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Guar gum improves insulin sensitivity, blood lipids,

blood pressure, and fibrinolysis in healthy men13


Kerstin Landin, G#{246}ranHolm, Lilian Tengborn, and U/f Smith

ABSTRACT A double-blind, placebo-controlled, cross-over The aim of the present study was to investigate the effect of
study was carried out in 25 healthy, nonobese middle-aged men guar on blood pressure, lipid and glucose metabolism, and fi-
to test the effect of guar gum on glucose and lipid metabolism, brinolytic variables in nonobese, healthy, middle-aged men in
blood pressure, and fibrinolysis. Ten grams guar or placebo a randomized, double-blind, placebo-controlled cross-over study
granulate was given three times a day for 6 wk with a 2-wk run- with run-in and wash-out periods.
in before and a wash-out period after. Decreases in fasting blood
glucose (P < 0.001), cholesterol (P < 0.001), triglycerides (P
< 0.05), plasminogen activator inhibitor-l activity (P < 0.01), Subjects and methods
systolic blood pressure (P < 0.01), and diastolic blood pressure
Twenty-five healthy, nonobese men aged 52.0 ± 5.2 (1 ± SD)

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(P < 0.00 1 ) were seen during guar treatment when compared
y with body mass index 24.6 ± 1.6 (in kg/m2) and waist-hip
with placebo. Insulin sensitivity, measured with the euglycemic-
ratio (WHR) 0.9 1 ± 0.02, were recruited with an advertisement
clamp technique, increased (P < 0.0 1 ). adipose tissue-glucose
in the local newspaper (Table 1). Six men were smokers. None
uptake measured in vitro increased (P <0.001), and 24-h urinary
were receiving medical treatment. All worked full-time and none
excretion ofsodium and potassium increased (P < 0.001) during
exercised regularly. The study was approved by the Ethical
guar treatment. Fasting plasma insulin, renin, aldosterone, and
Committee of the University of Goteborg and all participants
fibrinogen concentrations as well as skeletal-muscle electrolytes,
gave their informed consent.
urinary catecholamines, and body weight remained unaltered.
These findings support a role for guar in the treatment of the
Study design
metabolic syndrome in which insulin resistance seems to play
a pivotal role. Am J C/in Nutr 1992;56: 106 1-5. The study was double-blind and placebo-controlled. All sub-
jects participated in a 2-wk run-in period without treatment.
They were randomly assigned to a regimen of either placebo or
KEY WORDS Guar, glucose, insulin, cholesterol, blood guar gum for 6 wk followed by a 2-wk wash-out period to mm-
pressure, fibrinolysis imize carry-over effects. This was followed by another 6 wk of
placebo or guar, respectively.
Introduction Ten grams granulated guar or granulated gelling starch of
similar appearance (Culinar, Fjelkinge, Sweden) was given in a
Elevated blood pressure and blood lipids, and impaired glucose glass of water, 3 times a day before meals. Guar is a highly
viscous gel-forming galactomannan polysaccharide from the
tolerance are established risk factors for cardiovascular disease
(1 , 2). These abnormalities are often present in the same mdi- cluster bean (14).
vidual and commonly associated with obesity (3). It has been The subjects were asked not to alter their regular diet and
physical-activity habits during the entire study period. A 3-d
postulated that insulin resistance may be a common denomi-
nator in the pathogenesis ofboth lipid and glucose disturbances dietary recall was taken before and during the last 3 d of the
second treatment period with reference to the Swedish National
and, possibly, hypertension (4, 5). Both genetic and environ-
Food Administration’s food composition tables (1 5).
mental factors such as diet and physical activity seem to play a
role in the development ofthese disturbances. Intake was 12095 ± 984 kJ (2950 ± 240 kcal) (460 ± 55 g
Diet and weight reduction regimens are often difficult for pa- carbohydrate, 90 ± 1 1 g fat, 1 5 ± 4 g protein, 98 ± 22 mmol
tients to comply with. Therefore, supplementing the diet with
fiber such as guar gum, has been tested in healthy subjects (6),
I From the Department ofMedicine, Sahlgrenska Hospital, University
overweight individuals (7), hypertensive subjects (8), hypercho-
of Goteborg, Goteborg, Sweden.
lesterolemic women (9), and type I (10) and type II diabetic 2 Supported by Nordisk Insulinfond, the Swedish Nutrition Foundation
patients (1 1-1 3). Guar gum decreased glucose and lipid con-
(51K) and Goteborg Medical Society.
centrations, and reduced body weight and blood pressure in these 3 Address reprint requests to K Landin, Department of Medicine II,
studies. However, controlled guar gum studies in nonobese in- Sahlgrenska Hospital, 5-413 45 G#{246}teborg,Sweden.
dividuals are sparse, as are studies ofthe effect ofguar on blood Received January 30, 1992.
pressure and fibrinolysis. Accepted for publication July 9, 1992.

Am J C/in Nuir l992;56:l061-5. Printed in USA. © 1992 American Society for Clinical Nutrition I061
1062 LANDIN ET AL

TABLE I Serum aldosterone was determined by using a commercially


Anthropometric data for healthy men during a double-blind, available radioimmunoassay kit from International CIS (Paris,
placebo-controlled, guar-gum France).
Fibrinogen was analyzed by a syneresis method (20) with ye-
Placebo Guar
nous blood drawn into tubes containing trisodium citrate and
Age (y) 52.0 ± 5.2 - &arninocaproic acid. Samples for assay of plasminogen-activator
Height (cm) 178.1 ± 4.0 - inhibitor (PAl-i) activity were drawn into tubes containing tri-
Weight (kg) 78.5 ± 6.8 78.2 ± 6.9 sodium citrate and measured by using the reagent Spectrolyse
Body mass indext 24.6 ± 1.6 24.6 ± 1.7 (Biopool, Ume#{227},Sweden).
Lean body mass (kg) 61.5 ± 5.5 -

Body fat(kg) 19.1 ± 5.7 - G/ucose-c/amp technique


WHRt 0.91 ± 0.02 0.91 ± 0.02
A hyperinsulinemic, euglycemic glucose clamp was performed
to measure insulin action according to the method described by
5.±SD:n= 25.
DeFronzo et al (2 1). The insulin-infusion rate was 86 pmol - kg
t In kg/m2.
j: WHR. waist-hip circumference ratio. body wt . min ‘ which gave mean plasma insulin concentra-
tions of 1 5 14 ± 25 1 pmol/L on both occasions. The clamp lasted
for 2 h and the glucose-disposal rate was calculated from the
steady-state glucose-infusion rate during the last 30 mm. The
sodium, and 87 ± 25 mmol potassium) per person per day before
glucose disposal-rate was expressed as mg glucose - kglean body
the study and 1 1787 ± 1087 kJ (2875 ± 265 kcal) (445 ± 63 g
mass’ - min’.
carbohydrate, 92 ± 12 g fat, 14 ± 5 g protein, 95 ± 27 mmol
sodium and 83 ± 27 mmol potassium) per person per day at Urinalysis
the end of the second treatment period (fiber intake not in-

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Urine was collected for 24 h to analyze adrenaline and nor-
eluded).
adrenaline excretion. The hormone concentrations were deter-
Body weight and blood pressure were measured and blood
mined with a fluororneter that used an adsorption technique
samples were collected at entry to the study and after 3 and 6 with aluminum oxide (22). The results were expressed in nmol
wk in each treatment period. A hyperinsulinemic, euglycernic
per period. Urine was also collected for 24 h for sodium, po-
glucose clamp, urinalysis, and skeletal muscle and fat biopsies
tassium, and creatinine excretion, which were measured
were performed after each treatment period. with a flame photometer (FLM 3; Radiometer, Copenhagen,
Denmark).
A nthropomnetrr
Ske/eta/-mnuscie e/ectrolvtes
Body weight and height were measured in the fasting state
with the subject in underwear and without shoes. Waist circurn- Muscle needle biopsies were performed under local anesthesia
ference was measured with a soft tape midway between the lowest (1% Carbocaine, Astra, S#{246}dert#{228}lje,
Sweden) in the left femoral
rib margin and the iliac crest in the standing position. The hip vastus lateralis muscle. The muscle biopsy sample, 10-20 mg
circumference was measured over the widest part ofthe gluteal wet wt, was rapidly freeze dried, after which blood, connective
region and the waist-hip circumference ratio (WHR) was cal- tissue, and fat were carefully removed. The biopsy sample was
culated (16). reweighed, and potassium, sodium, and magnesium were mea-
Potassiurn-40 was measured in a whole-body counter (17) sured with an atomic absorption spectrophotometer (HGA-87B;
(Nuclear Enterprise Ltd. Edinburgh, UK) and lean body mass Perkin Elmer, Beaconsfield, UK) as reported in detail previously
calculated according to Forbes et al ( 18) where 1 kg tissue con- (23). The results are expressed as mmol/g fat-free dry weight
tains 68. 1 mrnol potassium. Body fat was calculated by sub- and are the mean values of duplicate samples. The coefficient
tracting lean body mass from total body weight. of variation was 4.4% for potassium, 4.2% for magnesium and
12.3% for sodium. The reproducibility and mean values are in
B/ood pressure accordance with previous studies (23-26).
Blood pressure was expressed as the mean of three measure- G/ucose transport in isolated adipocytes
ments to the nearest 2 mm Hg on the right arm, after a 10-mm
After subjects fasted overnight, a subcutaneous fat needle bi-
rest. Disappearance of Korotkoff sounds (phase V) was used to
opsy (to 300 mg) was obtained under local anesthesia (1% Car-
determine diastolic pressure, with random zero blood pressure
bocaine) from the abdominal region lateral to the umbilicus.
machine (Hawksley and Sons, Lancing, UK) (19).
Care was taken not to infiltrate the tissue to be excised with the
local anesthetic agent. Isolated fat cells were prepared (27) and
B/ood chemistry
incubated for 60 mm in Medium 199 (Statens Bakteriologiska
Venous blood samples were drawn, after an overnight fast, Laboratorium, Stockholm, Sweden) containing 50 moI/L
from an antecubital vein and analyzed for glucose with the glu- [U4C] glucose and 1% albumin. Basal and maximally insulin-
cose-oxidase method (Kabi, Stockholm, Sweden) and for insulin stimulated (7 175 pmol/L) glucose uptake was measured. The
with a radioimrnunoassay technique, by using a Phadebas insulin glucose-transport rate was calculated from the amount of glucose
kit (Pharmacia, Uppsala. Stockholm). Cholesterol and triglyc- cleared and expressed as fL . cell ‘ . sec .

erides were determined enzyrnatically (Boehringer Mannheim,


Mannheim, Germany). Plasma renin activity was analyzed Statistics
with a radioimmunoassay technique (Abbott, Wiesbaden- Mean values, SDs, and linear regressions were calculated with
Delkenheim, Germany) after a 30-mm rest in the supine position. conventional methods. Differences in results between placebo
mmHg
GUAR TREATMENT IN HEALTHY SUBJECTS 1063

150

Wash out Systolic


140

130

90
Diastolic

5*5 55*

80

-2 -1 0 3 6 i 2W..k.

FIG 1. Systolic and diastolic blood pressure during placebo and guar
treatment, respectively: n = 25. Differences between the two treatment FIG 2. Mean 24-h urine excretion ofsodium, potassium, and creatinine
periods are shown. . ± SE. 55P < 0.01, 555P < 0.001. during placebo and guar treatment in healthy men: n = 25. Differences
between treatments are shown. . ± SD. 555P < 0.001.

and guar treatment were calculated with Student’s paired t test


(28). P values < 0.05 were considered statistically significant. fibrinogen concentration was unchanged after guar treatment as
compared with placebo (Table 2). Plasma renin activity was 1.0
± 0.6 ng- mL . h and plasma aldosterone was 0.35 ± 0.07
Results

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nmol/L after both placebo and guar treatment.
Urine sodium excretion increased by 27 ± 1 1 mmol/24 h (P
Body weight and WHR were unchanged during both the guar < 0.00 1) and potassium increased 1 1 ± 7 rnmol/24 h (P < 0.001)
and placebo treatments (Table 1). The 3-d diet recalls at the after guar treatment compared with placebo (Fig 2). However,
beginning and at the end ofthe study showed no changes in the the urine sodium-potassium ratio was unaltered after guar treat-
intake of major nutrients. ment. The urine excretion ofadrenaline and noradrenaline was
Systolic blood pressure decreased 5 ± 6 mm Hg (P < 0.001) unaffected by guar treatment. Urinary creatinine indicated re-
and diastolic decreased 3 ± 2 mm Hg (P < 0.001), respectively, liable urine sampling on both occasions (Fig 2).
after 3 wk of guar treatment and 6 ± 9 mm Hg (P < 0.01) and The skeletal muscle sodium, potassium, sodium-potassium
3 ± 2 mm Hg (P < 0.001), respectively, after 6 wk of guar ratio, and magnesium content were unchanged throughout the
treatment for the treatment group compared with the placebo study. Basal glucose uptake by abdominal fat cells increased by
group (Fig I).
2.6 ± 1 .5 fL . cell ‘ - sec ‘ (P < 0.001) and maximally stimulated
Fasting blood glucose decreased 0.3 ± 0.2 mmol/L (P <0.001) glucose uptake increased by 2.9 ± 3.0 if. - cell . (P < 0.01)
after guar treatment whereas fasting plasma insulin was un- after guar (Table 3). There were no correlations between increase
changed. However, the mean insulin values were low, 57 ± 14 ofglucose-disposal rate and decrease in mean blood pressure or
prnol/L after both treatments. Glucose disposal, measured with excretion rate of electrolytes and blood pressure reduction, re-
the euglycemic-clamp technique, increased 1.2 ± 1.2 mg . kg
spectively.
lean body mass . min (P < 0.01). Serum cholesterol decreased Remaining guar or placebo granulate from all subjects after
0.6 ± 0.3 mmol/L (P < 0.00 1) and serum triglycerides 0.2 ± 0.6 each period was weighed and indicated that the prescribed
mrnol/L (P < 0.05) after guar treatment compared with placebo.
PAI-l activity decreased 2.9 ± 4.9 mU/L (P < 0.01) whereas

TABLE 3
Skeletal muscle electrolytes and fat-cell glucose transport during
TABLE 2 placebo and guar treatment in 25 healthy
Metabolic and fibrinolytic data during placebo and guar treatment
in 25 healthy 5 Placebo Guar P level

Placebo Guar P level Skeletal muscle sodium


(mmol/g dry weight)t 0.15 ± 0.04 0.15 ± 0.04 NS
Glucose (mmol/L) 4.8 ± 0.4 4.5 ± 0.5 < 0.00 1 Skeletal muscle potassium
Insulin (pmol/L) 57 ± 14 57 ± 14 NS (mmol/g dry weight)t 0.38 ± 0.03 0.38 ± 0.03 NS
Glucose disposal mg . kg Skeletal muscle magnesium
LBM . min t 13.9 ± 2.8 15.0 ± 2.4 < 0.01 (mmol/g dry weight)t 0.04 ± 0.004 0.04 ± 0.004 NS
Cholesterol (mmol/L) 5.5 ± 0.8 5.1 ± 0.9 < 0.001 Fat-cell transport rate
Triglycerides (mmol/L) 1.3 ± 0.8 1.1 ± 0.7 < 0.05 (fI.cell’ .sec)
Fibrinogen (gIL) 2.4 ± 0.5 2.3 ± 0.6 NS Basal medium 25.2 ± 10.6 27.7 ± 15.7 < 0.00 1
PAI-l activity (U/mL)f 14.5 ± 8.2 12.1 ± 6.1 < 0.01 + insulin (7175 pmol/L)[ 49.8 ± 19.8 52.6 ± 9.6 < 0.01

S g ± SD. S SD.
t LBM, lean body mass. t Values were measured per 100 g dry weight.
4: PAl-I. plasminogen-activator inhibitor. :: Basal medium with insulin added.
I064 LANDIN ET AL

amount had been consumed. Compliance expressed as the pressure was raised when subjects switched back to their usual
amount of guar gum consumed was similar in both periods. diet.
Four ofthe 25 men reported increased flatulence and soft stools It is still an open question whether insulin sensitivity or the
2-3 times per day during the guar treatment period. None refused effect ofinsulin on blood pressure is regulated through increased
to continue the study because of this. renal sodium reabsorption (36), increased sympathetic nerve ac-
tivity (37). or by other hormonal or vasoactive mechanisms.
However, a previous study showed (38) that enhanced insulin
Discussion
sensitivity by metformin treatment improved the metabolic risk-
Supplementary guar gum increased the effect of insulin and factor profile, fibrinolytic activity. as well as blood pressure in
lowered the glucose and lipid concentrations, as well as PAI-l nonobese, untreated hypertensive subjects. Thus, insulin resis-
activity and blood pressure with unaltered body weight in these tance seems to have preceded hypertension in these subjects. It
healthy. nonobese men in this study. Guar gum increases the is also obvious that many cardiovascular risk factors may be
gastric-emptying time and reduces the rate ofglucose absorption present in the same individual. Another controlled study (39)
in the small intestine (29-3 1). These effects probably play a role showed beneficial effects on blood glucose and lipid concentra-
in improved insulin sensitivity and lowered blood lipids, although tions by metformin as well as by guar gum in type II diabetics.
the mechanisms are not clear. The increased glucose-disposal It was recently demonstrated that nonobese hypertensive in-
rate probably reflects enhanced glucose utilization in the skeletal dividuals are not only more insulin resistant and have higher
muscles. However, the present study shows that glucose uptake blood lipid concentrations, but that they also have higher fi-
was also increased in adipose tissue during guar treatment. Sur- brinogen concentrations and PAI-l activity (40). Guar gum
prisingly, fasting insulin concentrations were unaffected by guar lowered the PAI-l activity in the present study, indicating a
treatment in spite of the increased effects in at least two major beneficial effect of guar gum on both atherogenic and throm-
organs. This may be because the insulin concentrations were bogenic factors. PAl-I activity correlates strongly with insulin

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already low in these individuals and, thus, it may be difficult to concentrations and degree ofinsulin resistance (40). An increase
detect a further reduction. Unfortunately, no measurements were in glucose uptake may decrease PAl- 1 activity, suggesting an
performed in connection with meals when more clear differences important regulatory role ofinsulin. Previous studies ofthe effect
may have been seen. A number ofstudies have shown decreased of dietary fiber on PAl- 1 activity have not been consistently
insulin concentrations during guar treatment. both in the fasting favorable (4 1). PAI-l activity is, however, lower in subjects con-
and postprandial states. in insulin-resistant conditions suming large amounts of vegetables and fruits (42).
(6-9. 12. 13). Guar gum among other fiber analogs, has been considered
Guar gum also had slight effects on blood pressure. Whether highly effective in decreasing postprandial hyperglycemia, body
this is a direct effect ofthe guar gum or an effect mediated through weight, cholesterol concentrations, and blood pressure in obese
increased insulin sensitivity is not known. In a previous study and diabetic subjects (6-1 3). Increased insulin sensitivity may
(8) guar gum decreased both blood pressure and urinary excretion increase the lipoprotein lipase activity and a reduction of lipo-
ofsodium and potassium in obese, hypertensive subjects. In the proteins and bile acids may be an effect of the guar gum (43).
present study with lean, normotensive subjects. however, sodium The viscosity ofthe guar gum, which increases gastric-emptying
and potassium excretion increased. This might be explained by time and prolongs the intestinal-absorption phase of fat, car-
a direct effect ofguar gum on sodium absorption or by increased bohydrates, and sodium without inducing malabsorption, seems
excretion (32). Increased excretion could be anticipated because to be the cornerstone of its efficacy (29-3 1, 44). Highly viscous
of increased insulin sensitivity and lower postprandial insulin or gel-forming fibers also increase satiety, possibly leading to
concentrations. leading to decreased sodium reabsorption in the weight reduction in obesity (7, 9).
renal tubuli. Electrolyte excretion did not seem to be mediated These findings support a role for guar gum in the treatment
by changes in plasma aldosterone or renin concentrations be- ofthe metabolic syndrome (4). Increased insulin sensitivity could
cause these hormone concentrations were unaltered. Also, no beneficially influence the various risk factors for cardiovascular
changes were seen in catecholamine excretion. disease seen in that syndrome. B
Blood pressure is to some extent volume dependent (33. 34).
We thank Sven Lindstedt, Department ofClinical Chemistry. for per-
However, even if the increased electrolyte excretion supported
forming the lipid assays, and Gunilla Nilsson, Kerstin Ahlkvist, Elisabeth
a loss of osmotically active ions, body weight remained un-
Ericson, Christine Berglof-Iornbratt. and Kaisa Torstensson for their
changed in these subjects. Furthermore, the skeletal muscle technical assistance.
electrolytes were unaffected, indicating an unaltered intracellular
cation homeostasis, which should not have been the case if a
reduction of the extracellular water had occurred. Previous References
studies ofskeletal muscle electrolytes showed an increased muscle
sodium and decreased muscle potassium content in obese sub- 1. Kannel WB, Gordon T, Castelli WP. Obesity. lipids. and glucose
jects (23. 24). Weight reduction improved the muscle potassium intolerance. The Framingham study. Am I Clin Nutr 1979:32:1238-
45.
content, supporting the concept that decreased extracellular vol-
2. Wilhelmsen L, Wedel H. Tibblin G. Multivariate analysis of risk
ume was partly responsible for the weight reduction (25). How-
factors for coronary heart disease. Circulation 1973:48:950-8.
ever, hypertension in nonobese subjects was not associated with
3. Modan M. Halkin H, Almog S. et al. Hyperinsulinemia. A link
any change in skeletal muscle electrolytes (26).
between hypertension. obesity and glucose intolerance. I Clin Invest
A previous controlled study (35) showed 3-5% reductions in 1985:75:809-17.
both systolic and diastolic blood pressure in hypertensive mdi- 4. Reaven GM. Role of insulin resistance in human disease. Diabetes
viduals after increasing their dietary-fiber intake for 6 wk. Blood I988:37:1595-607.
GUAR TREATMENT IN HEALTHY SUBJECTS 1065

5. Ferraninni E, Buzzigoli
G. Bonadonna R. et al. Insulin resistance 26. Landin K, Lindghrde F. Saltin B. Smith U. The skeletal muscle Na/
in essential N Engl I Med 1987:317:350-7.
hypertension. K-ratio is not increased in hypertension. Evidence for the importance
6. Jenkins DIA, Leeds AR, Gassull MA, Cochet B, Alberti KGMM. ofobesity and glucose intolerance. I Hypertens 199 1:9:65-9.
Decrease in postprandial insulin and glucose concentrations by guar 27. Smith U, Sj#{246}str#{246}m
L. Bjorntorp P. Comparison oftwo methods for
and pectin. Ann Intern Med 1977:86:20-3. determining human adipose cell size. I Lipid Res 1972:13:822-4.
7. Krotkiewski M. Effect ofguar gum on body-weight. hunger ratings
28. Colton T. Statistics in medicine. Boston: Little. Brown and Company,
and metabolism in obese subjects. Br J Nutr 1984:52:97-105.
1974.
8. Krotkiewski M. Effect of guar gum on the arterial blood pressure.
29. lenkins DIA, Wolever TMS, Leeds AR, et al. Dietary fibres, fibre
Acta Med Scand 1987:222:43-9.
analogues. and glucose tolerance: importance of viscosity. Br Med
9. Tuomilehto I. Voutilainen E, Huttunen I, Vinni 5, Homan K. Effect
I 1978:1:1392-4.
ofguar gum on body weight and serum lipids in hypercholesterolemic
30. Blackburn NA, Redfern IS. Jarjis H. et al. The mechanism of action
females. Acta Med Scand 1980:208:45-8.
10. Ebeling P. Yki-I#{228}rvinen H, Aro A. Helve E, Sinisalo M, Koivisto ofguar gum in improving glucose tolerance in man. Clin Sci I 984:66:
VA. Glucose and lipid metabolism and insulin sensitivity in type 1 329-36.

diabetes: the effect ofguar gum. Am I Clin Nutr 1988:48:98-103. 3 1 . Meyer JH, Doty JE. GI transit and absorption ofsolid food: multiple
1 1. Peterson DB, Ellis PR. Baylis IM. et al. Low dose guar in a novel effects ofguar. Am I Clin Nutr 1988:48:267-73.
food product: improved metabolic control in non-insulin-dependent 32. Karanja N, McCarron DA. Effects ofdietary carbohydrates on blood
diabetes. Diabetic Med 1987:4:1 11-5. pressure. Prog Biochem Pharmacol 1986:21:248-65.
I 2. Smith U. HoIm G. Effect of a modified guar gum preparation on 33. Tobian L Jr. Binlon IT. Tissue cations and water in arterial hyper-
glucose and lipid levels in diabetics and healthy volunteers. Athero- tension. Circulation 1952:5:724-58.
sclerosis 1982:45:1-10. 34. Hilton P1. Cellular sodium transport in essential hypertension. N
13. Uusitupa M, Tuomilehto I. Karttunen P. WolfE. Long term effects EngI I Med 1986:314:222-9.
of guar gum on metabolic control. serum cholesterol and blood 35. Rouse IL, Beilin U. Armstrong BK, Vandongen R. Blood-pressure-
pressure levels in type 2 (non-insulin-dependent) diabetic patients lowering effect ofa vegetarian diet: controlled trial in normotensive
with high blood pressure. Ann Clin Res 1984:16:126-3 1.

Downloaded from www.ajcn.org by on July 25, 2007


subjects. Lancet 1983:1:5-10.
14. Van Soest P1. Dietary fibers: their definition and nutritional prop-
36. DeFronzo RA, Cooke CR. Andres R, Faloona GR, Davis P1. The
erties. Am I Clin Nutr 1978:31:512-520.
effect of insulin on renal handling of sodium, potassium, calcium,
1 5. National Food Administration. Statens Livsmedelsverk. Energi och
and phosphate in man. I Clin Invest 1975:55:845-55.
N#{228}rings#{228}mnen.Stockholm: Liber Tryck AB. 1986.
16. Krotkiewski M. Bjorntorp P. Sj#{246}str#{246}m
L, Smith U. Impact of obesity 37. Landsberg L, Young lB. Fasting. feeding and regulation ofthe sym-
on metabolism in men and women. Importance ofregional adipose pathetic nervous system. N EngI I Med 1978:298:1295-1301.
tissue distribution. I Clin Invest 1983:72:1 150-62. 38. Landin K, Tengborn L. Smith U. Treating insulin resistance in hy-
I 7. SkOldborn H, Arvidsson B, Andersson M. A new whole body mon- pertension with metformin reduces both blood pressure and meta-
itoring laboratory. Acta Radiol 1972:(suppl 313):S233-4l. bolic risk factors. I Intern Med 1991:229:181-7.
18. Forbes GB, Gallup I. Hursh lB. Estimation of total body fat from 39. Lalor BC, Bhatnagar D, Winocour PH, et al. Placebo-controlled
potassium-40 content. Science I 961:133:101-2. trial of the effects of guar gum and metformin on fasting blood
19. Maxwell MH. Waks AU, Schroth PC, Karam M, Dornfeld LP. Error glucose and serum lipids in obese. Type 2 diabetic patients. Diabetic
in blood-pressure measurement due to incorrect cuff size in obese Med 1990:7:242-5.
patients. Lancet 1982:2:33-6. 40. Landin K, Tengborn L, Smith U. Elevated fibrinogen and plasmin-
20. Nilsson IM, Olow B. Determination of fibrinogen and fibrinogen- ogen activator inhibitor (PAl- 1) in hypertension are related to met-
olytic activity. Thromb Diath Haemorrh 1962:8:297-3 10. abolic risk factors for cardiovascular disease. I Intern Med 1990:227:
21. DeFronzo RA. Tobin ID. Andres R. Glucose clamp technique: a 273-8.
method for quantifying insulin secretion and resistance. Am I Physiol 4 1 . Sundell I. Nilsson TK, Hallmans G, Nygren C. The effect of body
1979:237:E214-23.
build, diet and endocrine factors on the extrinsic fibrinolytic system
22. von Euler US, Lishajko F. The estimation ofcatecholamines in urine.
in healthy young women. Scand I Clin Lab Invest 1988:48:557-64.
Acta Physiol Scand 1959:45:122-32.
42. Nilsson TK. Sundell I. Hellsten G. Hallmans G. Reduced plasmin-
23. Landin K. Lindg#{228}rdeF. Saltin B, Wilhelmsen L. Decreased skeletal
ogen activator inhibitor activity in high consumers of fruits. vege-
muscle potassium in obesity. Acta Med Scand 1988:223:507-13.
24. Landin K, Lindg#{228}rdeF. Saltin B, Wilhelmsen L. Increased skeletal tables and root vegetables. I Intern Med 1990:227:267-71.
muscle Na/K-ratio in obese men, but not in women, with glucose 43. Turner PR. Tuomilehto I, Happonen P. La Ville AE. Shaikh M,
intolerance. I Intern Med 1989:225:89-94. Lewis B. Metabolic studies on the hypolipidaemic effect of guar
25. Landin K. Lindg#{228}rde F. Saltin B. Skeletal muscle potassium increases gum. Atherosclerosis 1990:81:145-50.
after diet and weight reduction in obese subjects with normal and 44. Leeds AR. Dietary fibre: mechanisms of action. Int I Obes
impaired glucose tolerance. Acta Endocrinol 1989:121:21-6. 1987:1 l(suppl l):3-7.

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