In a somewhat older study researchers raised liquid levels in their test subjects and measured the effect on their metabolism. The subjects’ burned more fat and less proteins. It sounds impossible, but water is anabolic.
The researchers dehydrated their test subjects by giving them a salt solution. The salt drew the water out of their cells. The researchers imitated the effect of a high liquid level by introducing water, and used a hormone to reduce the amount of liquid lost through the urine.
Below you can see the effect of liquid on the release of fats from the fat cells, so that the body can burn them. The concentration of glycerol in the body rises as the fat cells release more fatty acids.
The ‘hypo-osmality study’ bars show what happens in the bodies of the completely hydrated test subjects.
Below you can see the effect of an increased level of liquid on protein burning. Hypo = hydrated cells, hyper = dehydrated cells, iso = control group. The researchers measured the breakdown of protein via the oxidation of the amino acid leucine.
The conclusion: fat cells that are saturated with water release fats more easily; muscle cells that are full of water save proteins. Water is a perfect anabolic.
Effects of changes in hydration on protein, glucose and lipid metabolism in man: impact on health.
Alterations of cell volume induced by changes of extracellular osmolality have been reported to regulate intracellular metabolic pathways. Hypo-osmotic cell swelling counteracts proteolysis and glycogen breakdown in the liver, whereas hyperosmotic cell shrinkage promotes protein breakdown, glycolysis and glycogenolysis. To investigate the effect of acute changes of extracellular osmolality on whole-body protein, glucose and lipid metabolism in vivo, we studied 10 male subjects during three conditions: (i) hyperosmolality was induced by fluid restriction and intravenous infusion of hypertonic NaCl (2-5%, wt/vol) during 17 h; (ii) hypo-osmolality was produced by intravenous administration of desmopressin, liberal water drinking and infusion of hypotonic saline (0.4%); and (iii) the iso-osmolality study comprised oral water intake ad libitum. Plasma osmolality increased from 285+/-1 to 296+/-1 mosm/kg (P<0.001 during hyperosmolality, and decreased from 286+/-1 to 265+/-1 mosm/kg during hypo-osmolality (P<0.001). Total body leucine flux ([1-(13)C]leucine infusion technique), reflecting whole-body protein breakdown, as well as whole-body leucine oxidation rate (irreversible loss of amino acids) decreased significantly during hypo-osmolality. The glucose metabolic clearance rate during hyperinsulinaemic-euglycemic clamping increased significantly less during hypo-osmolality than iso-osmolality, indicating diminished peripheral insulin sensitivity. Glycerol turnover (2-[(13)C]glycerol infusion technique), reflecting whole-body lipolysis, increased significantly during hypo-osmolar conditions. The results demonstrate that the metabolic adaptation to acute hypo-osmolality resembles that of acute fasting, that is, it results in protein sparing associated with increased lipolysis, ketogenesis and lipid oxidation and impaired insulin sensitivity of glucose metabolism.
PMID: 14681716 [PubMed – indexed for MEDLINE]