Type 2 diabetes as a disease of ectopic fat?

Background Although obesity and diabetes commonly co-exist, the evidence base to support obesity as the major driver of type 2 diabetes mellitus (T2DM), and the mechanisms by which this occurs, are now better appreciated. Discussion This review briefly examines several sources of evidence - epidemio...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Sattar, Naveed [verfasserIn] Gill, Jason MR

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Insulin resistance NAFLD Pancreas Adiposity Sex Ethnicity Family history of diabetes

Anmerkung:	© Sattar and Gill; licensee BioMed Central Ltd. 2014

Übergeordnetes Werk:	Enthalten in: BMC medicine - London : BioMed Central, 2003, 12(2014), 1 vom: 26. Aug.
Übergeordnetes Werk:	volume:12 ; year:2014 ; number:1 ; day:26 ; month:08

Links:	Volltext

DOI / URN:	10.1186/s12916-014-0123-4

Katalog-ID:	SPR028351983

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520			\|a Background Although obesity and diabetes commonly co-exist, the evidence base to support obesity as the major driver of type 2 diabetes mellitus (T2DM), and the mechanisms by which this occurs, are now better appreciated. Discussion This review briefly examines several sources of evidence - epidemiological, genetic, molecular, and clinical trial - to support obesity being a causal risk factor for T2DM. It also summarises the ectopic fat hypothesis for this condition, and lists several pieces of evidence to support this concept, extending from rare conditions and drug effects to sex- and ethnicity-related differences in T2DM prevalence. Ectopic liver fat is the best-studied example of ectopic fat, but more research on pancreatic fat as a potential cause of β-cell dysfunction seems warranted. This ectopic fat concept, in turn, broadly fits with the observation that individuals of similar ages can develop diabetes at markedly different body mass indexes (BMIs). Those with risk factors leading to more rapid ectopic fat gain - for example, men (compared with women), certain ethnicities, and potentially those with a family history of diabetes, as well as others with genes linked to a reduced subcutaneous adiposity - are more likely to develop diabetes at a younger age and/or lower BMI than those without. Summary Obesity is the major risk factor for T2DM and appears to drive tissue insulin resistance in part via gain of ectopic fat, with the best-studied organ being the liver. However, ectopic fat in the pancreas may contribute to β-cell dysfunction. In line with this observation, rapid resolution of diabetes linked to a preferential and rapid reduction in liver fat has been noted with significant caloric reduction. Whether these observations can help develop better cost-effective and sustainable lifestyle /medical interventions in patients with T2DM requires further study.
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allfields	10.1186/s12916-014-0123-4 doi (DE-627)SPR028351983 (SPR)s12916-014-0123-4-e DE-627 ger DE-627 rakwb eng Sattar, Naveed verfasserin aut Type 2 diabetes as a disease of ectopic fat? 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sattar and Gill; licensee BioMed Central Ltd. 2014 Background Although obesity and diabetes commonly co-exist, the evidence base to support obesity as the major driver of type 2 diabetes mellitus (T2DM), and the mechanisms by which this occurs, are now better appreciated. Discussion This review briefly examines several sources of evidence - epidemiological, genetic, molecular, and clinical trial - to support obesity being a causal risk factor for T2DM. It also summarises the ectopic fat hypothesis for this condition, and lists several pieces of evidence to support this concept, extending from rare conditions and drug effects to sex- and ethnicity-related differences in T2DM prevalence. Ectopic liver fat is the best-studied example of ectopic fat, but more research on pancreatic fat as a potential cause of β-cell dysfunction seems warranted. This ectopic fat concept, in turn, broadly fits with the observation that individuals of similar ages can develop diabetes at markedly different body mass indexes (BMIs). Those with risk factors leading to more rapid ectopic fat gain - for example, men (compared with women), certain ethnicities, and potentially those with a family history of diabetes, as well as others with genes linked to a reduced subcutaneous adiposity - are more likely to develop diabetes at a younger age and/or lower BMI than those without. Summary Obesity is the major risk factor for T2DM and appears to drive tissue insulin resistance in part via gain of ectopic fat, with the best-studied organ being the liver. However, ectopic fat in the pancreas may contribute to β-cell dysfunction. In line with this observation, rapid resolution of diabetes linked to a preferential and rapid reduction in liver fat has been noted with significant caloric reduction. Whether these observations can help develop better cost-effective and sustainable lifestyle /medical interventions in patients with T2DM requires further study. Insulin resistance (dpeaa)DE-He213 NAFLD (dpeaa)DE-He213 Pancreas (dpeaa)DE-He213 Adiposity (dpeaa)DE-He213 Sex (dpeaa)DE-He213 Ethnicity (dpeaa)DE-He213 Family history of diabetes (dpeaa)DE-He213 Gill, Jason MR aut Enthalten in BMC medicine London : BioMed Central, 2003 12(2014), 1 vom: 26. Aug. (DE-627)377271225 (DE-600)2131669-7 1741-7015 nnns volume:12 year:2014 number:1 day:26 month:08 https://dx.doi.org/10.1186/s12916-014-0123-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2014 1 26 08
spelling	10.1186/s12916-014-0123-4 doi (DE-627)SPR028351983 (SPR)s12916-014-0123-4-e DE-627 ger DE-627 rakwb eng Sattar, Naveed verfasserin aut Type 2 diabetes as a disease of ectopic fat? 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sattar and Gill; licensee BioMed Central Ltd. 2014 Background Although obesity and diabetes commonly co-exist, the evidence base to support obesity as the major driver of type 2 diabetes mellitus (T2DM), and the mechanisms by which this occurs, are now better appreciated. Discussion This review briefly examines several sources of evidence - epidemiological, genetic, molecular, and clinical trial - to support obesity being a causal risk factor for T2DM. It also summarises the ectopic fat hypothesis for this condition, and lists several pieces of evidence to support this concept, extending from rare conditions and drug effects to sex- and ethnicity-related differences in T2DM prevalence. Ectopic liver fat is the best-studied example of ectopic fat, but more research on pancreatic fat as a potential cause of β-cell dysfunction seems warranted. This ectopic fat concept, in turn, broadly fits with the observation that individuals of similar ages can develop diabetes at markedly different body mass indexes (BMIs). Those with risk factors leading to more rapid ectopic fat gain - for example, men (compared with women), certain ethnicities, and potentially those with a family history of diabetes, as well as others with genes linked to a reduced subcutaneous adiposity - are more likely to develop diabetes at a younger age and/or lower BMI than those without. Summary Obesity is the major risk factor for T2DM and appears to drive tissue insulin resistance in part via gain of ectopic fat, with the best-studied organ being the liver. However, ectopic fat in the pancreas may contribute to β-cell dysfunction. In line with this observation, rapid resolution of diabetes linked to a preferential and rapid reduction in liver fat has been noted with significant caloric reduction. Whether these observations can help develop better cost-effective and sustainable lifestyle /medical interventions in patients with T2DM requires further study. Insulin resistance (dpeaa)DE-He213 NAFLD (dpeaa)DE-He213 Pancreas (dpeaa)DE-He213 Adiposity (dpeaa)DE-He213 Sex (dpeaa)DE-He213 Ethnicity (dpeaa)DE-He213 Family history of diabetes (dpeaa)DE-He213 Gill, Jason MR aut Enthalten in BMC medicine London : BioMed Central, 2003 12(2014), 1 vom: 26. Aug. (DE-627)377271225 (DE-600)2131669-7 1741-7015 nnns volume:12 year:2014 number:1 day:26 month:08 https://dx.doi.org/10.1186/s12916-014-0123-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2014 1 26 08
allfields_unstemmed	10.1186/s12916-014-0123-4 doi (DE-627)SPR028351983 (SPR)s12916-014-0123-4-e DE-627 ger DE-627 rakwb eng Sattar, Naveed verfasserin aut Type 2 diabetes as a disease of ectopic fat? 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sattar and Gill; licensee BioMed Central Ltd. 2014 Background Although obesity and diabetes commonly co-exist, the evidence base to support obesity as the major driver of type 2 diabetes mellitus (T2DM), and the mechanisms by which this occurs, are now better appreciated. Discussion This review briefly examines several sources of evidence - epidemiological, genetic, molecular, and clinical trial - to support obesity being a causal risk factor for T2DM. It also summarises the ectopic fat hypothesis for this condition, and lists several pieces of evidence to support this concept, extending from rare conditions and drug effects to sex- and ethnicity-related differences in T2DM prevalence. Ectopic liver fat is the best-studied example of ectopic fat, but more research on pancreatic fat as a potential cause of β-cell dysfunction seems warranted. This ectopic fat concept, in turn, broadly fits with the observation that individuals of similar ages can develop diabetes at markedly different body mass indexes (BMIs). Those with risk factors leading to more rapid ectopic fat gain - for example, men (compared with women), certain ethnicities, and potentially those with a family history of diabetes, as well as others with genes linked to a reduced subcutaneous adiposity - are more likely to develop diabetes at a younger age and/or lower BMI than those without. Summary Obesity is the major risk factor for T2DM and appears to drive tissue insulin resistance in part via gain of ectopic fat, with the best-studied organ being the liver. However, ectopic fat in the pancreas may contribute to β-cell dysfunction. In line with this observation, rapid resolution of diabetes linked to a preferential and rapid reduction in liver fat has been noted with significant caloric reduction. Whether these observations can help develop better cost-effective and sustainable lifestyle /medical interventions in patients with T2DM requires further study. Insulin resistance (dpeaa)DE-He213 NAFLD (dpeaa)DE-He213 Pancreas (dpeaa)DE-He213 Adiposity (dpeaa)DE-He213 Sex (dpeaa)DE-He213 Ethnicity (dpeaa)DE-He213 Family history of diabetes (dpeaa)DE-He213 Gill, Jason MR aut Enthalten in BMC medicine London : BioMed Central, 2003 12(2014), 1 vom: 26. Aug. (DE-627)377271225 (DE-600)2131669-7 1741-7015 nnns volume:12 year:2014 number:1 day:26 month:08 https://dx.doi.org/10.1186/s12916-014-0123-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2014 1 26 08
allfieldsGer	10.1186/s12916-014-0123-4 doi (DE-627)SPR028351983 (SPR)s12916-014-0123-4-e DE-627 ger DE-627 rakwb eng Sattar, Naveed verfasserin aut Type 2 diabetes as a disease of ectopic fat? 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sattar and Gill; licensee BioMed Central Ltd. 2014 Background Although obesity and diabetes commonly co-exist, the evidence base to support obesity as the major driver of type 2 diabetes mellitus (T2DM), and the mechanisms by which this occurs, are now better appreciated. Discussion This review briefly examines several sources of evidence - epidemiological, genetic, molecular, and clinical trial - to support obesity being a causal risk factor for T2DM. It also summarises the ectopic fat hypothesis for this condition, and lists several pieces of evidence to support this concept, extending from rare conditions and drug effects to sex- and ethnicity-related differences in T2DM prevalence. Ectopic liver fat is the best-studied example of ectopic fat, but more research on pancreatic fat as a potential cause of β-cell dysfunction seems warranted. This ectopic fat concept, in turn, broadly fits with the observation that individuals of similar ages can develop diabetes at markedly different body mass indexes (BMIs). Those with risk factors leading to more rapid ectopic fat gain - for example, men (compared with women), certain ethnicities, and potentially those with a family history of diabetes, as well as others with genes linked to a reduced subcutaneous adiposity - are more likely to develop diabetes at a younger age and/or lower BMI than those without. Summary Obesity is the major risk factor for T2DM and appears to drive tissue insulin resistance in part via gain of ectopic fat, with the best-studied organ being the liver. However, ectopic fat in the pancreas may contribute to β-cell dysfunction. In line with this observation, rapid resolution of diabetes linked to a preferential and rapid reduction in liver fat has been noted with significant caloric reduction. Whether these observations can help develop better cost-effective and sustainable lifestyle /medical interventions in patients with T2DM requires further study. Insulin resistance (dpeaa)DE-He213 NAFLD (dpeaa)DE-He213 Pancreas (dpeaa)DE-He213 Adiposity (dpeaa)DE-He213 Sex (dpeaa)DE-He213 Ethnicity (dpeaa)DE-He213 Family history of diabetes (dpeaa)DE-He213 Gill, Jason MR aut Enthalten in BMC medicine London : BioMed Central, 2003 12(2014), 1 vom: 26. Aug. (DE-627)377271225 (DE-600)2131669-7 1741-7015 nnns volume:12 year:2014 number:1 day:26 month:08 https://dx.doi.org/10.1186/s12916-014-0123-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2014 1 26 08
allfieldsSound	10.1186/s12916-014-0123-4 doi (DE-627)SPR028351983 (SPR)s12916-014-0123-4-e DE-627 ger DE-627 rakwb eng Sattar, Naveed verfasserin aut Type 2 diabetes as a disease of ectopic fat? 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sattar and Gill; licensee BioMed Central Ltd. 2014 Background Although obesity and diabetes commonly co-exist, the evidence base to support obesity as the major driver of type 2 diabetes mellitus (T2DM), and the mechanisms by which this occurs, are now better appreciated. Discussion This review briefly examines several sources of evidence - epidemiological, genetic, molecular, and clinical trial - to support obesity being a causal risk factor for T2DM. It also summarises the ectopic fat hypothesis for this condition, and lists several pieces of evidence to support this concept, extending from rare conditions and drug effects to sex- and ethnicity-related differences in T2DM prevalence. Ectopic liver fat is the best-studied example of ectopic fat, but more research on pancreatic fat as a potential cause of β-cell dysfunction seems warranted. This ectopic fat concept, in turn, broadly fits with the observation that individuals of similar ages can develop diabetes at markedly different body mass indexes (BMIs). Those with risk factors leading to more rapid ectopic fat gain - for example, men (compared with women), certain ethnicities, and potentially those with a family history of diabetes, as well as others with genes linked to a reduced subcutaneous adiposity - are more likely to develop diabetes at a younger age and/or lower BMI than those without. Summary Obesity is the major risk factor for T2DM and appears to drive tissue insulin resistance in part via gain of ectopic fat, with the best-studied organ being the liver. However, ectopic fat in the pancreas may contribute to β-cell dysfunction. In line with this observation, rapid resolution of diabetes linked to a preferential and rapid reduction in liver fat has been noted with significant caloric reduction. Whether these observations can help develop better cost-effective and sustainable lifestyle /medical interventions in patients with T2DM requires further study. Insulin resistance (dpeaa)DE-He213 NAFLD (dpeaa)DE-He213 Pancreas (dpeaa)DE-He213 Adiposity (dpeaa)DE-He213 Sex (dpeaa)DE-He213 Ethnicity (dpeaa)DE-He213 Family history of diabetes (dpeaa)DE-He213 Gill, Jason MR aut Enthalten in BMC medicine London : BioMed Central, 2003 12(2014), 1 vom: 26. Aug. (DE-627)377271225 (DE-600)2131669-7 1741-7015 nnns volume:12 year:2014 number:1 day:26 month:08 https://dx.doi.org/10.1186/s12916-014-0123-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2014 1 26 08
language	English
source	Enthalten in BMC medicine 12(2014), 1 vom: 26. Aug. volume:12 year:2014 number:1 day:26 month:08
sourceStr	Enthalten in BMC medicine 12(2014), 1 vom: 26. Aug. volume:12 year:2014 number:1 day:26 month:08
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Insulin resistance NAFLD Pancreas Adiposity Sex Ethnicity Family history of diabetes
isfreeaccess_bool	true
container_title	BMC medicine
authorswithroles_txt_mv	Sattar, Naveed @@aut@@ Gill, Jason MR @@aut@@
publishDateDaySort_date	2014-08-26T00:00:00Z
hierarchy_top_id	377271225
id	SPR028351983
language_de	englisch
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spellingShingle	Sattar, Naveed misc Insulin resistance misc NAFLD misc Pancreas misc Adiposity misc Sex misc Ethnicity misc Family history of diabetes Type 2 diabetes as a disease of ectopic fat?
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topic_title	Type 2 diabetes as a disease of ectopic fat? Insulin resistance (dpeaa)DE-He213 NAFLD (dpeaa)DE-He213 Pancreas (dpeaa)DE-He213 Adiposity (dpeaa)DE-He213 Sex (dpeaa)DE-He213 Ethnicity (dpeaa)DE-He213 Family history of diabetes (dpeaa)DE-He213
topic	misc Insulin resistance misc NAFLD misc Pancreas misc Adiposity misc Sex misc Ethnicity misc Family history of diabetes
topic_unstemmed	misc Insulin resistance misc NAFLD misc Pancreas misc Adiposity misc Sex misc Ethnicity misc Family history of diabetes
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title	Type 2 diabetes as a disease of ectopic fat?
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title_full	Type 2 diabetes as a disease of ectopic fat?
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title_sort	type 2 diabetes as a disease of ectopic fat?
title_auth	Type 2 diabetes as a disease of ectopic fat?
abstract	Background Although obesity and diabetes commonly co-exist, the evidence base to support obesity as the major driver of type 2 diabetes mellitus (T2DM), and the mechanisms by which this occurs, are now better appreciated. Discussion This review briefly examines several sources of evidence - epidemiological, genetic, molecular, and clinical trial - to support obesity being a causal risk factor for T2DM. It also summarises the ectopic fat hypothesis for this condition, and lists several pieces of evidence to support this concept, extending from rare conditions and drug effects to sex- and ethnicity-related differences in T2DM prevalence. Ectopic liver fat is the best-studied example of ectopic fat, but more research on pancreatic fat as a potential cause of β-cell dysfunction seems warranted. This ectopic fat concept, in turn, broadly fits with the observation that individuals of similar ages can develop diabetes at markedly different body mass indexes (BMIs). Those with risk factors leading to more rapid ectopic fat gain - for example, men (compared with women), certain ethnicities, and potentially those with a family history of diabetes, as well as others with genes linked to a reduced subcutaneous adiposity - are more likely to develop diabetes at a younger age and/or lower BMI than those without. Summary Obesity is the major risk factor for T2DM and appears to drive tissue insulin resistance in part via gain of ectopic fat, with the best-studied organ being the liver. However, ectopic fat in the pancreas may contribute to β-cell dysfunction. In line with this observation, rapid resolution of diabetes linked to a preferential and rapid reduction in liver fat has been noted with significant caloric reduction. Whether these observations can help develop better cost-effective and sustainable lifestyle /medical interventions in patients with T2DM requires further study. © Sattar and Gill; licensee BioMed Central Ltd. 2014
abstractGer	Background Although obesity and diabetes commonly co-exist, the evidence base to support obesity as the major driver of type 2 diabetes mellitus (T2DM), and the mechanisms by which this occurs, are now better appreciated. Discussion This review briefly examines several sources of evidence - epidemiological, genetic, molecular, and clinical trial - to support obesity being a causal risk factor for T2DM. It also summarises the ectopic fat hypothesis for this condition, and lists several pieces of evidence to support this concept, extending from rare conditions and drug effects to sex- and ethnicity-related differences in T2DM prevalence. Ectopic liver fat is the best-studied example of ectopic fat, but more research on pancreatic fat as a potential cause of β-cell dysfunction seems warranted. This ectopic fat concept, in turn, broadly fits with the observation that individuals of similar ages can develop diabetes at markedly different body mass indexes (BMIs). Those with risk factors leading to more rapid ectopic fat gain - for example, men (compared with women), certain ethnicities, and potentially those with a family history of diabetes, as well as others with genes linked to a reduced subcutaneous adiposity - are more likely to develop diabetes at a younger age and/or lower BMI than those without. Summary Obesity is the major risk factor for T2DM and appears to drive tissue insulin resistance in part via gain of ectopic fat, with the best-studied organ being the liver. However, ectopic fat in the pancreas may contribute to β-cell dysfunction. In line with this observation, rapid resolution of diabetes linked to a preferential and rapid reduction in liver fat has been noted with significant caloric reduction. Whether these observations can help develop better cost-effective and sustainable lifestyle /medical interventions in patients with T2DM requires further study. © Sattar and Gill; licensee BioMed Central Ltd. 2014
abstract_unstemmed	Background Although obesity and diabetes commonly co-exist, the evidence base to support obesity as the major driver of type 2 diabetes mellitus (T2DM), and the mechanisms by which this occurs, are now better appreciated. Discussion This review briefly examines several sources of evidence - epidemiological, genetic, molecular, and clinical trial - to support obesity being a causal risk factor for T2DM. It also summarises the ectopic fat hypothesis for this condition, and lists several pieces of evidence to support this concept, extending from rare conditions and drug effects to sex- and ethnicity-related differences in T2DM prevalence. Ectopic liver fat is the best-studied example of ectopic fat, but more research on pancreatic fat as a potential cause of β-cell dysfunction seems warranted. This ectopic fat concept, in turn, broadly fits with the observation that individuals of similar ages can develop diabetes at markedly different body mass indexes (BMIs). Those with risk factors leading to more rapid ectopic fat gain - for example, men (compared with women), certain ethnicities, and potentially those with a family history of diabetes, as well as others with genes linked to a reduced subcutaneous adiposity - are more likely to develop diabetes at a younger age and/or lower BMI than those without. Summary Obesity is the major risk factor for T2DM and appears to drive tissue insulin resistance in part via gain of ectopic fat, with the best-studied organ being the liver. However, ectopic fat in the pancreas may contribute to β-cell dysfunction. In line with this observation, rapid resolution of diabetes linked to a preferential and rapid reduction in liver fat has been noted with significant caloric reduction. Whether these observations can help develop better cost-effective and sustainable lifestyle /medical interventions in patients with T2DM requires further study. © Sattar and Gill; licensee BioMed Central Ltd. 2014
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score	7.4003124

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Type 2 diabetes as a disease of ectopic fat?

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Zugang & Verfügbarkeit

Vorhandene Bände

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