nmbj68P7r-afy4vLj5_O3F2VQFamyCjoQyTq0SDJoUsq44FlT46HpQLvOoFetluBlMIG8Iw7ALTdtaE0unInn89xNHH9MnLZ23afAq5UbeJyS1TWairD5L8TaAElJGT77C96MUxzyJ2wOFWqjsdJZvZhViGNKkTu7if3axX1GB2dsDt8ewrc5_MyfHIdOfs3tH3xMOwOcwa5f8f6fw-zlu--IWuWeYu4Z3HaK_Lsp44Od9z6dSedG65axT_bqiwQkgMagAUO_AFStoOI</recordid><startdate>200411</startdate><enddate>200411</enddate><creator>Roth, J</creator><creator>Qiang, X</creator><creator>Marban, S.L</creator><creator>Redelt, H</creator><creator>Lowell, B.C</creator><general>Blackwell Publishing Ltd</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200411</creationdate><title>obesity pandemic: Where have we been and where are we going?</title><author>Roth, J ; Qiang, X ; Marban, S.L ; Redelt, H ; Lowell, B.C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5435-4c6c3327cd132c63558acbe639b09f06af81b5d620b2c8c3ba3ec0ede9dcd88c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adipose Tissue - pathology</topic><topic>Adipose Tissue - secretion</topic><topic>adiposity</topic><topic>Aging</topic><topic>Body Composition</topic><topic>Humans</topic><topic>Hydrocortisone - biosynthesis</topic><topic>Insulin Resistance</topic><topic>Islets of Langerhans</topic><topic>Liver</topic><topic>Macrophages - pathology</topic><topic>Metabolic Syndrome</topic><topic>Muscles</topic><topic>Obesity - epidemiology</topic><topic>Obesity - genetics</topic><topic>Obesity - physiopathology</topic><topic>Obesity - therapy</topic><topic>pandemic</topic><topic>Signal Transduction</topic><topic>Weight Loss</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Roth, J</creatorcontrib><creatorcontrib>Qiang, X</creatorcontrib><creatorcontrib>Marban, S.L</creatorcontrib><creatorcontrib>Redelt, H</creatorcontrib><creatorcontrib>Lowell, B.C</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Obesity (Silver Spring, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Roth, J</au><au>Qiang, X</au><au>Marban, S.L</au><au>Redelt, H</au><au>Lowell, B.C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>obesity pandemic: Where have we been and where are we going?</atitle><jtitle>Obesity (Silver Spring, Md.)</jtitle><addtitle>Obes Res</addtitle><date>2004-11</date><risdate>2004</risdate><volume>12</volume><issue>90002</issue><spage>88S</spage><epage>101S</epage><pages>88S-101S</pages><issn>1071-7323</issn><issn>1930-7381</issn><eissn>1550-8528</eissn><eissn>1930-739X</eissn><abstract>Obesity, a new pandemic, is associated with an increased risk of death, morbidity, and accelerated aging. The multiple therapeutic modalities used to promote weight loss are outlined with caution, especially for patients who are very young or old. Except for very rare single gene defects, the inheritance of obesity is complex and still poorly understood, despite active investigations. Recent advances that have shed light on the pathophysiology of obesity are the recognition that 1) excess fat is deposited in liver, muscle, and pancreatic islets; 2) fat tissue secretes a large number of active signaling molecules including leptin, adiponectin, and resistin, as well as free fatty acids; and 3) activated macrophages colonize the adipose tissue. Other candidates for key roles in the causes and consequences of obesity include 1) metabolic programming, where food acts as a developmental regulator; 2) the constellation of defects known as the “metabolic syndrome;” 3) cortisol overproduction in the adipose tissue; and especially, 4) insulin resistance. The possible etiologies of insulin resistance include cytokine excess, elevated free fatty acids, and hyperinsulinemia itself, as with transgenic overproduction of insulin in mice.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>15601956</pmid><doi>10.1038/oby.2004.273</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1071-7323
ispartof Obesity (Silver Spring, Md.), 2004-11, Vol.12 (90002), p.88S-101S
issn 1071-7323
1930-7381
1550-8528
1930-739X
language eng
recordid cdi_proquest_miscellaneous_67184319
source Wiley
subjects Adipose Tissue - pathology
Adipose Tissue - secretion
adiposity
Aging
Body Composition
Humans
Hydrocortisone - biosynthesis
Insulin Resistance
Islets of Langerhans
Liver
Macrophages - pathology
Metabolic Syndrome
Muscles
Obesity - epidemiology
Obesity - genetics
Obesity - physiopathology
Obesity - therapy
pandemic
Signal Transduction
Weight Loss
title obesity pandemic: Where have we been and where are we going?
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T20%3A59%3A07IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=obesity%20pandemic:%20Where%20have%20we%20been%20and%20where%20are%20we%20going?&rft.jtitle=Obesity%20(Silver%20Spring,%20Md.)&rft.au=Roth,%20J&rft.date=2004-11&rft.volume=12&rft.issue=90002&rft.spage=88S&rft.epage=101S&rft.pages=88S-101S&rft.issn=1071-7323&rft.eissn=1550-8528&rft_id=info:doi/10.1038/oby.2004.273&rft_dat=%3Cproquest_cross%3E17803223%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c5435-4c6c3327cd132c63558acbe639b09f06af81b5d620b2c8c3ba3ec0ede9dcd88c3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1030786146&rft_id=info:pmid/15601956&rfr_iscdi=true