Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals

Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabet...
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Autor*in:	Fuqiang Liu [verfasserIn] Ronghuai Zhang [verfasserIn] Wei Zhang [verfasserIn] Ling Zhu [verfasserIn] Qi Yu [verfasserIn] Zhongwei Liu [verfasserIn] Yong Zhang [verfasserIn] Shuo Pan [verfasserIn] Yang Wang [verfasserIn] Chao Chu [verfasserIn] Li Hu [verfasserIn] Qingyu Wang [verfasserIn] Jiadong Yu [verfasserIn] Jianjun Mu [verfasserIn] Junkui Wang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	Dietary intervention Insulin resistance Retinol‐binding protein 4

Übergeordnetes Werk:	In: Journal of Diabetes Investigation - Wiley, 2014, 12(2021), 4, Seite 658-663
Übergeordnetes Werk:	volume:12 ; year:2021 ; number:4 ; pages:658-663

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1111/jdi.13376

Katalog-ID:	DOAJ00268604X

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520			\|a Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = −0.506, P < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. Our pioneer work has contributed to the present understanding of salt‐induced insulin resistance or type 2 diabetes mellitus.
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650		4	\|a Insulin resistance
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653		0	\|a Diseases of the endocrine glands. Clinical endocrinology
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700	0		\|a Shuo Pan \|e verfasserin \|4 aut
700	0		\|a Yang Wang \|e verfasserin \|4 aut
700	0		\|a Chao Chu \|e verfasserin \|4 aut
700	0		\|a Li Hu \|e verfasserin \|4 aut
700	0		\|a Qingyu Wang \|e verfasserin \|4 aut
700	0		\|a Jiadong Yu \|e verfasserin \|4 aut
700	0		\|a Jianjun Mu \|e verfasserin \|4 aut
700	0		\|a Junkui Wang \|e verfasserin \|4 aut
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allfields	10.1111/jdi.13376 doi (DE-627)DOAJ00268604X (DE-599)DOAJf87d4fbc8bf94b26b43d2abfb2076346 DE-627 ger DE-627 rakwb eng RC648-665 Fuqiang Liu verfasserin aut Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = −0.506, P < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. Our pioneer work has contributed to the present understanding of salt‐induced insulin resistance or type 2 diabetes mellitus. Dietary intervention Insulin resistance Retinol‐binding protein 4 Diseases of the endocrine glands. Clinical endocrinology Ronghuai Zhang verfasserin aut Wei Zhang verfasserin aut Ling Zhu verfasserin aut Qi Yu verfasserin aut Zhongwei Liu verfasserin aut Yong Zhang verfasserin aut Shuo Pan verfasserin aut Yang Wang verfasserin aut Chao Chu verfasserin aut Li Hu verfasserin aut Qingyu Wang verfasserin aut Jiadong Yu verfasserin aut Jianjun Mu verfasserin aut Junkui Wang verfasserin aut In Journal of Diabetes Investigation Wiley, 2014 12(2021), 4, Seite 658-663 (DE-627)620769297 (DE-600)2542077-X 20401124 nnns volume:12 year:2021 number:4 pages:658-663 https://doi.org/10.1111/jdi.13376 kostenfrei https://doaj.org/article/f87d4fbc8bf94b26b43d2abfb2076346 kostenfrei https://doi.org/10.1111/jdi.13376 kostenfrei https://doaj.org/toc/2040-1116 Journal toc kostenfrei https://doaj.org/toc/2040-1124 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021 4 658-663
spelling	10.1111/jdi.13376 doi (DE-627)DOAJ00268604X (DE-599)DOAJf87d4fbc8bf94b26b43d2abfb2076346 DE-627 ger DE-627 rakwb eng RC648-665 Fuqiang Liu verfasserin aut Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = −0.506, P < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. Our pioneer work has contributed to the present understanding of salt‐induced insulin resistance or type 2 diabetes mellitus. Dietary intervention Insulin resistance Retinol‐binding protein 4 Diseases of the endocrine glands. Clinical endocrinology Ronghuai Zhang verfasserin aut Wei Zhang verfasserin aut Ling Zhu verfasserin aut Qi Yu verfasserin aut Zhongwei Liu verfasserin aut Yong Zhang verfasserin aut Shuo Pan verfasserin aut Yang Wang verfasserin aut Chao Chu verfasserin aut Li Hu verfasserin aut Qingyu Wang verfasserin aut Jiadong Yu verfasserin aut Jianjun Mu verfasserin aut Junkui Wang verfasserin aut In Journal of Diabetes Investigation Wiley, 2014 12(2021), 4, Seite 658-663 (DE-627)620769297 (DE-600)2542077-X 20401124 nnns volume:12 year:2021 number:4 pages:658-663 https://doi.org/10.1111/jdi.13376 kostenfrei https://doaj.org/article/f87d4fbc8bf94b26b43d2abfb2076346 kostenfrei https://doi.org/10.1111/jdi.13376 kostenfrei https://doaj.org/toc/2040-1116 Journal toc kostenfrei https://doaj.org/toc/2040-1124 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021 4 658-663
allfields_unstemmed	10.1111/jdi.13376 doi (DE-627)DOAJ00268604X (DE-599)DOAJf87d4fbc8bf94b26b43d2abfb2076346 DE-627 ger DE-627 rakwb eng RC648-665 Fuqiang Liu verfasserin aut Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = −0.506, P < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. Our pioneer work has contributed to the present understanding of salt‐induced insulin resistance or type 2 diabetes mellitus. Dietary intervention Insulin resistance Retinol‐binding protein 4 Diseases of the endocrine glands. Clinical endocrinology Ronghuai Zhang verfasserin aut Wei Zhang verfasserin aut Ling Zhu verfasserin aut Qi Yu verfasserin aut Zhongwei Liu verfasserin aut Yong Zhang verfasserin aut Shuo Pan verfasserin aut Yang Wang verfasserin aut Chao Chu verfasserin aut Li Hu verfasserin aut Qingyu Wang verfasserin aut Jiadong Yu verfasserin aut Jianjun Mu verfasserin aut Junkui Wang verfasserin aut In Journal of Diabetes Investigation Wiley, 2014 12(2021), 4, Seite 658-663 (DE-627)620769297 (DE-600)2542077-X 20401124 nnns volume:12 year:2021 number:4 pages:658-663 https://doi.org/10.1111/jdi.13376 kostenfrei https://doaj.org/article/f87d4fbc8bf94b26b43d2abfb2076346 kostenfrei https://doi.org/10.1111/jdi.13376 kostenfrei https://doaj.org/toc/2040-1116 Journal toc kostenfrei https://doaj.org/toc/2040-1124 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021 4 658-663
allfieldsGer	10.1111/jdi.13376 doi (DE-627)DOAJ00268604X (DE-599)DOAJf87d4fbc8bf94b26b43d2abfb2076346 DE-627 ger DE-627 rakwb eng RC648-665 Fuqiang Liu verfasserin aut Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = −0.506, P < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. Our pioneer work has contributed to the present understanding of salt‐induced insulin resistance or type 2 diabetes mellitus. Dietary intervention Insulin resistance Retinol‐binding protein 4 Diseases of the endocrine glands. Clinical endocrinology Ronghuai Zhang verfasserin aut Wei Zhang verfasserin aut Ling Zhu verfasserin aut Qi Yu verfasserin aut Zhongwei Liu verfasserin aut Yong Zhang verfasserin aut Shuo Pan verfasserin aut Yang Wang verfasserin aut Chao Chu verfasserin aut Li Hu verfasserin aut Qingyu Wang verfasserin aut Jiadong Yu verfasserin aut Jianjun Mu verfasserin aut Junkui Wang verfasserin aut In Journal of Diabetes Investigation Wiley, 2014 12(2021), 4, Seite 658-663 (DE-627)620769297 (DE-600)2542077-X 20401124 nnns volume:12 year:2021 number:4 pages:658-663 https://doi.org/10.1111/jdi.13376 kostenfrei https://doaj.org/article/f87d4fbc8bf94b26b43d2abfb2076346 kostenfrei https://doi.org/10.1111/jdi.13376 kostenfrei https://doaj.org/toc/2040-1116 Journal toc kostenfrei https://doaj.org/toc/2040-1124 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021 4 658-663
allfieldsSound	10.1111/jdi.13376 doi (DE-627)DOAJ00268604X (DE-599)DOAJf87d4fbc8bf94b26b43d2abfb2076346 DE-627 ger DE-627 rakwb eng RC648-665 Fuqiang Liu verfasserin aut Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = −0.506, P < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. Our pioneer work has contributed to the present understanding of salt‐induced insulin resistance or type 2 diabetes mellitus. Dietary intervention Insulin resistance Retinol‐binding protein 4 Diseases of the endocrine glands. Clinical endocrinology Ronghuai Zhang verfasserin aut Wei Zhang verfasserin aut Ling Zhu verfasserin aut Qi Yu verfasserin aut Zhongwei Liu verfasserin aut Yong Zhang verfasserin aut Shuo Pan verfasserin aut Yang Wang verfasserin aut Chao Chu verfasserin aut Li Hu verfasserin aut Qingyu Wang verfasserin aut Jiadong Yu verfasserin aut Jianjun Mu verfasserin aut Junkui Wang verfasserin aut In Journal of Diabetes Investigation Wiley, 2014 12(2021), 4, Seite 658-663 (DE-627)620769297 (DE-600)2542077-X 20401124 nnns volume:12 year:2021 number:4 pages:658-663 https://doi.org/10.1111/jdi.13376 kostenfrei https://doaj.org/article/f87d4fbc8bf94b26b43d2abfb2076346 kostenfrei https://doi.org/10.1111/jdi.13376 kostenfrei https://doaj.org/toc/2040-1116 Journal toc kostenfrei https://doaj.org/toc/2040-1124 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021 4 658-663
language	English
source	In Journal of Diabetes Investigation 12(2021), 4, Seite 658-663 volume:12 year:2021 number:4 pages:658-663
sourceStr	In Journal of Diabetes Investigation 12(2021), 4, Seite 658-663 volume:12 year:2021 number:4 pages:658-663
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Dietary intervention Insulin resistance Retinol‐binding protein 4 Diseases of the endocrine glands. Clinical endocrinology
isfreeaccess_bool	true
container_title	Journal of Diabetes Investigation
authorswithroles_txt_mv	Fuqiang Liu @@aut@@ Ronghuai Zhang @@aut@@ Wei Zhang @@aut@@ Ling Zhu @@aut@@ Qi Yu @@aut@@ Zhongwei Liu @@aut@@ Yong Zhang @@aut@@ Shuo Pan @@aut@@ Yang Wang @@aut@@ Chao Chu @@aut@@ Li Hu @@aut@@ Qingyu Wang @@aut@@ Jiadong Yu @@aut@@ Jianjun Mu @@aut@@ Junkui Wang @@aut@@
publishDateDaySort_date	2021-01-01T00:00:00Z
hierarchy_top_id	620769297
id	DOAJ00268604X
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ00268604X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230309171547.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230225s2021 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1111/jdi.13376</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ00268604X</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJf87d4fbc8bf94b26b43d2abfb2076346</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC648-665</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Fuqiang Liu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = −0.506, P < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. 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callnumber-first	R - Medicine
author	Fuqiang Liu
spellingShingle	Fuqiang Liu misc RC648-665 misc Dietary intervention misc Insulin resistance misc Retinol‐binding protein 4 misc Diseases of the endocrine glands. Clinical endocrinology Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals
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topic_title	RC648-665 Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals Dietary intervention Insulin resistance Retinol‐binding protein 4
topic	misc RC648-665 misc Dietary intervention misc Insulin resistance misc Retinol‐binding protein 4 misc Diseases of the endocrine glands. Clinical endocrinology
topic_unstemmed	misc RC648-665 misc Dietary intervention misc Insulin resistance misc Retinol‐binding protein 4 misc Diseases of the endocrine glands. Clinical endocrinology
topic_browse	misc RC648-665 misc Dietary intervention misc Insulin resistance misc Retinol‐binding protein 4 misc Diseases of the endocrine glands. Clinical endocrinology
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title	Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals
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title_full	Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals
author_sort	Fuqiang Liu
journal	Journal of Diabetes Investigation
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author_browse	Fuqiang Liu Ronghuai Zhang Wei Zhang Ling Zhu Qi Yu Zhongwei Liu Yong Zhang Shuo Pan Yang Wang Chao Chu Li Hu Qingyu Wang Jiadong Yu Jianjun Mu Junkui Wang
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doi_str_mv	10.1111/jdi.13376
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title_sort	potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals
callnumber	RC648-665
title_auth	Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals
abstract	Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = −0.506, P < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. Our pioneer work has contributed to the present understanding of salt‐induced insulin resistance or type 2 diabetes mellitus.
abstractGer	Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = −0.506, P < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. Our pioneer work has contributed to the present understanding of salt‐induced insulin resistance or type 2 diabetes mellitus.
abstract_unstemmed	Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = −0.506, P < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. Our pioneer work has contributed to the present understanding of salt‐induced insulin resistance or type 2 diabetes mellitus.
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title_short	Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals
url	https://doi.org/10.1111/jdi.13376 https://doaj.org/article/f87d4fbc8bf94b26b43d2abfb2076346 https://doaj.org/toc/2040-1116 https://doaj.org/toc/2040-1124
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author2	Ronghuai Zhang Wei Zhang Ling Zhu Qi Yu Zhongwei Liu Yong Zhang Shuo Pan Yang Wang Chao Chu Li Hu Qingyu Wang Jiadong Yu Jianjun Mu Junkui Wang
author2Str	Ronghuai Zhang Wei Zhang Ling Zhu Qi Yu Zhongwei Liu Yong Zhang Shuo Pan Yang Wang Chao Chu Li Hu Qingyu Wang Jiadong Yu Jianjun Mu Junkui Wang
ppnlink	620769297
callnumber-subject	RC - Internal Medicine
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doi_str	10.1111/jdi.13376
callnumber-a	RC648-665
up_date	2024-07-03T13:29:46.090Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ00268604X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230309171547.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230225s2021 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1111/jdi.13376</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ00268604X</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJf87d4fbc8bf94b26b43d2abfb2076346</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC648-665</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Fuqiang Liu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = −0.506, P < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. 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Clinical endocrinology</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Ronghuai Zhang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Wei Zhang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Ling Zhu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Qi Yu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Zhongwei Liu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yong Zhang</subfield><subfield code="e">verfasserin</subfield><subfield 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Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals

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