Low Water Intake and Risk for New-Onset Hyperglycemia
Open accessAbstract
OBJECTIVE: Water intake alters vasopressin secretion. Recent findings reveal an independent association between plasma copeptin, a surrogate for vasopressin, and risk of diabetes. RESEARCH DESIGN AND METHODS: Participants were 3,615 middle-aged men and women, with normal baseline fasting glycemia (FG), who were recruited in a 9-year follow-up study. Odds ratios (ORs) and 95% CIs for the incidence of hyperglycemia (FG ≥6.1 mmol/L or treatment for diabetes) were calculated according to daily water intake classes based on a self-administered questionnaire. RESULTS: During follow-up, there were 565 incident cases of hyperglycemia. After adjustment for confounding factors, ORs (95% CIs) for hyperglycemia associated with classes of water intake (<0.5 L, n = 677; 0.5 to <1.0 L, n = 1,754; and >1.0 L, n = 1,184) were 1.00, 0.68 (0.52–0.89), and 0.79 (0.59–1.05), respectively (P = 0.016). CONCLUSIONS: Self-reported water intake was inversely and independently associated with the risk of developing hyperglycemia.
AI snapshot
Written from the paper’s full text.
TL;DR
In a 9-year French cohort of 3,615 initially normoglycemic middle-aged adults, self-reported daily water intake was inversely associated with new-onset hyperglycemia. The association was independent of multiple metabolic risk factors and other beverage intake, though the study is observational and cannot establish causality.
Key findings
- During follow-up, 565 participants developed hyperglycemia and 202 developed diabetes.
- After adjustment for known diabetes risk factors and other beverages, ORs for incident hyperglycemia by daily water intake were 1.00 for <0.5 L (n = 677), 0.68 (95% CI 0.52–0.89) for 0.5 to <1.0 L (n = 1,754), and 0.79 (0.59–1.05) for >1.0 L (n = 1,184); P = 0.016.
- With the two upper water-intake classes combined, the OR was 0.72 (0.56–0.92). The relation was not linear.
- For new-onset diabetes, the same trend was nonsignificant: ORs were 0.68 (0.41–1.15) and 0.75 (0.43–1.32) for 0.5–1.0 L and >1.0 L versus <0.5 L, respectively; P = 0.36.
Methods
- Prospective analysis within the D.E.S.I.R. study: 3,615 French men and women aged 30–65 years with baseline fasting glycemia <6.1 mmol/L, followed over 9 years with examinations at years 3, 6, and 9.
- Daily water intake was assessed by self-administered questionnaire and grouped into three classes: <0.5 L, 0.5 to 1.0 L, and >1.0 L.
- Logistic regression models estimated ORs and 95% CIs for incident hyperglycemia, adjusted for age, sex, BMI, baseline fasting glucose, physical activity, smoking, triglycerides, HOMA-IR, total cholesterol, and further for intake of other beverages.
Limitations
- Stated: diabetes incidence was low, limiting statistical power; 24-h urine volume was not measured, though urinary density was inversely associated with self-reported water intake; residual confounding cannot be excluded because healthier behaviors may correlate with higher water drinking; only volunteers were included, so results may not be extrapolated to the general population.
- Evident from the text: the observational design does not establish causality, and water intake was self-reported via questionnaire rather than directly measured.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
0 of 35 cited sources checked · 0 supported · 0 flagged
- Findingown data
With the two upper water intake classes combined, the odds ratio for new-onset hyperglycemia was 0.72 (95% CI 0.56-0.92).
“With the two upper classes combined, the OR was 0.72 (0.56–0.92) (Supplementary Fig. 1).”
Quote in the paperSubstantial claim - Findingown data
The relation between water intake and risk of new-onset hyperglycemia was not linear.
“The relation was not linear (data not shown).”
Quote in the paperNot a substantial claim - Findingown data
During follow-up, 565 incident cases of hyperglycemia occurred.
“During follow-up, there were 565 incident cases of hyperglycemia.”
- Also stated in: § RESULTS · plain
“Among them, during follow-up, 565 subjects became hyperglycemic and 202 developed diabetes.”
Quote in the paperNot a substantial claim - Also stated in: § RESULTS · plain
- Findingown data
There was no interaction between water intake and several important characteristics, including self-reported alcohol or tobacco consumption, on the risk of new-onset hyperglycemia.
“There was no interaction with several important characteristics, including those related to self-reported alcohol or tobacco consumption (Supplementary Table 1).”
Quote in the paperNot a substantial claim - Findingown data
In Model 2, after further adjustment for intake of other beverages, the odds ratios for new-onset hyperglycemia were 0.68 (95% CI 0.52-0.89) for 0.5-1.0 L and 0.79 (0.59-1.05) for >1.0 L compared with <0.5 L, with P = 0.016.
“After further adjustments for intake of other beverages, the ORs were slightly attenuated: 0.68 (0.52–0.89) and 0.79 (0.59–1.05) for classes of 0.5–1.0 L and >1.0 L, respectively (P = 0.016) (Table 1).”
- Also stated in: § RESULTS · plain
“After adjustment for confounding factors, ORs (95% CIs) for hyperglycemia associated with classes of water intake (<0.5 L, n = 677; 0.5 to <1.0 L, n = 1,754; and >1.0 L, n = 1,184) were 1.00, 0.68 (0.52–0.89), and 0.79 (0.59–1.05), respectively (P = 0.016).”
Quote in the paperSubstantial claim - Also stated in: § RESULTS · plain
- Findingown data
Self-reported daily water intake was inversely and independently associated with the risk of new-onset hyperglycemia after adjustment for multiple metabolic risk factors.
“The daily W-Intake was negatively associated with the risk of new-onset hyperglycemia, even after adjustment for multiple metabolic risk factors.”
- Also stated in: § CONCLUSIONS · plain
“Self-reported water intake was inversely and independently associated with the risk of developing hyperglycemia.”
- Also stated in: § CONCLUSIONS · plain
“Risk for hyperglycemia was negatively and independently related with self-reported W-Intake in normoglycemic middle-aged individuals from the French general population.”
Quote in the paperSubstantial claim - Also stated in: § CONCLUSIONS · plain
- Findingown data
Almost 20% of participants in this cohort reported drinking <0.5 L of water per day.
“as did almost 20% of the participants in this cohort.”
Quote in the paperNot a substantial claim - Findingown data
The association between water intake and hyperglycemia risk was moderately attenuated when important metabolic risk factors and potential confounders, including intake of other beverages, were introduced as covariables.
“However, the association was moderately attenuated when important metabolic risk factors and potential confounders were introduced as covariables in the analysis, including intake of other classes of beverages with known adverse long-term effects (sweet and alcohol-containing drinks).”
Quote in the paperSubstantial claim - Interpretationown data
The data support the idea that vasopressin, besides its role in urine concentration, is an important actor in glucose homeostasis.
“Our data support the novel idea that vasopressin, besides its role in urine concentration, is also an important actor in glucose homeostasis (1).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [1] Enhörning, 2010, Plasma copeptin and the risk of diabetes mellitus, Circulation source
Not checked in the free run.
- Interpretationown data
Identification of individuals with water intake <0.5 L may be widely relevant to target preventive interventions regarding metabolic risk.
“This indicates that identification of individuals with a W-Intake of <0.5 L may be widely relevant to target preventive interventions regarding the metabolic risk.”
Quote in the paperSubstantial claim - Premisecitation
Vasopressin induces gluconeogenesis in the rat liver.
“A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”
Quote in the paperSubstantial claim0 of 8 sources checked- cites [2] Zerbe, 1979, Plasma vasopressin in uncontrolled diabetes mellitus, Diabetes source
Not checked in the free run.
- cites [3] Bankir, 2001, Vasopressin and diabetes mellitus, Nephron source
Not checked in the free run.
- cites [4] Whitton, 1978, Stimulation by vasopressin, angiotensin and oxytocin of gluconeogenesis in hepatocyte suspensions, Biochem J source
Not checked in the free run.
- cites [5] Spruce, 1985, The effect of vasopressin infusion on glucose metabolism in man, Clin Endocrinol (Oxf) source
Not checked in the free run.
- cites [6] Phillips, 1990, Localization of vasopressin binding sites in rat tissues using specific V1 and V2 selective ligands, Endocrinology source
Not checked in the free run.
- cites [7] Serradeil-Le Gal, 1994, Binding of [3H] SR 49059, a potent nonpeptide vasopressin V1a antagonist, to rat and human liver membranes, Biochem Biophys Res Commun source
Not checked in the free run.
- cites [8] Folny, 2003, Pancreatic vasopressin V1b receptors: characterization in In-R1-G9 cells and localization in human pancreas, Am J Physiol Endocrinol Metab source
Not checked in the free run.
- cites [9] Oshikawa, 2004, Vasopressin stimulates insulin release from islet cells through V1b receptors: a combined pharmacological/knockout approach, Mol Pharmacol source
Not checked in the free run.
- Interpretationreasoning
An increase in water intake could prevent or delay the onset of hyperglycemia and subsequent diabetes.
“It suggests that an increase in W-Intake, an easy and costless intervention, could prevent or delay the onset of hyperglycemia and subsequent diabetes.”
Quote in the paperSubstantial claim - Premisecitation
Vasopressin transiently increases glycemia in healthy humans.
“A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”
Quote in the paperSubstantial claim0 of 8 sources checked- cites [2] Zerbe, 1979, Plasma vasopressin in uncontrolled diabetes mellitus, Diabetes source
Not checked in the free run.
- cites [3] Bankir, 2001, Vasopressin and diabetes mellitus, Nephron source
Not checked in the free run.
- cites [4] Whitton, 1978, Stimulation by vasopressin, angiotensin and oxytocin of gluconeogenesis in hepatocyte suspensions, Biochem J source
Not checked in the free run.
- cites [5] Spruce, 1985, The effect of vasopressin infusion on glucose metabolism in man, Clin Endocrinol (Oxf) source
Not checked in the free run.
- cites [6] Phillips, 1990, Localization of vasopressin binding sites in rat tissues using specific V1 and V2 selective ligands, Endocrinology source
Not checked in the free run.
- cites [7] Serradeil-Le Gal, 1994, Binding of [3H] SR 49059, a potent nonpeptide vasopressin V1a antagonist, to rat and human liver membranes, Biochem Biophys Res Commun source
Not checked in the free run.
- cites [8] Folny, 2003, Pancreatic vasopressin V1b receptors: characterization in In-R1-G9 cells and localization in human pancreas, Am J Physiol Endocrinol Metab source
Not checked in the free run.
- cites [9] Oshikawa, 2004, Vasopressin stimulates insulin release from islet cells through V1b receptors: a combined pharmacological/knockout approach, Mol Pharmacol source
Not checked in the free run.
- Study design and conductown data
Urinary density was inversely associated with self-reported water intake, supporting the validity of the questionnaire.
“24-h urine volume was not measured, but the urinary density was inversely associated with self-reported W-Intake, arguing for the validity of the questionnaire (Table 1).”
Quote in the paperNot a substantial claim- Rests on an assumption: Urinary density is a valid marker of water intake or hydration.
- Premisecitation
Plasma copeptin, a surrogate for vasopressin, is an independent risk factor for diabetes.
“Recent findings reveal an independent association between plasma copeptin, a surrogate for vasopressin, and risk of diabetes.”
- Also stated in: § CONCLUSIONS · plain
“Copeptin, a stable glycopeptide comprising the COOH-terminal portion of the preprovasopressin, released in equimolar amounts as vasopressin, recently has been shown to represent an independent risk factor for diabetes (1).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [1] Enhörning, 2010, Plasma copeptin and the risk of diabetes mellitus, Circulation source
Not checked in the free run.
- Also stated in: § CONCLUSIONS · plain
- Premisecitation
Vasopressin receptors are expressed in hepatocytes and pancreatic islets.
“A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”
Quote in the paperSubstantial claim0 of 8 sources checked- cites [2] Zerbe, 1979, Plasma vasopressin in uncontrolled diabetes mellitus, Diabetes source
Not checked in the free run.
- cites [3] Bankir, 2001, Vasopressin and diabetes mellitus, Nephron source
Not checked in the free run.
- cites [4] Whitton, 1978, Stimulation by vasopressin, angiotensin and oxytocin of gluconeogenesis in hepatocyte suspensions, Biochem J source
Not checked in the free run.
- cites [5] Spruce, 1985, The effect of vasopressin infusion on glucose metabolism in man, Clin Endocrinol (Oxf) source
Not checked in the free run.
- cites [6] Phillips, 1990, Localization of vasopressin binding sites in rat tissues using specific V1 and V2 selective ligands, Endocrinology source
Not checked in the free run.
- cites [7] Serradeil-Le Gal, 1994, Binding of [3H] SR 49059, a potent nonpeptide vasopressin V1a antagonist, to rat and human liver membranes, Biochem Biophys Res Commun source
Not checked in the free run.
- cites [8] Folny, 2003, Pancreatic vasopressin V1b receptors: characterization in In-R1-G9 cells and localization in human pancreas, Am J Physiol Endocrinol Metab source
Not checked in the free run.
- cites [9] Oshikawa, 2004, Vasopressin stimulates insulin release from islet cells through V1b receptors: a combined pharmacological/knockout approach, Mol Pharmacol source
Not checked in the free run.
- Premisecitation
A causal link between vasopressin and glucose homeostasis is plausible.
“A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”
Quote in the paperSubstantial claim0 of 8 sources checked- cites [2] Zerbe, 1979, Plasma vasopressin in uncontrolled diabetes mellitus, Diabetes source
Not checked in the free run.
- cites [3] Bankir, 2001, Vasopressin and diabetes mellitus, Nephron source
Not checked in the free run.
- cites [4] Whitton, 1978, Stimulation by vasopressin, angiotensin and oxytocin of gluconeogenesis in hepatocyte suspensions, Biochem J source
Not checked in the free run.
- cites [5] Spruce, 1985, The effect of vasopressin infusion on glucose metabolism in man, Clin Endocrinol (Oxf) source
Not checked in the free run.
- cites [6] Phillips, 1990, Localization of vasopressin binding sites in rat tissues using specific V1 and V2 selective ligands, Endocrinology source
Not checked in the free run.
- cites [7] Serradeil-Le Gal, 1994, Binding of [3H] SR 49059, a potent nonpeptide vasopressin V1a antagonist, to rat and human liver membranes, Biochem Biophys Res Commun source
Not checked in the free run.
- cites [8] Folny, 2003, Pancreatic vasopressin V1b receptors: characterization in In-R1-G9 cells and localization in human pancreas, Am J Physiol Endocrinol Metab source
Not checked in the free run.
- cites [9] Oshikawa, 2004, Vasopressin stimulates insulin release from islet cells through V1b receptors: a combined pharmacological/knockout approach, Mol Pharmacol source
Not checked in the free run.
- Classified as probably not a substantial claim. 6
- May combine two claims. 9
Probably not a substantial claim: may not pass S3 (load-bearing).
Findingown dataDuring follow-up, 202 subjects developed diabetes.
“Among them, during follow-up, 565 subjects became hyperglycemic and 202 developed diabetes.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataIn Model 1, compared with daily water intake <0.5 L, the odds ratios for new-onset hyperglycemia were 0.64 (95% CI 0.49-0.83) for 0.5-1.0 L and 0.73 (0.55-0.97) for >1.0 L, with P = 0.003.
“Compared with daily W-Intake of <0.5 L, ORs were 0.64 (95% CI 0.49–0.83) and 0.73 (0.55–0.97) for classes of 0.5–1.0 L and >1.0 L, respectively (P = 0.003).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataThe negative association of water intake and risk for hyperglycemia was relevant among many subsets of participants, and those reporting low water intake (<0.5 L) had a higher risk for hyperglycemia, for example in the high physical activity group.
“The negative association of W-Intake and risk for hyperglycemia was relevant among many subsets of participants, and those reporting a low W-Intake (<0.5 L) had a higher risk for hyperglycemia (for example, participants in the high physical activity group) (Supplementary Table 1).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataFor new-onset diabetes, the same trend was observed but was nonsignificant: compared with daily water intake <0.5 L, odds ratios were 0.68 (95% CI 0.41-1.15) for 0.5-1.0 L and 0.75 (0.43-1.32) for >1.0 L, with P = 0.36.
“The same trend, although nonsignificant, was observed for the association with new-onset diabetes: compared with participants with a daily W-Intake <0.5 L, ORs for those drinking 0.5–1.0 L and >1.0 L water per day were 0.68 (95% CI 0.41–1.15) and 0.75 (0.43–1.32), respectively, P = 0.36.”
Quote in the paperNot a substantial claimMay combine two claims.
Interpretationown dataThe study extends the observation of an association between copeptin and diabetes, drawing attention to low water intake as a possible new risk factor for impaired glycemia.
“Our study extends this observation, drawing attention to a low W-Intake as a possible new risk factor for impaired glycemia.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone given24-hour urine volume was not measured.
“24-h urine volume was not measured”
Quote in the paperNot a substantial claimMay combine two claims.
Study design and conductown dataDiabetes incidence was low and statistical power was thus limited.
“Diabetes incidence was low and statistical power was thus limited”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
Study design and conductnone givenAdjustment variables were either known risk factors for type 2 diabetes or factors associated (P < 0.10) with hyperglycemia and water intake in the study population.
“Adjustment variables were either known risk factors for type 2 diabetes or factors associated (P < 0.10) with hyperglycemia and W-Intake in our population.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationWater intake alters vasopressin secretion, and vasopressin and copeptin secretion depends on the level of hydration.
“Water intake alters vasopressin secretion.”
- Also stated in: § CONCLUSIONS · boosted
“Vasopressin and copeptin secretion is known to depend on the level of hydration (10).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [10] Meijer, 2010, Copeptin, a surrogate marker of vasopressin, is associated with microalbuminuria in a large population cohort, Kidney Int source
Not checked in the free run.
- Also stated in: § CONCLUSIONS · boosted
May combine two claims.
Study design and conductreasoningResidual confounding cannot be excluded; healthier behaviors correlating with higher water drinking could account for the observed association.
“In addition, we cannot exclude residual confounding: healthier behaviors correlating with higher water drinking could account for the observed association.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Interpretationnone givenOnly volunteers were included and the results may not be extrapolated to the general population.
“Finally, only volunteers were included and the results may not be extrapolated to the general population.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductnone givenParticipants provided written informed consent, and the protocol was approved by the ethics committee of Bicêtre Hospital, Kremlin-Bicêtre, France.
“Participants provided written informed consent, and the protocol was approved by the ethics committee of Bicêtre Hospital, Kremlin-Bicêtre, France.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
Study design and conductnone givenThis observational study does not establish causality.
“This observational study does not establish causality.”
Quote in the paperSubstantial claim
The paper relies on this without support.
Baseline self-reported water intake reflects habitual water intake over the 9-year follow-up.
“Mean daily intake of water, wine, beer or cider, and sweet beverages was categorized in the questionnaire into six mutually exclusive levels: none, <0.5, 0.5 to 1, 1 to 1.5, 1.5 to 2.0, and >2 L.”
“The daily W-Intake was negatively associated with the risk of new-onset hyperglycemia, even after adjustment for multiple metabolic risk factors.”
The paper relies on this without support.
Urinary density is a valid marker of water intake or hydration.
“24-h urine volume was not measured, but the urinary density was inversely associated with self-reported W-Intake, arguing for the validity of the questionnaire (Table 1).”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Water intake is inversely and independently associated with the risk of developing hyperglycaemia in a general French population cohort.
“We reported that water intake was inversely and independently associated with the risk of developing hyperglycaemia in a cohort of the general French population [19].”
From Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats (2015) · cites this paper as [19]
Cites
Plasma Copeptin and the Risk of Diabetes Mellitus
Enhörning, S., Wang, T. J., Nilsson, P. M., Almgren, P., Hedblad, B., Berglund, G., Struck, J., Morgenthaler, N. G., Bergmann, A., Lindholm, E., et al. (2010) · Circulation · doi:10.1161/circulationaha.109.909663 · Cited by 299 · cited 3× · see citing works
“Knowing the rise of vasopressin in diabetes, its effect on glycemia, gluconeogenesis, and glucagon release, it is surprising that no attention had been given to vasopressin as a possible risk factor for hyperglycemia and diabetes until a recent report of an association between copeptin and the incidence of diabetes (1…”
BackgroundPredicting Diabetes: Clinical, Biological, and Genetic Approaches
Balkau, B., Lange, C., Fezeu, L., Tichet, J., de Lauzon‐Guillain, B., Czernichow, S., Fumeron, F., Froguel, P., Vaxillaire, M., Cauchi, S., et al. (2008) · Diabetes Care · doi:10.2337/dc08-0368 · Cited by 296 · see citing works
Self-citationPlasma Vasopressin in Uncontrolled Diabetes Mellitus
Zerbe, R. L., Vinicor, F., & Robertson, G. L. (1979) · Diabetes · doi:10.2337/diab.28.5.503 · Cited by 158 · see citing works
Localization of Vasopressin Binding Sites in Rat Tissues Using Specific Vi and V2 Selective Ligands*
PHILLIPS, P. A., ABRAHAMS, J. M., KELLY, J. M., MOOSER, V., TRINDER, D., & JOHNSTON, C. I. (1990) · Endocrinology · doi:10.1210/endo-126-3-1478 · Cited by 127 · see citing works
Stimulation by vasopressin, angiotensin and oxytocin of gluconeogenesis in hepatocyte suspensions
Whitton, P. D., Rodrigues, L. M., & Hems, D. A. (1978) · Biochemical Journal · doi:10.1042/bj1760893 · Cited by 123 · see citing works
Meijer, E., Bakker, S. J. L., Halbesma, N., de Jong, P. E., Struck, J., & Gansevoort, R. T. (2010) · Kidney International · doi:10.1038/ki.2009.397 · Cited by 123 · see citing works
THE EFFECT OF VASOPRESSIN INFUSION ON GLUCOSE METABOLISM IN MAN
SPRUCE, B. A., MCCULLOCH, A. J., BURD, J., ØRSKOV, H., HEATON, A., BAYLIS, P. H., & ALBERTI, K. G. M. M. (1985) · Clinical Endocrinology · doi:10.1111/j.1365-2265.1985.tb00145.x · Cited by 114 · cited 1× · see citing works
“Knowing the rise of vasopressin in diabetes, its effect on glycemia, gluconeogenesis, and glucagon release, it is surprising that no attention had been given to vasopressin as a possible risk factor for hyperglycemia and diabetes until a recent report of an association between copeptin and the incidence of diabetes (1…”
BackgroundVasopressin and diabetes mellitus
Bankir, L., Bardoux, P., & Ahloulay, M. (2001) · Nephron · doi:10.1159/000045879 · Cited by 110 · see citing works
Self-citationOshikawa, S., Tanoue, A., Koshimizu, T.-A., Kitagawa, Y., & Tsujimoto, G. (2004) · Molecular Pharmacology · doi:10.1124/mol.65.3.623 · Cited by 105 · see citing works
Folny, V., Raufaste, D., Lukovic, L., Pouzet, B., Rochard, P., Pascal, M., & Serradeil-Le Gal, C. (2003) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00148.2003 · Cited by 61 · see citing works
Characterization of receptors mediating AVP- and OT-induced glucagon release from the rat pancreas
Yibchok‐anun, S., Cheng, H., Heine, P. A., & Hsu, W. H. (1999) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1999.277.1.e56 · Cited by 42 · see citing works
Serradeillegal, C., Raufaste, D., Marty, E., Garcia, C., Maffrand, J. P., & Lefur, G. (1994) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1994.1236 · Cited by 40 · see citing works
for the DESIR Study Group, Gautier, A., Balkau, B., et al. (2009) · Diabetologia · doi:10.1007/s00125-009-1602-6 · Cited by 38 · see citing works
Self-citationAlcohol intake and fasting insulin in French men and women. The D.E.S.I.R. Study.
Konrat, C., Mennen, L., Cacès, E., et al. (2002) · PubMed · Cited by 26 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Vasopressin: a novel target for the prevention and retardation of kidney disease?
Bankir, L., Bouby, N., & Ritz, E. (2013) · Nature Reviews Nephrology · doi:10.1038/nrneph.2013.22 · Cited by 214 · see citing works
Self-citationPlain-water intake and risk of type 2 diabetes in young and middle-aged women
Pan, A., Malik, V. S., Schulze, M. B., Manson, J. E., Willett, W. C., & Hu, F. B. (2012) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.111.032698 · Cited by 113 · see citing works
Taveau, C., Chollet, C., Waeckel, L., Desposito, D., Bichet, D. G., Arthus, M.-F., Magnan, C., Philippe, E., Paradis, V., Foufelle, F., et al. (2015) · Diabetologia · doi:10.1007/s00125-015-3496-9 · Cited by 86 · see citing works
Self-citation
- Authors
- Roussel, R., Fezeu, L., Bouby, N., Balkau, B., Lantieri, O., Alhenc-Gelas, F., Marre, M., Bankir, L., & for the D.E.S.I.R. Study Group
- Affiliations
- Inserm (FR)
- Institut Inter-Régional pour la Santé, La Riche, France
- INSERM Unité 872, Centre de Recherche des Cordeliers, Paris, France
- Corresponding author
- Roussel, Ronan
- Venue
- Diabetes Care
- Publisher
- American Diabetes Association
- Published
- 2011-11-14
- Volume
- 34
- Issue
- 12
- Pages
- 2551-2554
- ISSN
- 0149-5992 (ISSN-L)
- 1935-5548
- PMC
- PMC3220834
- OpenAlex
- W2148254906
- Semantic Scholar
- 03f98de4d5166198ac37a02e16b4738ccc5fc145
- Cited by
- 165
- References
- 14
- Citations by year
- 2026: 10 · 2025: 8 · 2024: 14 · 2023: 10 · 2022: 9 · 2021: 11 · 2020: 14 · 2019: 16 · 2018: 11 · 2017: 14 · 2016: 19 · 2015: 17 · 2014: 5 · 2013: 5 · 2012: 2
- FWCI
- 3.14
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Diabetes Care (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- Institut National de la Santé et de la Recherche Médicale
- Centre National de la Recherche Scientifique
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Electrolyte and hormonal disorders
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Nutritional Studies and Diet
- Keywords
- water intake, hyperglycemia, diabetes risk, copeptin, vasopressin, fasting blood glucose, middle-aged adults
- MeSH terms
- Adult, Diabetes Mellitus, Drinking, Female, Follow-Up Studies, France, Glycopeptides, Humans, Hyperglycemia, Male, Middle Aged, Risk, Cohort Studies
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-06.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-06.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review