Reply to Letter to the Editor

International Journal of Obesity (2009) 33, 386; doi:10.1038/ijo.2008.276; published online 20 January 2009

Response to ‘Hydration increases cell metabolism’

M L Mathai1,2 and R S Weisinger3

  1. 1School of Biomedical and Health Sciences, Victoria University, St Albans, Victoria, Australia
  2. 2Howard Florey Institute, University of Melbourne, Melbourne, Victoria, Australia
  3. 3School of Psychological Science, LaTrobe University, Bundoora, Victoria, Australia

Correspondence: ML Mathai, E-mail: michael.mathai@vu.edu.au

Blockade with an angiotensin-converting enzyme inhibitor has often resulted in increased water intake in animals. The mechanism for this phenomenon is unknown, and we have suggested that it could be due to a primary thirst sensation mediated by the brain to increase water intake, or a compensatory response secondary to increased urinary water loss, possibly due to a reduction in angiotensin II-mediated vasopressin release.1 In their letter (above), Thornton and colleagues make the interesting observation that increased water intake is associated in the literature with lean body weight and increased cellular metabolism, which suggests that the drinking of water could be a useful strategy in the pursuit of reduced body weight and improved glucose control.

One of the major points made by our correspondents is the slow growth rate of the Brattleboro rat. This animal cannot synthesise vasopressin, so the drive to drink 250ml per day (which is more than three times what we observed in rats treated with an angiotensin-converting enzyme inhibitor) is secondary to the water loss due to an inability to concentrate the urine. In these animals, increased energy expenditure could be due to the increased locomotor activity involved in obtaining and drinking the water and warming it from room to core temperature. Furthermore, Boschmann et al.2 found that ingestion of 500ml of water, but not saline, increased thermogenesis, suggesting that reduced osmolality may be involved in the increased energy expenditure.

In all these studies, including our own, vasopressin secretion would be reduced. Vasopressin administration decreases thermogenesis,3 so it is possible that the reduction in vasopressin drives increased metabolism. Recent evidence4 shows that genetic deletion of the vasopressin V1a receptor in mice leads to increased β-oxidation of fat. Interestingly, these animals also have a reduction in activation of the renin–angiotensin system, whereby release of renin from the kidney is reduced in the absence of V1a-receptor-mediated signalling.5 This evidence links the increase in metabolic rate back with a reduction in angiotensin that we observed in our study. Moreover, other studies have shown that blockade of angiotensin with AT1 receptor antagonists also reduces body fat, without increasing water intake.6, 7

Finally our recent data in mice with a genetic deletion of angiotensin-converting enzyme indicate that hepatic fatty oxidation may be a key component of the increase in metabolic rate that drives a reduction in body fat.8 These animals drink more water on a daily basis; however, vasopressin levels were not measured. Thus, the available evidence leaves open a role for vasopressin in the increased metabolic rate and a possible interaction between the renin–angiotensin system and vasopressin release. It is not yet possible to conclude whether the increase in metabolism and reduction in fat mass is mediated by a reduction in vasopressin due to increased water intake and hypo-osmolality, or whether a reduction in the activity of angiotensin is the primary mechanism.

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References

  1. Gohlke P, Weiss S, Jansen A, Wienen W, Stangier J, Rascher W et al. AT1 receptor antagonist telmisartan administered peripherally inhibits central responses to angiotensin II in conscious rats. J Exp Pharmacol Ther 2001; 298: 62–70. | ChemPort |
  2. Boschmann M, Steiniger J, Franke G, Birkenfeld AL, Luft FC, Jordan J. Water drinking induces thermogenesis through osmosensitive mechanisms. J Clin Endocrinol Metab 2007; 92: 3334–3337. | Article | PubMed | ChemPort |
  3. Shido O, Kifune A, Nagasaka T. Baroreflexive suppression of heat production and fall in body temperature following peripheral administration of vasopressin in rats. Jpn J Physiol 1984; 34: 397–406. | Article | PubMed | ChemPort |
  4. Hiroyama M, Aoyagi T, Fujiwara Y, Birumachi J, Shigematsu Y, Kiwaki K et al. Hypermetabolism of fat in V1a vasopressin receptor knockout mice. Mol Endocrinol 2007; 21: 247–258. | Article | PubMed | ChemPort |
  5. Aoyagi T, Izumi Y, Hiroyama M, Matsuzaki T, Yasuoka Y, Sanbe A et al. Vasopressin regulates the renin–angiotensin system via V1a receptors in macula densa cells. Am J Physiol 2008; 295: F100–F107. | Article | ChemPort |
  6. Sugimoto K, Qi NR, Kazdova L, Pravenec M, Ogihara T, Kurtz TW. Telmisartan but not valsartan increases caloric expenditure and protects against weight gain and hepatic steatosis. Hypertension 2006; 47: 1003–1009. | Article | PubMed | ChemPort |
  7. Zorad S, Dou JT, Benicky J, Hutanu D, Tybitnaclova K, Zhou J et al. Long-term angiotensin II AT1 receptor inhibition produces adipose tissue hypotrophy accompanied by increased expression of adiponectin and PPARgamma. Eur J Pharmacol 2006; 552: 112–122. | Article | PubMed | ChemPort |
  8. Jayasooriya AP, Mathai ML, Begg DP, Denton DA, Jois M, Rodger P et al. Mice lacking angiotensin converting enzyme have increased energy expenditure with reduced fat mass and improved glucose tolerance. Proc Nat'l Acad Sci USA 2008; 105: 6531–6536. | Article |

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