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Dietary acid load, insulin sensitivity and risk of type 2 diabetes in community-dwelling older men

Aims/hypothesis We tested the hypothesis that dietary acid load may increase the risk of type 2 diabetes, and studied the association between acid load and insulin sensitivity as a possible mechanism involved. Methods An observational survey with prospective follow-up including 911 non-diabetic Swed... Full description

Journal Title: Diabetologia 2014-05-31, Vol.57 (8), p.1561-1568
Main Author: Xu, Hong
Other Authors: Jia, Ting , Huang, Xiaoyan , Risérus, Ulf , Cederholm, Tommy , Ärnlöv, Johan , Sjögren, Per , Lindholm, Bengt , Carrero, Juan-Jesús
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Berlin/Heidelberg: Springer Berlin Heidelberg
ID: ISSN: 0012-186X
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title: Dietary acid load, insulin sensitivity and risk of type 2 diabetes in community-dwelling older men
format: Article
creator:
  • Xu, Hong
  • Jia, Ting
  • Huang, Xiaoyan
  • Risérus, Ulf
  • Cederholm, Tommy
  • Ärnlöv, Johan
  • Sjögren, Per
  • Lindholm, Bengt
  • Carrero, Juan-Jesús
subjects:
  • Acids
  • Aged
  • Algorithms
  • Article
  • Biological and medical sciences
  • Clinical Medicine
  • Diabetes incidence
  • Diabetes incidence
  • Dietary acid load
  • Insulin resistance
  • Insulin sensitivity
  • Kidney function
  • Diabetes Mellitus, Type 2 - epidemiology
  • Diabetes Mellitus, Type 2 - etiology
  • Diabetes Mellitus, Type 2 - physiopathology
  • Diabetes. Impaired glucose tolerance
  • Diet
  • Diet therapy
  • Dietary acid load
  • Endocrine pancreas. Apud cells (diseases)
  • Endocrinology and Diabetes
  • Endocrinopathies
  • Endokrinologi och diabetes
  • Etiopathogenesis. Screening. Investigations. Target tissue resistance
  • Glucose tolerance tests
  • Health and Welfare
  • Human Physiology
  • Humans
  • Hälsa och välfärd
  • Incidence
  • Insulin
  • Insulin resistance
  • Insulin Resistance - physiology
  • Insulin sensitivity
  • Internal Medicine
  • Kidney function
  • Klinisk medicin
  • Male
  • Medical and Health Sciences
  • Medical colleges
  • Medical sciences
  • Medicin och hälsovetenskap
  • Medicine
  • Medicine & Public Health
  • Metabolic Diseases
  • Residence Characteristics
  • Risk
  • Risk factors
  • Type 2 diabetes
ispartof: Diabetologia, 2014-05-31, Vol.57 (8), p.1561-1568
description: Aims/hypothesis We tested the hypothesis that dietary acid load may increase the risk of type 2 diabetes, and studied the association between acid load and insulin sensitivity as a possible mechanism involved. Methods An observational survey with prospective follow-up including 911 non-diabetic Swedish men aged 70–71 years was carried out. The gold standard euglycaemic–hyperinsulinaemic clamp technique and the OGTT were used to determine insulin sensitivity and beta cell function, respectively. Diabetes incidence was assessed during 18 years of follow-up. Renal function was estimated from serum cystatin C concentrations. Dietary acid load was calculated as potential renal acid load (PRAL) and net endogenous acid production (NEAP) algorithms from 7 day food records. Adequate dietary reporters were identified by Goldberg cut-offs. Results PRAL and NEAP were not associated with insulin sensitivity or beta cell function. Underlying kidney function or consideration of dietary adequate reporters did not modify these null findings. During follow-up, 115 new cases of diabetes were validated. Neither PRAL nor NEAP was associated with diabetes incidence. Conclusions/interpretation Our results do not support the hypothesis that dietary acid load influences insulin sensitivity, beta cell function or diabetes risk. Interventional studies modifying acid–base dietary intake are needed to further elucidate a possible role of acid load in the development of type 2 diabetes.
language: eng
source:
identifier: ISSN: 0012-186X
fulltext: no_fulltext
issn:
  • 0012-186X
  • 1432-0428
  • 1432-0428
url: Link


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titleDietary acid load, insulin sensitivity and risk of type 2 diabetes in community-dwelling older men
creatorXu, Hong ; Jia, Ting ; Huang, Xiaoyan ; Risérus, Ulf ; Cederholm, Tommy ; Ärnlöv, Johan ; Sjögren, Per ; Lindholm, Bengt ; Carrero, Juan-Jesús
creatorcontribXu, Hong ; Jia, Ting ; Huang, Xiaoyan ; Risérus, Ulf ; Cederholm, Tommy ; Ärnlöv, Johan ; Sjögren, Per ; Lindholm, Bengt ; Carrero, Juan-Jesús
descriptionAims/hypothesis We tested the hypothesis that dietary acid load may increase the risk of type 2 diabetes, and studied the association between acid load and insulin sensitivity as a possible mechanism involved. Methods An observational survey with prospective follow-up including 911 non-diabetic Swedish men aged 70–71 years was carried out. The gold standard euglycaemic–hyperinsulinaemic clamp technique and the OGTT were used to determine insulin sensitivity and beta cell function, respectively. Diabetes incidence was assessed during 18 years of follow-up. Renal function was estimated from serum cystatin C concentrations. Dietary acid load was calculated as potential renal acid load (PRAL) and net endogenous acid production (NEAP) algorithms from 7 day food records. Adequate dietary reporters were identified by Goldberg cut-offs. Results PRAL and NEAP were not associated with insulin sensitivity or beta cell function. Underlying kidney function or consideration of dietary adequate reporters did not modify these null findings. During follow-up, 115 new cases of diabetes were validated. Neither PRAL nor NEAP was associated with diabetes incidence. Conclusions/interpretation Our results do not support the hypothesis that dietary acid load influences insulin sensitivity, beta cell function or diabetes risk. Interventional studies modifying acid–base dietary intake are needed to further elucidate a possible role of acid load in the development of type 2 diabetes.
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1ISSN: 1432-0428
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3DOI: 10.1007/s00125-014-3275-z
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languageeng
publisherBerlin/Heidelberg: Springer Berlin Heidelberg
subjectAcids ; Aged ; Algorithms ; Article ; Biological and medical sciences ; Clinical Medicine ; Diabetes incidence ; Diabetes incidence; Dietary acid load; Insulin resistance; Insulin sensitivity; Kidney function ; Diabetes Mellitus, Type 2 - epidemiology ; Diabetes Mellitus, Type 2 - etiology ; Diabetes Mellitus, Type 2 - physiopathology ; Diabetes. Impaired glucose tolerance ; Diet ; Diet therapy ; Dietary acid load ; Endocrine pancreas. Apud cells (diseases) ; Endocrinology and Diabetes ; Endocrinopathies ; Endokrinologi och diabetes ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Glucose tolerance tests ; Health and Welfare ; Human Physiology ; Humans ; Hälsa och välfärd ; Incidence ; Insulin ; Insulin resistance ; Insulin Resistance - physiology ; Insulin sensitivity ; Internal Medicine ; Kidney function ; Klinisk medicin ; Male ; Medical and Health Sciences ; Medical colleges ; Medical sciences ; Medicin och hälsovetenskap ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Residence Characteristics ; Risk ; Risk factors ; Type 2 diabetes
ispartofDiabetologia, 2014-05-31, Vol.57 (8), p.1561-1568
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3Risérus, Ulf
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7Lindholm, Bengt
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descriptionAims/hypothesis We tested the hypothesis that dietary acid load may increase the risk of type 2 diabetes, and studied the association between acid load and insulin sensitivity as a possible mechanism involved. Methods An observational survey with prospective follow-up including 911 non-diabetic Swedish men aged 70–71 years was carried out. The gold standard euglycaemic–hyperinsulinaemic clamp technique and the OGTT were used to determine insulin sensitivity and beta cell function, respectively. Diabetes incidence was assessed during 18 years of follow-up. Renal function was estimated from serum cystatin C concentrations. Dietary acid load was calculated as potential renal acid load (PRAL) and net endogenous acid production (NEAP) algorithms from 7 day food records. Adequate dietary reporters were identified by Goldberg cut-offs. Results PRAL and NEAP were not associated with insulin sensitivity or beta cell function. Underlying kidney function or consideration of dietary adequate reporters did not modify these null findings. During follow-up, 115 new cases of diabetes were validated. Neither PRAL nor NEAP was associated with diabetes incidence. Conclusions/interpretation Our results do not support the hypothesis that dietary acid load influences insulin sensitivity, beta cell function or diabetes risk. Interventional studies modifying acid–base dietary intake are needed to further elucidate a possible role of acid load in the development of type 2 diabetes.
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5Clinical Medicine
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9Diabetes Mellitus, Type 2 - etiology
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14Dietary acid load
15Endocrine pancreas. Apud cells (diseases)
16Endocrinology and Diabetes
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19Etiopathogenesis. Screening. Investigations. Target tissue resistance
20Glucose tolerance tests
21Health and Welfare
22Human Physiology
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25Incidence
26Insulin
27Insulin resistance
28Insulin Resistance - physiology
29Insulin sensitivity
30Internal Medicine
31Kidney function
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35Medical colleges
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37Medicin och hälsovetenskap
38Medicine
39Medicine & Public Health
40Metabolic Diseases
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44Type 2 diabetes
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titleDietary acid load, insulin sensitivity and risk of type 2 diabetes in community-dwelling older men
authorXu, Hong ; Jia, Ting ; Huang, Xiaoyan ; Risérus, Ulf ; Cederholm, Tommy ; Ärnlöv, Johan ; Sjögren, Per ; Lindholm, Bengt ; Carrero, Juan-Jesús
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8Diabetes Mellitus, Type 2 - epidemiology
9Diabetes Mellitus, Type 2 - etiology
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15Endocrine pancreas. Apud cells (diseases)
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date2014-05-31
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abstractAims/hypothesis We tested the hypothesis that dietary acid load may increase the risk of type 2 diabetes, and studied the association between acid load and insulin sensitivity as a possible mechanism involved. Methods An observational survey with prospective follow-up including 911 non-diabetic Swedish men aged 70–71 years was carried out. The gold standard euglycaemic–hyperinsulinaemic clamp technique and the OGTT were used to determine insulin sensitivity and beta cell function, respectively. Diabetes incidence was assessed during 18 years of follow-up. Renal function was estimated from serum cystatin C concentrations. Dietary acid load was calculated as potential renal acid load (PRAL) and net endogenous acid production (NEAP) algorithms from 7 day food records. Adequate dietary reporters were identified by Goldberg cut-offs. Results PRAL and NEAP were not associated with insulin sensitivity or beta cell function. Underlying kidney function or consideration of dietary adequate reporters did not modify these null findings. During follow-up, 115 new cases of diabetes were validated. Neither PRAL nor NEAP was associated with diabetes incidence. Conclusions/interpretation Our results do not support the hypothesis that dietary acid load influences insulin sensitivity, beta cell function or diabetes risk. Interventional studies modifying acid–base dietary intake are needed to further elucidate a possible role of acid load in the development of type 2 diabetes.
copBerlin/Heidelberg
pubSpringer Berlin Heidelberg
pmid24875749
doi10.1007/s00125-014-3275-z