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Articles

Use of Bioimpedance Spectroscopy to Estimate Body Water Distribution in Rats Fed High Dietary Sulfur Amino Acids^{1 ,2 ,3 ,4}

U.S. Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, North Dakota 58202-9034

⁵To whom correspondence should be addressed at U.S. Department of Agriculture, ARS, GFHNRC, P.O. Box 9034, Grand Forks, ND 58202-9034. E-mail: kyokoi{at}gfhnrc.ars.usda.gov

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
The effect of dietary sulfur amino acids on bioelectric properties was studied in rats by using bioimpedance spectroscopy. Weanling rats were assigned to one of 12 groups in a factorially arranged experiment with dietary variables of supplemental sulfur amino acid (none, 10 g DL-methionine/kg or 10 g DL-homocystine/kg), pyridoxine hydrochloride (0 or 7.5 mg/kg) and nickel (0 or 1 mg/kg). After 9 wk of feeding, 20-h urine specimens were collected from food-deprived rats for measurements of creatinine, and then bioimpedance was measured with multifrequency (Hydra ECF/ICF 4200) and single-frequency (RJL Systems model 101) analyzers. Urinary creatinine excretion was measured by intracellular water (ICW), total body solid and urinary volume (R² = 0.675). Extracellular water (ECW) did not add significantly to the model. Rats fed methionine had significantly lower total body water, ICW and ECW than rats fed no supplemental sulfur amino acid. Rats fed homocystine had significantly lower ECW and a significantly higher ratio of ICW to ECW. Rats fed methionine or homocystine had significantly lower capacitance corrected for body length and ICW than those fed no supplemental sulfur amino acids. These results suggest that dietary homocystine changes the distribution of body water and that sulfur amino acids can affect membrane porosity and/or membrane thickness.

KEY WORDS: • bioimpedance • capacitance • extracellular water • methionine • homocysteine • rats

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Assessment of body fluid distribution would be useful to evaluate nutritional status, renal function and cardiovascular function. Bioimpedance spectroscopy (BIS)⁶ is a versatile noninvasive method of evaluating body fluids and cell membrane porosity in humans (1 2 3 4) . We believe that this is the first report that applies BIS to experimental animals.

Usually, BIS data are fit to the Cole-Cole model that determines R_E [resistance of extracellular water (ECW)], R_I [resistance of intracellular water (ICW)] and Cm (whole body capacitance). The volume of ECW is calculated from R_E, body height, body weight and k_ECW (a variable empirically scaled with a correction factor of body geometry), resistivity of ECW and body density. Then, the volume of ICW is determined based on the Hanai mixture theory (1) . In humans, Ht² · Cm/ICW [the product of the square of body height (Ht) and capacitance (Cm) divided by ICW] is an indicator of cell membrane porosity and thickness (1) .

Daniel and Waisman (5) found that excessive amounts of sulfur amino acids (SAA) dose-dependently depressed growth; 10 g L-methionine (MET)/kg diet had a slight growth-depressing effect. In a previous study, we also found decreased body weight of rats fed 10 g kg-MET/kg diet (6) . Although excessive dietary SAA depress body weight, the effect of SAA on body composition is not clear.

Excessive MET and homocysteine are potentially atherogenic (7) . Homocysteine is produced from MET in the body. Because homocysteine is remethylated into MET or converted into cysteine via the transsulfuration pathway, homocysteine concentrations in the body are maintained at lower levels than other amino acids. Dietary MET overload increases plasma homocysteine in humans (8) and induces endothelial damage (9) , vascular dysfunction (10) and atherosclerotic morphology of arteries (11 ,12) in experimental animals.

Homocysteine and biological thiols can attack cell membranes through several modalities, i.e., direct protein binding, inhibition of protein repair and lipid and protein peroxidation. Homocysteine and cysteine are biological thiols that bind to the cellular proteins via cysteine residues (13 ,14) . Homocysteine, cysteine and mercaptoethanol damage the cell wall of yeast cells and increase the cell wall porosity (15 ,16) . Protein methylation is a key process of enzymatic repair of protein damaged by spontaneous deamidation, isomerization and racemization (17) . Perna et al. (18) found that hyperhomocysteinemia reduced membrane protein methylation in patients with chronic renal failure. Ventura et al. (19) revealed that hyperhomocysteinemia during MET oral loading increased plasma markers of lipid and protein peroxidation in humans.

Vitamin B-6 is involved in many steps of the transsulfuration pathway and cysteine catabolism (20) . Nielsen et al. (21) found that dietary nickel (Ni) deprivation enhanced alterations in trace element metabolism associating with vitamin B-12 deficiency. Uthus and Poellot (22) found that Ni deprivation increased plasma MET and that it exacerbated an increase in urinary N-formimino-L-glutamic acid excretion by folate deficiency (23) . They proposed an involvement of Ni in the MET cycling and hence in homocysteine metabolism (22) .

Because vitamin B-12 is involved in SAA metabolism, other research determined whether responses to changes in other nutrients involved in SAA (and vitamin B-12) metabolism would be affected by dietary Ni. The response of dietary Ni to both folic acid deprivation and vitamin B-6 deprivation was similar to the response to vitamin B-12 deprivation (6 ,21 22 23) . These findings suggested that Ni has a function that is related to a change caused by the lack of each of these three vitamins; an alteration in SAA metabolism is one possibility. Because of these findings, we hypothesized that Ni has a function that is markedly affected by changes in SAA status.

If dietary MET and homocystine (HCY) loading and vitamin B-6 and Ni deprivation can affect cell membranes in the whole body, the whole body capacitance corrected for body length and ICW may be altered. If dietary SAA can affect the cardiovascular and renal function, body water distribution may be altered. Thus, this experiment was designed to determine the effects of altering SAA metabolism (through dietary manipulation of SAA and vitamin B-6 status) and Ni deprivation on bioelectrical properties in rats by using BIS.

	MATERIALS AND METHODS

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Ninety-five weanling male Sprague-Dawley rats weighing 30–40 g (Charles River/SASCO, Wilmington, MA) were used. The rats were housed individually in plastic cages in a laminar flow rack; the room was maintained at 23°C and 47% relative humidity with a 12-h light/dark cycle. The rats were divided into the 12 groups of a 3 x 2 x 2 factorially arranged experiment. Rats had free access to food and deionized drinking water (Super Q; Millipore, Bedford, MA). Dietary factors were SAA: no supplemental SAA (NSAA), 10 g/kg DL-MET or 10 g/kg DL-HCY; pyridoxine hydrochloride (PN) (0 or 7.5 mg supplemental PN/kg); and Ni (0 or 1 mg supplemental Ni as Ni chloride/kg). The composition of the basal diet is shown in Table 1 .

Immediately after the collection of urine, bioimpedance was measured with a tetrapolar single-frequency (50 kHz, 800 µA current) analyzer (model 101; RJL Systems, Mt. Clemens, MI) and an impedance analyzer (Hydra ECF/ICF 4200; Xitron Technologies, San Diego, CA). Placement of the electrodes was that of Hall et al. (27) . Twenty-gauge stainless steel hypodermic needles bent at the tip to form a right angle were used as electrodes.

Rats were anesthetized with ether. Hair was removed from the dorsal surface of the head and body for electrode placement. The rats were placed in prone recumbency on a nonconductive surface to eliminate interference of electrical induction. Body orientation was standardized according to Hall et al. (27) . On the midline, source electrode 1 was placed at the anterior edge of the orbit, source electrode 2 was placed 4 cm from the base of the tail, detector electrode 1 was placed at the anterior opening of pinna and detector electrode 2 was placed at mid-pelvis of the rats.

The weight of the rats was recorded to the nearest 0.1 g. Body length was measured from the narium to the pelvic-caudal junction.

After 10 wk of treatment, blood was collected with a heparin-coated syringe from rats under ether anesthesia. Plasma cysteine and homocyst(e)ine were measured by HPLC (28) . The livers were collected, frozen in liquid nitrogen and stored at -70°C until analyses. Livers were homogenized with 0.25 mol sucrose/0.01 mol sodium phosphate per L buffer (pH 7.4). Liver alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were measured with commercial assay kits (Infinity ALT reagent and Infinity AST reagent; Sigma Chemical Co., St. Louis, MO). Protein concentration was measured with a Coomassie brilliant blue G binding method (29) .

Estimation of body composition variables.

Total body water weight (W_TBW, g) was estimated from the empirical formula of Hall et al. (27) :W_TBW = 15.47 + 97.44 L²/WBR, where L is body length (cm) and WBR is whole body resistance () from single-frequency bioimpedance measurements.

Total body solid (TBS, g) was calculated as body weight (g) minus W_TBW.

The ratio of ICW to ECW was estimated from the BIS data. The BIS data were fit to the Cole-Cole model, and R_E, R_I and Cm in the Cole-Cole model were estimated.

The ratio of ICW to ECW volume (V_ICW/V_ECW, mL/mL) was estimated by solving the following equation, which was derived by De Lorenzo et al. (1) on the basis of the Hanai mixture theory:

(1)

where k = (_ICW/_ECW), the ratio of resistivity of ICW to ECW; R_E is the value from the Cole-Cole model fitting (); and R_I is the value from the Cole-Cole model fitting ().

Using the V_ICW/V_ECW ratio, ^{eq. 1} can be rewritten as

(2)

where Q is the V_ICW/V_ECW ratio.

^{Equation 2} can be solved through an iterative procedure for the value of Q without information on body geometry. The k was set at 3.60 based on human data (1) because the corresponding data for rats were unavailable. The values for k are 3.82 for men and 3.40 for women.

De Lorenzo et al. (1) scaled _ICW, _ECW and k based on the dilution study in humans (1) . Hence, k was scaled to the mole amount of water rather than the physical volume of fluid. Therefore, ICW and ECW weights were calculated as follows:

where W_ICW is ICW weight (g), and W_ECW is ECW weight (g).

Because the urinary excretion rate of creatinine is proportional to the skeletal muscle mass in rats as well as in humans (30) , the following equation is given:

where E is the excretion rate of urinary creatinine (µmol/h), c is the excretion rate constant from muscle mass [µmol/(h · g)] and M is muscle cell mass (g).

Muscle cell mass is the composite of the W_ICW (W_m) and solid weight (S_m) in muscle. The following equation is derived:

where p_mw is the proportion of muscle cell water in the ICW, p_ms is the proportion of muscle cell solid in the TBS and S is TBS.

Based on the above equations, both ICW and TBS, but not ECW, are expected to be independent variables for urinary creatinine excretion. The c p_mw and c p_ms values are empirically determined as regression coefficients of multiple regression for the urinary creatinine excretion rate (E) on W_ICW and TBS (S). Then, the ICW content in muscle cells (C_mw) is derived as follows:

(3)

Data were statistically analyzed by using the simple correlation analysis, multiple regression analysis, ANOVA and Dunnett’s simultaneous multiple comparison test found in the statistical package SYSTAT version 5 (Systat, Evanston, IL).

	RESULTS

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BIS measurements of body compositions.

The physical characteristics and the bioimpedance data are shown in Table 2 . The water content of the whole body was 61.3 g/100 g. ICW and ECW occupied 70.6 and 29.4% of TBW, respectively. The correlation coefficient between ICW and TBW was larger than that between ECW and TBW (0.977 versus 0.923, P < 0.001).

Table 4 shows the result of multiple regression analysis for urinary creatinine excretion rate (E) using ICW, ECW, TBS, UV (urine flow rate - 0.83), and UV² (square of UV) as independent variables. The contributions of ECW and the intercept were not significant. The partial correlation coefficient between urinary creatinine excretion rate and ECW was markedly smaller than the simple correlation coefficient, after both urinary creatinine excretion rate and ECW were adjusted for ICW, TBS, UV and UV².

where W_ICW is the ICW weight (g) and S is TBS (g).

Therefore, the estimated c p_mw was 0.0498 µmol/(h · g) and the estimated c p_ms was 0.0283 µmol/h/g. The mean estimated water content of muscle cells from ^{eq. 3} was 66.5 g/100 g with a SD of 3.7 g/100 g.

Status of SAA and vitamin B-6 of rats.

The main effect of SAA on plasma homocyst(e)ine was significant (Table 6 ). Mean plasma homocyst(e)ine was 6.42, 5.95 and 9.55 µmol/L for rats fed NSAA, MET and HCY, respectively. The plasma homocyst(e)ine concentration of HCY-fed rats was significantly higher than in rats fed NSAA (P = 0.0001). The main effect of SAA on urinary inorganic sulfate excretion was significant. Mean urinary inorganic sulfate excretion was 10.5, 18.2 and 19.2 µmol/h for rats fed NSAA, MET and HCY, respectively. The urinary inorganic sulfate excretion of MET- and HCY-fed rats was significantly higher than rats fed NSAA (P = 0.0001). Plasma cysteine concentration was not affected by dietary treatments (data not shown).

Liver ALT activity was 271 and 319 U/g protein for rats fed no supplemental PN and those fed supplemental PN, respectively. No significant effect of dietary treatments was found in the liver AST activity (data not shown).

SAA and body composition.

The main effect of SAA on TBW was significant (Table 7 ). Mean TBW was 200, 187 and 194 g for rats fed NSAA, MET and HCY, respectively. That of MET-fed rats was significantly lower than that of rats fed NSAA (P = 0.003).

The main effects of SAA on the ICW/ECW ratio, ICW, ECW and the ECW/TBW ratio were significant. The ICW was 140, 132 and 138 g for rats fed NSAA, MET and HCY, respectively. The ICW of MET-fed rats was significantly lower than that of rats fed NSAA (P = 0.004). The ECW was 59.4, 55.1 and 56.1 g for rats fed NSAA, MET and HCY, respectively. ECW of MET-fed rats and HCY-fed rats were significantly lower than that of rats fed NSAA (P = 0.009 and P = 0.040, respectively). The ICW/ECW ratio was 2.37, 2.40 and 2.48 for rats fed NSAA, MET and HCY, respectively. The ICW/ECW ratio of HCY-fed rats was significantly higher than that of rats fed NSAA (P = 0.010). The ECW/TBW ratio was 0.297, 0.295 and 0.288 for rats fed NSAA, MET and HCY, respectively. The ECW/TBW ratio of HCY-fed rats was significantly lower than that of rats fed NSAA (P = 0.009).

The main effect of SAA on L² · Cm, a product of squared L (body length) and Cm (whole body capacitance) was significant. The L² · Cm was 1352, 1179 and 1238 cm² · nF for rats fed NSAA, MET and HCY, respectively. The L² · Cm of MET- and HCY-fed rats was significantly lower than that of rats fed NSAA (P = 0.001 and P = 0.026, respectively). The main effect of SAA on L² · Cm/ICW was significant. The L² · Cm/ICW ratio was 9.62, 8.93 and 8.91 cm² · nF/g for rats fed NSAA, MET and HCY, respectively. The L² · Cm/ICW ratio of MET- and HCY-fed rats was significantly lower than rats with NSAA (P = 0.016 and P = 0.012, respectively). The L² · Cm/ICW ratio was 8.90 and 9.41 cm² · nF/g for rats fed no supplemental PN and those fed supplemental PN, respectively.

Dietary treatments did not affect other variablers, i.e., body weight, body length, whole body water content, and muscle cell water content.

	DISCUSSION

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BIS measurements of body compositions.

BIS is promising as a method for assessing rat body composition including the ICW/ECW ratio because it is rapid and easy to use with minimum disturbance to the rats. For the calculation of the ICW to ECW ratio, no parameters related to the body geometry and the resistivities of intracellular and extracellular fluids are used. The only assumed constant in ^{eq. 2} is the k term. Although the k for rats is not available, the k is purely a scaler and has no significant effect on correlations or comparisons among groups (1) . We made the assumption that the k derived for humans is sufficient for testing hypotheses in animal experiments. The k was scaled to the body fluid volumes measured by the in vivo dilution study (1) . Therefore, the body fluid volumes defined were actually an indicator of the mole amount of water (H₂O) but not the physical volume of the fluids (1) , although the mole amount of water and the physical volume of the fluids are highly correlated. The ratio of ICW to ECW found in this study (2.42) was similar to the reported values by Lyons and Riedesel (31) , who found 181.8 mL of intracellular fluid and 63.3 mL of extracellular fluid and hence an intracellular to extracellular fluid ratio of 2.87 in 5 male Sprague-Dawley rats with mean body weight of 362 g. They measured TBW volume by in vivo dilution of ³H₂O and extracellular fluid volume by in vivo dilution of ¹⁴C-inulin by using the measurement of radioactivity in plasma. Therefore, the TBW volume and the extracellular fluid volume were defined as a plasma equivalent volume or a proportional scale to the molar amount of water rather than a "true" physical volume of liquid in the Hanai mixture theory.

Hall et al. (27) determined the empirical formula to predict TBW from body length and whole body resistance measured at 50 kHz. They measured TBW by direct chemical analysis, i.e., body weight (g) minus whole body dry matter (g). In this study, ICW and ECW were estimated from TBW and ICW/ECW ratio. To validate the method, the theoretical relationship between urinary creatinine excretion and body compartments was tested. A linear relationship between urinary excretion rate of creatinine and skeletal muscle mass has been established in humans. Rikimaru et al. (30) found a similar relationship in rats. If the proportion of muscular intracellular fluid in the whole body ICW and the proportion of muscular solid in the TBS are relatively invariate in the rats studied here, multiple regression analysis can detect ICW and TBS but not ECW as significant explanatory variables for urinary excretion of creatinine. Multiple regression analysis revealed the expected results. However, the high correlation of urinary creatinine with ICW and TBS may depend on the fact that body metrics of rats were relatively invariate in this study. Hence the above results demonstrate that ICW and TBS will not always be found as explanatory variables for urinary creatinine excretion when heterogeneous populations are tested. Body proportions are expected to be significantly affected by some conditions, i.e., sexual difference, growth, severe malnutrition, obesity, endocrinopathy, etc.

Based on the regression coefficients for ICW and TIS in the multiple regression using urinary creatinine excretion as a dependent variable, the ICW content in muscle cells was estimated to be 66.5 g/100 g. This figure was higher than the whole body water content (61.3 g/100 g). According to Burton (32) , the solute concentration in erythrocytes is about 360 g/L. The conversion factor from molal concentration to molar concentration is 0.72 at the indicated concentration. Hence, the water content in erythrocytes becomes 66.7 g/100 g. Ciesler et al. (33) reported 0.755 mL/g wet total water content and 0.124 mL/g wet extracellular inulin space in skeletal muscle of rats. Assuming the specific gravity of muscle is 1.08, water content of muscle cells is calculated to be 66.0 g/100 g. Our indirect estimation of water content in muscle cells is close to these values.

Status of SAA and vitamin B-6 of rats.

Compared to NSAA, both dietary MET and HCY similarly increased urinary excretion of inorganic sulfate, a major final catabolite of SAA, suggesting that dietary SSA supplementation significantly burdened the SAA catabolic pathway.

TBS was slightly but significantly decreased in rats fed diets containing no supplemental PN; urinary excretion of 4-PA was decreased in these rats. Liver ALT activity, which is dependent on vitamin B-6, of the rats fed no supplemental PN was approximately 85% of those fed supplemental PN; however, no effect of PN was found in liver AST. Therefore, the rats fed no supplemental PN were considered to be marginal in vitamin B-6 nutriture.

SAA and body composition.

Although significant effects of SAA were not observed for body weight and TBW, SAA significantly affected ICW, ECW, ICW/ECW and ECW/TBW, which were measured by BIS. MET significantly decreased TBW, ICW and ECW compared with values in rats fed NSAA. These results suggest that MET decreases ECW and ICW proportionally. In contrast, HCY decreased only ECW.

The major part of the body’s capacitance is derived from the cell membrane (34) . With cell death or cell destruction, the cell membrane loses its high resistive properties, and the capacitance decreases (1 ,35) . In humans, Ht² · Cm/ICW (the product of the square of body height (Ht) and capacitance (Cm) divided by ICW) is an index of cell membrane porosity and thickness (1) . In this study, the body length (L) of rats was used in place of body height of humans to obtain L² · Cm/ICW. Supplemental MET and HCY and dietary vitamin B-6 deprivation decreased L² · Cm/ICW, suggesting an increased cell membrane porosity and/or a decreased cell membrane thickness. Biriuzova et al. (15) found an increased cell wall porosity of Candida utilis (Torula yeast) cells treated by cysteine and homocysteine, not by MET. Because their exposure time for the yeast was up to 4 h and the yeast is monocellular organism, the conversion of MET to homocysteine or cysteine and the secretion of these thiol amino acids into the medium are negligible. In the rats of this experiment, both dietary MET and HCY were presumably catabolized through the transsulfuration pathway via cysteine. The changes of bioelectric properties in HCY-fed rats might be the result of direct exposure to the increased circulating homocysteine and/or through the metabolic changes in the whole body. There was no evidence of increased circulating thiol amino acids in MET-fed rats. The changes in bioelectric properties in MET-fed rats could be secondary to the metabolic changes due to MET in the whole body, although the mechanism is not clear.

In conclusion, we have shown that BIS is a versatile measure to assess body compartments in rats. Excessive SAA may increase cell membrane porosity through cell membrane damage. Dietary HCY may affect body water distribution.

	ACKNOWLEDGMENTS

 
The authors thank LuAnn K. Johnson for statistical analysis; Clint B. Hall, Rhonda A. Poellot, Eugene Korynta, Kim K. Baurichter and Thomas J. Zimmerman for their excellent technical assistance; Jim Lindlauf and Karin Tweton for rat diet preparation and Denice Schafer and her staff for the care of the rats.

	FOOTNOTES

 
¹ Supported by a grant from the Nickel Producers Environmental Research Association (NiPERA).

² The U.S. Department of Agriculture, Agricultural Research Service, Northern Plains Area, is an equal opportunity/affirmative action employer and all agency services are available without discrimination.

³ Mention of a trademark or proprietary product does not constitute a guarantee or warranty of the product by the U.S. Department of Agriculture and does not imply its approval to the exclusion of the products that may also be suitable.

⁴ Presented in part at Experimental Biology 2000, San Diego, CA, April 15–18, 2000 [Yokoi, K., Hall, C. B., Lukaski, H. C., Uthus, E. O. & Nielsen, F. H. (2000) Estimation of body water by impedance spectroscopy (BIS) in rats fed methionine or homocystine. FASEB J. 14: A497].

⁶ Abbreviations used: ALT, alanine aminotransferase; AST, aspartate aminotransferase; BIS, bioimpedance spectroscopy; ECW, extracellular water; HCY, homocystine; ICW, intracellular water; MET, methionine; Ni, nickel; NSAA, no sulfur amino acids; 4-PA, 4-pyridoxic acid; PN, pyridoxine hydrochloride; SAA, sulfur amino acid; TBS, total body solid; TBW, total body water.

Manuscript received October 2, 2000. Initial review completed October 28, 2000. Revision accepted January 3, 2001.

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