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靈芝對糖尿病患者降血糖之輔助治療

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(1)

2 0 1 0

2 . 5 2 4

( 95% ) 2

( UKPDS )

2

4 6 3000 mg

1 2 ( HbA1C )

4 ( p<0.01 )

-0.2 0.3 mg/dl.h 4 5 42.1 mg/dl.h ( p<0.05 )

( 180 mg/dl H b A1C 8% )

H b A1C ( p<0.01 )

2

H b A1C

2 ( Type 2 diabetes )

( )

( HbA

1

C )

( Fasting blood glucose )

( Postprandial blood glucose )

(2)

2

3(The Diabetes Control and Complications Tr i a l )

4( United Kingdom Prospective Diabetes Study )

U K P D S

6 4 4 %

4

5

6

7 - 9

2

5 0 2

( )

8 1 5 0 - 2 5 0

m g / d l

( )

3

2 ( 500 mg )

1 2

5 0 4

( 1 ) ( 1 )

( 2 ) 4 4 6

1 2

4 6 2 3 ( 12 11

p- v a l u e

2 3 2 3 -

( / ) 1 2 / 11 1 2 / 11 -

( years ) 6 . 5 0 . 8 8 . 5 1 . 2 0 . 2 2 1

( years ) 5 8 . 6 2 . 3 6 1 . 8 2 . 4 0 . 3 8 6

( kgs ) 6 5 . 5 2 . 7 6 5 . 9 2 . 6 0 . 7 8 3

( kg/m2 ) 2 6 . 5 1 . 0 2 5 . 3 0 . 7 0 . 9 11

FPG ( mg/dl) 1 8 0 . 1 6 . 5 1 8 4 . 7 3 . 2 0 . 4 1 5

2h PC ( mg/dl) 2 8 2 . 9 8 . 5 2 6 4 . 6 4 . 7 0 . 1 2 5

H b A1C ( %) 8 . 2 1 . 3 8 . 5 1 . 4 0 . 4 0 1

( mmHg ) 1 2 7 . 3 2 . 9 1 3 1 . 1 3 . 6 0 . 4 6 6

( mmHg ) 7 4 . 2 2 . 0 7 5 . 6 1 . 9 0 . 4 6 1

S u l f o n y l u r e a 1 3 1 4 0 . 9 8 8

M e t f o r m i n 2 3 0 . 8 3 6

S u l f o n y l u r e a M e t f o r m i n 8 6 0.838

Student's t-test F P G

2h PC 2

H b A1C

(3)

) 2 3 ( 12 11 )

( body mass index ) 2

( )

( Ganoderma tsugae ) t r i t e r-

penoids nucleosid p o l y s a c c h a r i d e f i n g e r p r i n t ( Ganoderma lucidum )

E D TA 1 0

2000 xg 1 5 - 7 0

H b A1C e n z y m a t i c

m e t h o d s 1 0

( Meal Tolerance Test ) 2 ( 30Kcal/kg/day )

(

1 / 5 5 5 %

3 0 % 15% )

1 2 3 4

SPSS 8.0

t - t e s t

paired Student t -t est

4 8 1 2

A

B (

180 mg/dl 180 mg/dl )

F P G H b A1C Glu cose Area 2h PC

B e f o r e A f t e r 1 B e f o r e A f t e r 2

FPG ( mg/dl ) 1 8 0 . 1 6 . 5 1 8 0 . 9 8 . 1 0 . 8 0 . 2 1 8 4 . 7 3 5 . 2 1 8 7 . 9 4 9 3 . 2 3 . 1

HbA1C ( % ) 8 . 2 1 . 3 7 . 9 0 . 6 - 0 . 3 0 . 1 8 . 5 1 . 4 8 . 5 1 . 7 0 . 1 0 . 2

Glucose Area ( mg/dl.h ) 8 9 7 . 3 3 7 . 7 8 9 7 . 1 3 8 . 2 - 0 . 2 0 . 3 9 0 1 . 1 3 4 . 4 9 4 6 . 5 5 6 . 3 4 5 . 0 4 2 . 1

2h PC ( mg/dl ) 2 8 2 . 9 8 . 5 2 9 2 . 7 1 4 . 0 9 . 8 8 . 1 2 6 4 . 8 4 . 7 2 8 0 . 5 11 . 0 1 6 . 1 7.8

p 0 . 0 5 p 0 . 0 5

F P G

B

A

(4)

4 8

1 2 ( A )

( 180 mg/dl 180 mg/dl )

1 8 0

m g / d l 4

( B )

( -0.2 0.3, 45 42.1 mg/dl.h p<0.05 )

( )

( 180 mg/dl

180 mg/dl 2 250 mg/dl 2 5 0

m g / d l 9 0 0

m g / d l . h 9 0 0

m g / d l . h H b A1C 8 % 8% ) ( ) F P G 180 mg/dl

F P G ( -3.3 8.4, 7.7

8.3 mg/dl p<0.05 ) F P G 1 8 0

m g / d l

2

P C 250 mg/dl 250 mg/dl

900 mg/ dl.h

1 4 6 . 2 42.1 mg/dl.h 7 0 . 0 16.4 mg/dl.h p 0 . 0 1

900 mg/ dl. h

H b A1C 8 %

H b A1C - 0 . 6 0 . 3 0 . 4

0 . 3 % p < 0 . 0 1 8 %

H b A1C

( )

2 ( HbA1C 8 % 8% )

1 2 6 5 . 4 5 1. 7 m g/ d l 2 7 1 . 9 42.4 mg/ dl 2 3 4

F P G 2h PC Glu cose Area H b A1C ( )

FPG ( mg/dl )

1 8 0 1 2 - 3 . 3 8 . 4 7 . 7 8 . 3

1 8 0 11 1 4 . 1 9 . 0 1 4 . 7 9 . 5

2h PC ( mg/dl )

2 5 0 1 2 9 . 8 8 . 1 1 6 . 1 7 . 8

2 5 0 11 3 1 . 4 8 . 6 3 0 . 0 8 . 1

Glucose Area ( mg/dl.h )

9 0 0 1 2 - 1 4 6 . 2 4 2 . 1 7 0 . 0 1 6 . 4

9 0 0 11 9 0 . 2 2 6 . 1 9 0 . 0 2 6 . 0

H b A1C ( % )

8 % 1 2 - 0 . 6 0 . 3 0 . 4 0 . 3

8 % 11 0 . 5 0 . 2 0 . 6 0.4

Student's t-test p 0 . 0 5 p 0 . 0 1

F P G

2h PC 2

H b A1C

(5)

( p 0.01 )

( 1 2 3 4 )

H b A1C

( )

1 2 4

4

1 2

4

1 0

1 5

Monnier

H b A1C

1 6 1 7

"DECODE"

2 1 8

1 9

2 0

1 8 0

m g / d l 4

8 1 2

1 2

8 % 900 mg/dl.h

1 8 0 m g / d l ( HbA1C 8% )

Type I error ( H b A1C

8 % 8% )

(6)

1.Jervell J. Type II Diabetes (NIDDM) can be prevented. IDF Bulletin 1997; 42: 1-3.

2.Tseng CH, Tseng CP, Chong CK, et al. Increasing incidence of diagnosed type 2 diabetes in Taiwan: analysis of data from a na- tional cohort. Diabetologia 2006 49: 1755-60.

3.Eisenberg DM, Kessler RC, Foster C, Norlock FE, Calkins DR, Dellbanco TL. Unconventional medicine in the United States.

N Engl J Med 1993; 328: 246-52.

4.Matthews DR, Cull CA, Stratton IM, Holman RR, Turner RC.

Sulphonylurea failure in non-insulin-dependent diabetic pa- tients over six years .UK Prospective Diabetes Study (UKPDS) Group. Diabet Med 1998 ; 15: 297-303.

5.Garrow D, Egede LE. National patterns and correlates of com- plementary and alternative medicine use in adults with diabetes.

J Altern Complement Med 2006; 12: 895-902.

6.Bell RA, Suerken CK, Grzywacz JG , Lang W, Quandt SA, Arcury TA. Complementary and alternative medicine use among adults with diabetes in the United States. Altern Ther Health Med 2006; 12: 16-22.

7.Min BS, Gao JJ, Nakamura N, and Hattori M. Triperpenes from the spores of Ganoderma lucidum and their cytotoxicity against Meth-A and LLC tumor cells. Chem Pharm Bull 2000; 48: 1026- 33.

8.Shiao MS. Natural products of the medical fungus Ganoderma lucidum: occurrence, biological activities, and pharmacological functions. Chemical Record 2003; 3: 172-80.

9.Zhabg HN, He JH, Yuan L, Lin ZB. In vitro and in vivo protec- tive effect of Ganoderma lucidum polysaccharides on alloxan- induced pancreatic islets damage Life Sci 2003; 73: 2307-19.

10.Kadish AH, Litle RC, Sternberg JC. A new and rapid method for the determination of glucose by measurement of rate of oxy- gen consumption. Clin Chem 1968; 14: 116-31.

11.Hikino H, Ishiyama M, Suzuki Y, and Konno C. Mechanisms of hypoglycemic activity of ganoderan B: glycan of Ganoderma lucidum fruit bodies. Planta Med 1989; 55: 423-8.

12.Hikino H, Konno C, Mirin Y, Hayashi T. Isolation and hypo- glycem ic ac tivity of G anodera ns A a nd B , G lycans of Ganoderma lucidum fruit bodies1. Planta Med 1985; 51: 339- 40.

13.Kino K, Mizumoto K, Sone T, et al. An immunomodulating pro- tein, Ling Zhi-8 (LZ-8) prevents insulitis in non-obese diabetic mice. Diabetologia 1990; 33: 713-8.

14.Zhang HN, Lin ZB. Hypoglycemic effect of Ganoderma lucidum polysaccharides. Acta Pharmacol Sin 2004; 25: 191-5.

15. Kimura Y, Okuda H , A ric hi S. Effects of the extracts of Ganoderma lucidum on blood glucose level in rats. Planta Med 1988; 54: 290-4.

16.Monnier L, Lapinski H, Colette C. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of type 2 diabetic patients: variations with in- creasing levels of HbA(1c). Diabetes Care 2003; 26: 881-5.

17.Monnier L, Colette C, Dunseath GJ, Owens DR. The loss of postprandial glycemic control precedes stepwise deterioration of fasting with worsening diabetes. Diabetes Care 2007; 30: 263- 9.

18.Anonymous. Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria.

The DECODE study group. European Diabetes Epidemiology Group. Diabetes epidemiology : collaborative analysis of diag- nostic criteria in Europe. Lancet 1999; 354: 617-21.

19.Ceriello A, Davidson J, Hanefeld M, et al. International Prandial Glucose Regulation Study Group. Postprandial hyperglycaemia and cardiovascular complications of diabetes: an update. Nutr Metab Cardiovasc Dis 2006; 16: 453-6.

20.Hanefeld M, Temelkova KT. The postprandial state and the risk of atherosclerosis. Diabetic Medicine 1997; 14: S6-11.

(7)

on Metabolic Control in Type 2 Diabetes Subjects

- -- A Double Blinded Placebo Control Study

Chen-Wen Wang, Johannes Scheng-Ming Tschen , and Wayne Huey-Herng Sheu1

Diabetes mellitus has become one of leading causes of death worldwide. Owing to progressive deteriora- tion of current available hypoglycemic agents, Ganoderma lucidum , one of the most widely used herbs, was re- ported to lower blood glucose level in animal studies. We therefore undertook a clinical study to investigate the effect of Ganoderma lucidum on blood glucose control in subjects with type 2 diabetes mellitus. We conducted a double-blind, placebo-controlled trial in which 46 patients completed the trial. Subjects were randomized to take dry extract of Ganoderma lucidum 3000 mg or placebo in addition to regular oral hypoglycemic agents for a pe- riod of 12 weeks. As a group, no differences were found in values of fasting glucose, HbA1c before versus after treatment both in placebo and Ganoderma lucidum groups. However, plasma glucose under the curve during meal tolerance test reduced more significantly in those of taking Ganoderma lucidum than those taking placebo (p 0.01, 2-way ANOVA). In those subjects with poor glycemic control (fasting glucose 180 mg/dl, A1c 8.0%), treatment by Ganoderma lucidum revealed a greater reduction in values of fasting glucose (p 0.05) and glucose area under cruve (p 0.01). Results of this study suggest that Ganoderma lucidum might play some role in providing postprandial glucose lowering as supplementary therapy in treating subjects with type 2 diabetes mellitus. ( J Intern Med Taiwan 2008; 19: 54- 60 )

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