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	Recovery of Coronary Microangiopathy in Patients with Type 2 Diabetes
Ikuo Yokoyama M.D. a, Yusuke Inoue M.D. b, Toshiyuki Moritan M.D. c ,
 a Department of Cardiovascular Medicine, Clinical Research Center, Sanno Hospital of International University of Health and Welfare, Tokyo, Japan, b Department of Radiology, Institute of Medical Science, Graduate School of Medicine University of Tokyo, Tokyo, Japan, c Department of Clinical Engineering, Faculty of Medical Engineering, Suzuka University of Medical Science, Suzuka, Japan

Correspondence to: Dr Ikuo Yokoyama, Department of Cardiovascular Medicine, Sanno Hospital, International University of Health and Welfare 8-10-16 Akasaka, Minato-ku, Tokyo 107-0052, Japan
TEL: +81-3-3402-3151
FAX: +81-3-3402-3652
E-mail: yokochan-tky@umin.ac.jp

No conflict of interest exists in connection with this article.

Abstract 
Background: Hyperglycemia has been suggested as a significant factor in coronary microangiopathy in patients with type 2 diabetes (T2DM), but whether it can be reversed through treatment of hyperglycemia is still unknown.
Aim: To clarify whether glycemic control can improve coronary microangiopathy in T2DM. 
Methods: Subjects were 34 T2DM patients who underwent coronary angiography and 17 age-matched controls. Myocardial segments perfused by angiographically normal coronary arteries were studied. Baseline myocardial blood flow (MBF, ml/min/100g) and MBF during dipyridamole administration (0.56 mg/kg/min) were measured using positron emission tomography (PET). Myocardial flow reserve (MFR) was calculated by the ratio of MBF during dipyridamole administration to the baseline MBF. After the first PET study, patients were subdivided into an additional intensive therapy group (ATG) and no-additional therapy (NATG) group. Second PET scan was performed 6 to 9 months later.
Results: Baseline MBF was comparable among the ATG (87.5� 24.1), NATG (87.2�16.9) and controls (78.2�33.3). However, MBF during dipyridamole administration was significantly lower in both the ATG (170�52.0) and NATG (192�52.6) than in controls (293�159, p<.01) as was the MFR (ATG,1.96�0.52; NATG, 2.27�0.63; controls, 3.69�1.09; p<.01 respectively). MFR was significantly improved in the ATG (2.51�.77; p<.05), but not in the NATG (2.14�0.69; p=ns). There was a significant inverse relationship between percent change in MFR and percent change in glycemic control. However, no significant relationships were seen between the percent change in MFR and percent change in plasma lipid fractions. 
Conclusion: Coronary microangiopathy in T2DM can be reversed by intensive therapy for hyperglycemia.

Key Words: Hyperglycemia, type-2 diabetes mellitus, flow reserve, coronary microangiopathy, positron emission tomography (PET), glucoseIntroduction
	Impaired myocardial perfusion, such as coronary microangiopathy, is an important pathophysiological feature of diabetes 1-2) and an important unresolved clinical question. 3) The importance of glycemic control in the development of atherosclerosis in patients with diabetes has been suggested. 4-10) Recently, we reported that myocardial flow reserve (MFR) was related to glycemic control rather than to the mode of therapy or to insulin resistance in patients with type 2 diabetes (T2DM). 11-12) In addition, reduced MFR in angiographycally normal coronary arteries in patients with T2DM was shown and such reduced MFR was shown to be related to glycemic control in patients with T2DM. 13) Such results have highly indicated that glycemic control is an essential factor for diabetic coronary microangipathy. However, it has not been clear if such coronary microangiopathy can be reversed or not?. We have now examined whether the reduced MFR in segments that were perfused by angiographically normal coronary arteries in patients with T2DM can be improved by the control of hyperglycemia.
Materials and Methods
Study population
	 General characteristics of study subjects: Thirty-four patients with T2DM with indications for coronary angiography (CAG), such as symptoms or signs of myocardial ischemia or coronary artery disease, were entered into the study. Patients with hypercholesterolemia (plasma total cholesterol e"232 mg/dl) and those with left ventricular hypertrophy (wall thickness e"13 mm) were excluded. Patients who had undergone coronary artery bypass operation or percutaneous coronary angioplasty were excluded. Patients with well-controlled essential hypertension using long-acting calcium antagonists (Cilnidipine 5-10 mg; Amlodipine, 2.5-5 mg/day), diuretics, any angiotensin converting enzyme inhibitor (enalapril, 5-10 mg/day; Lisinopril, 10-20 mg/day) and any angiotensin II receptor blocker (losartan, 25-50 mg/day; candesartan cilexetil, 4-8 mg/day; valsartan, 40-80 mg/day) or both were included. Seventeen (13 males, 4 females) normo-lipidemic, normo-glycemic asymptomatic age-matched individuals without a history of heart disease or chronic disease were selected as control subjects. Details of coronary angiographic findings of study patients are shown in Table 1. General characteristics of the study subjects are summarized in Table 2. There were no significant differences among the two groups in age, gender, body weight, height, body mass index, blood pressure at rest and during dipyridamole administration, heart rate at rest and during dipyridamole administration, and levels of plasma total cholesterol (TC), low density lipoprotein cholesterol (LDL), high density lipoprotein cholesterol (HDL) and triglycerides (TG). Fasting plasma glucose concentrations (FBS) and hemoglobin A1c values averaged for the previous 6 months from data gathered at regular clinic visits for diabetes were significantly higher in the T2DM patients than in control subjects. Data for control subjects were reviewed from records at local health service centers. Hemoglobin A1c was assayed by the latex aggregation method (normal range 4.3%-5.8%). Plasma fasting glucose concentration was measured after an overnight fast of greater than 12 hours. Plasma insulin concentrations were measured by radioimmunoassay (normal range under fasting was 3-18 m�U/ml). Participants were informed of the nature of the study before agreeing to take part in the study protocol, which was approved by the local Ethics Committee. 
	Subjects with T2DM:  T2DM was diagnosed according to the following criteria: FBS greater than 7.3 mmol/liter and hemoglobin A1c level greater than 6.5% before the initiation of therapy. All of these patients had undergone coronary angiography (CAG) and were proven to have one, two or three normal coronary arteries within the three major branches as diagnosed by three independent specialists (0% stenosis). Among the 34 patients with T2DM were 8 with well-controlled essential hypertension. These study subjects were not common to those used in our other recent publications. 11-17)
	 The 34 patients were subdivided into two groups. One group was treated with additional intensive treatment of hyperglycemia including insulin, acarbose, poglybose and troglitazone and the other T2DM patients were not treated with additional therapy. Patient profiles and therapies are shown in Table 3. 
 	Control subjects: In all 17 control subjects, the resting electrocardiogram was normal. All potential control subjects underwent a symptom-limited treadmill test and those with typical chest pain or abnormal electrocardiogram indicating myocardial ischemia were excluded. Cardiac normality was not confirmed by CAG; however, since these subjects were selected among those with a low probability of cardiac disease they can be considered to be appropriate as normal control subjects as reported by Rozanski et al. 18) Due to the difficulty of recruiting normal control subjects for studies using positron emission tomography (PET), all but two of these control subjects were those used for our other studies. 11-17)  
PET
	Regional baseline myocardial blood flow (MBF) and that during dipyridamole administration were measured using PET and 13N-ammonia. Twenty-four hours before PET, we stopped all medications and caffeine intake. For all patients, follow-up PET study was performed 6 to 9 months after the first study.
	 Myocardial flow images were obtained using a Headtome IV scanner (Shimadzu Corp., Kyoto, Japan). This scanner has seven imaging planes; in-plane resolution is 4.5 mm at full width at half maximum and the z-axial resolution is 9.5 mm at full width at half maximum. Effective in-plane resolution is 7 mm after using a smoothing filter. The sensitivities of the Headtome IV scanners are 14 and 24 kilo counts per sec (�Ci/ml) for direct and cross planes, respectively.
	After acquiring transmission data to correct for photon attenuation prior to obtaining images, 15-20 mCi of 13N-ammonia was injected and dynamic PET was performed for 2 min and static scan for 8 min. After waiting 45 min to allow for decay of the radioactivity of 13N ammonia, dipyridamole (0.56 mg/kg) was administrated intravenously. Five min after dipyridamole administration, 15-20 mCi of 13N-ammonia was injected and, exactly at the same time, a second dynamic scan was performed for 2 min and a static scan for 8 min. The dynamic scan was performed every 15 sec (8 times) during the 2-min period and dynamic data were obtained for seven slices. Only one channel electrocardiographic monitoring in limb leads was made during the scan.
Determination of myocardial blood flow (MBF) and myocardial flow reserve (MFR)
	Regional MBF was calculated basically according to the two-compartment 13N-ammonia tracer kinetic model. 19-20) This model has been well validated 19-20) and has been used frequently in the studies of MFR. 11-17) 21-22) Metabolites of 13N-ammonia can be negligible during the first 90 sec after infusion of 13N-ammonia. 23) The time activity curve of the left ventricular cavity was used as an input function. Tracer spillover was corrected by least square nonlinear regression analysis on our program to calculate the MBF with the assumption that both myocardial and left ventricular radioactivity were influenced by each other. Details were given in our recent papers. 12-15)
	All data were corrected for dead time effects to reduce error to less than 1%. To avoid the influence of the partial volume effect associated with the object's size, recovery coefficients obtained from experimental phantom studies in our laboratory were used. The recovery coefficient was 0.8 when myocardial wall thickness was 10 mm. For correction of the partial volume effect, wall thickness was measured with two dimensional echocardiography by specialists in our hospital. The recovery coefficients were taken into consideration in our program to measure MBF.
	To determine MBF, regions of interest were placed on the transaxial images manually. Only myocardial segments which were perfused by anatomically normal coronary arteries were selected in this study. Those segments which were perfused by coronary arteries after percutaneous transluminal angioplasty or coronary artery bypass grafting were excluded. As has been reported previously, 11-15) each transaxial image was divided into 8 segments. Segments for the mid to mid-lower septum, upper septum, anterior wall on the mid-ventricular transaxial slice and mid to mid-lower septum, upper septum, and anterior wall on the lower slice were defined as the left descending coronary artery region. Segments for the lateral wall (mid-upper, mid-lower) on the middle slice and lateral wall on the lower slice were defined as the left circumflex coronary artery region. Segments for the lower septum and lower lateral wall on the middle slice and lower septum and lower lateral wall on the lower slice were defined as the right coronary artery region. When there was not enough space to place a region of interest on the right coronary arterial region visually, those segments were excluded. To obtain input function, small regions of interest were placed on the left ventricular cavity of each slice. Averages of the regional MBF corresponding to the same target coronary artery were used for this study. We then determined the MFR as follows:
MFR = regional MBF during dipyridamole administration/regional baseline MBF
Statistics
	Baseline MBF, MBF during dipyridamole loading, MFR, body weight, systolic blood pressure, diastolic blood pressure, height, body mass index and lipid parameters in the two groups were compared using analysis of variance, and then individual data were analyzed by the two-tailed unpaired t-test.  Wilcoxon signed-rank test was used to determine whether each therapy was effective for the improvement in MFR. Spearman rank order correlation coefficient analysis was used to determine the relationship between percent change in FBS and percent change in MFR. Values are expressed as the mean� standard deviation. 
RESULTS
Hemodynamic and electrocardiographic responses to dipyridamole administration
	There were no significant differences in systolic blood pressure at rest and during dipyridamole administration and rate pressure product between T2DM and control subjects (Table 2). During dipyridamole administration, typical chest pain or chest oppression accompanied by electrocardiographic changes were observed in 17 study patients. Due to difficulty in recording the radiolucent electrocardiogram in the precordial leads during PET, a detailed description of electrocardiographic response to dipyridamole was not possible.
Baseline MBF and MBF during dipyridamole administration 
	Baseline MBF (ml /min /100 g) was comparable among T2DM (86.8�22.3 ml /min /100 g) and control subjects (78.2�33.3 ml /min /100 g). However, MBF during dipyridamole administration was significantly lower in those with T2DM (188�60.4 ml /min /100 g) than in control subjects (293�159 ml /min /100 g, p<.01). 
MFR
	MFR was significantly lower in all 34 patients with T2DM (2.12�.58) than in control subjects (3.69�1.09, unpaired t test: p<.01). 
Effect of anti-hyperglycemic therapy on MBF and MFR
	After randomization, additional medications were introduced. In these patients, the MFR significantly improved (pre 1.96�.52 vs. post 2.51�.77, p<.05, Figure 1 on the left) as was the MBF during dipyridamole administration (pre 170�52.0 ml/min/100 g vs. post 224�56.5 ml/min/100 g, p<.05). However, baseline MBF did not change significantly (pre 87.5�24.1 vs. post 94.7�32.3). In these 17 patients, the hemoglobin A1c value was significantly reduced, (8.06�1.38% vs. 7.08�1.03% p<0.01) as were the FBS (188�44.8 mg/ dl vs. 151�33.0 mg/dl) and TC (188�36.2 mg/dl vs. 170�30.2 mg/dl, p<.05). LDL tended to be reduced (119�26.0 mg/dl vs. 102�26.9 mg/dl, p<0.1). On the other hand, HDL (39.2�8.72 mg/dl vs. 41.6�11.5 mg/dl), TG (151�78.9 mg/dl vs. 133�54.8 mg/dl) and blood pressures (systolic pressure, 132�30.6 mmHg vs. 130�28.9 mmHg; diastolic pressure, 79.9�7.18 vs. 78.3�7.01 mmHg) did not significantly change.
	In 17 patients for whom additional therapy was not given, MFR did not significantly change (pre 2.27�.63 vs. post 2.14�.69, p=ns (Figure 1 on the right) nor did baseline MBF (pre 87.2�16.9 vs. post 89.5�32.0). MBF during dipyridamole administration tended to be reduced (pre 192�52.6 vs. post 164�43.7). Values for hemoglobin A1c, (pre 7.7�1.2% vs. post 7.6�1.0%), FBS (pre 176�81.4 mg/dl vs. post 169�48.7 mg/dl) and plasma lipid fractions (TC, pre 188�31.8 mg/dl vs, post 187�37.5 mg/dl; HDL, pre 46.5�9.49 mg/dl vs. post 46.1�13.2 mg/dl; TG, pre 173�134 mg/dl vs. post 135�60.4 mg/dl; LDL, pre 107�22.6 mg/dl vs. post 115�28.9 mg/dl) and blood pressures (systolic pressure, pre 129�29.0 mmHg vs. post 131�25.1 mmHg; diastolic pressure, pre 78.6�7.03 mmHg vs. post 77.6�6.87 mmHg) were comparable between the first and second PET study. 
There were significant inverse relationships between the percent change in MFR and the percent change in FBS (r=-.54, p<0.01, Figure 1) as well as hemoglobin A1c. (r=-.54, p<0.01, Figure 2) However, there was no significant relationship between the percent change in MFR and percent change in plasma lipid fractions. Spearman rank order correlation coefficient analysis also showed that there were significant inverse relationships between the percent change in MFR and percent change in FBS (r=-.56, p<0.01) as well as hemoglobin A1c. (r=-.61, p<0.01) 
DISCUSSION
Reduced MFR in diabetes
	It has been recognized that MFR is inversely correlated with the severity of coronary stenosis. 24) However, contrary to that well-known general concept, it has been shown that MFR can be reduced without overt coronary stenosis or without evidence of ischaemia in the presence of a variety of coronary risk factors. 2-3, 11-16) 25-26) Improvement in MFR after therapy for coronary risk factors, including hyperlipidemia 17, 27-28) and hypertension, 26) has been reported. However, prior to our present study, there have been no reports of investigations as to whether the MFR in diabetic individuals can be improved by improvements in hyperglycemia. The present study, which addressed this issue, showed just such an effect. Several factors could contribute to the reduced MFR in T2DM, including coronary microangiopathy, 2-3) endothelial dysfunction, 2) an abnormal smooth muscle cellular mutation associated with atherosclerosis and angiographically undetectable balanced diffuse atherosclerosis. 29) Since we studied reduced MFR in myocardial segments which were perfused by angiographycally normal coronary arteries, coronary microangiopathy is an essential factor for the reduced MFR in our study subjects with T2DM. Thus, ineffective glycemic control, which would contribute to such microvascular damage, could be a major factor in the reduced MFR. However, improvement in glycemic control would improve MFR and, in turn, be reflected by an additional improvement in other factors such as myocardial vasodilatation and diffuse macrovascular balanced atherosclerosis.
	Lipid disorders 14-16) 25) have been shown to reduce MFR. In the present study, plasma TC was significantly reduced and plasma LDL cholesterol values showed a tendency toward worsening in patients to whom intensive therapy for hyperglycemia was introduced. Meaning It may therefore be considered that a reduction in lipid fractions would be a factor in the improvement of MFR in T2DM patients for whom additional therapy for glycemic control was introduced. However, there were no significant relationships between the percent change in the MFR and the percent change in plasma lipid fractions. The change in lipid parameters in MFR can be thought to be secondary to the improvement in hyperglycemia. 
Glycemic control and reduced MFR in myocardial segments which were perfused by anatomically normal coronary arteries in patients with T2DM
	A relationship between hyperglycemia and diabetic vascular complications 4-10) 30) has been shown as well as a relationship between glycemic control and MFR in T2DM. 11-13) Our current study showed an improvement in MFR in all 17 patients who received intensified treatment with additional medications, whereas a tendency toward the worsening of MFR was seen in patients who were not provided this additional treatment. There was a significant relationship between percent change in control of hyperglycemia and percent change in MFR. In support of our recent report that hyperglycemia rather than insulin resistance is related to the reduced MFR in T2DM, 12) our current results confirm the concept that glycemic control is the most essential factor for diabetic microangiopathy in these patients. However, in the strict sense of the word, it remains uncertain whether improvement in MFR can be explained by the coronary microvascular vasodilatory function or coronary microvascular structural changes or both. Minor contribution of macrovascular vasodilatory dysfunction should also be considered. Although MFR improved after successful anti-glycemic therapy, MFR remained significantly lower than that of control subjects. In general, it can be supposed that damage to the myocardial vascular structure due to a reduction in the microvascular bed could not easily be reversed 2) and that a longer period of time and more stringent control of hyperglycemia may be required for such a reversal. Therefore, the effect of anti-hyperglycemic therapy in MFR should be thought to examine in relation to the reduced MFR in T2DM over a much longer period of time.
Conclusions 
	Reduced MFR in angiographically normal coronary arteries in T2DM can be reversed by an improvement in glycemic control.
References
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2. Nahser, PJ Jr, Brown, RE, Oskarsson, H, Winnifold, MD, Rossen, JD: Maximal coronary flow reserve and metabolic coronary vasodilation in patients with diabetes mellitus. Circulation 1995;91: 635-40.
3.  HYPERLINK "http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Camici%20PG%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus" Camici PG, HYPERLINK "http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Crea%20F%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus" Crea F. Coronary microvascular dysfunction. HYPERLINK "javascript:AL_get(this, 'jour', 'N Engl J Med.');" N Engl J Med. 2007 22;356:830-40
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12. Yokoyama I, Ohtake T, Momomura S et al: Hyperglycemia rather than insulin resistance is related to coronary flow reserve in patients with non-insulin dependent diabetes mellitus. Diabetes 1998;47:119-124.
13 Yokoyama I., Yonekura K, Ohtake T et al : Coronary Microangiopathy in type 2 Diabetic Patients: Relation to Glycemic Control, Sex and Microvascular Angina Rather Than to Coronary Artery Disease. J Nucl Med 41:978-85 2000
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16. Yokoyama I, Ohtake T, Momomura S et al: Reduced myocardial vasodilatation in hyperiglyceridemic patients without overt coronary stenosis. Arterioscl Thromb Vasc Biol 1998;18: 294-299. 
17. Yokoyama I, Momomura S, Ohtake T et al. Improvement of myocardial vasodilatation in hypelipidemics due to diffuse coronary arterosclerosis after lipid lowering therapy. Circulation 1999;100:117-22
18. Rozanski A, Diamond GA, Forrester JS, Berman DS, Morris D, Swan JC: Alternative referent standard for cardiac normality. Implication for diagnostic testing. Ann Intern Med 1984;101:164-171.
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21. Czernin J, Muller P, Chan S et al: Influence of age and hemodynamics on myocardial blood flow and flow reserve. Circulation 1993;88:62-69. 
22. Czernin J, Bernard RJ, Sun KT et al. Effect of cardiovascular conditioning and low fat diet on myocardial blood flow and flow reserve. Circulation 1995;92:197-204.
23. Schelbert HR, Phelps ME, Hoffman EJ, Huang SC, Selin CE, Kuhl DE: N-13 ammonia as an indicator of myocardial blood flow. Circulation 1981;63:1259-1272.
24. Gould KL, Lipscomb K: Effects of coronary stenoses on coronary flow reserve and resistance. Am J Cardiol 1974;34:48-55.
25. Dayanikli F, Grambow D, Muzil O, Mosca L, Rubenfire M, Schwaiger M: Early detection of abnormal coronary flow reserve in asymptomatic men at high risk for CAD using positron emission tomography. Circulation 1994;90: 808 - 817.
26. Motz W, Strauer BE: Improvement of coronary flow reserve after long-term therapy with enalapril. Hypertension 1996; 27:1031-8.
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28. Mellwig KP, Baller D, Gleichmann U et al; Improvement of coronary vasodilatation capacity through single LDL apheresis. Atherosclerosis  1998;139:173-8. 
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Figure legends

Figure 1. left. Plotted data of myocardial flow reserve (MFR) pre and post additional therapy 

Figure 1. right Plotted data of myocardial flow reserve (MFR) pre and post in patients who were not given additional therapy 

Figure 2. Significant relationship between % change in myocardial flow reserve (MFR) and % change in fasting plasma glucose concentration (FBS).

Figure 3. Significant relationship between % change in myocardial flow reserve (MFR) and % change in hemoglobin A1c.
Table 1. Coronary angiographic findings in study patients
							T2DM    
Coronary angiographic findings
	Zero vessel disease			20
		normal coronary arteries		20
	One vessel disease				8		
		LAD					4		
		LCX					2	
		RCA					2	
	Two vessel disease				6		
		LAD+LCX				0		
		LAD+RCA				3	
		LCX+RCA				3	
Number of patients with 				
	old myocardial infarction			3	
                  
T2DM: type 2 diabetes mellitus. LAD: left descending coronary artery, LCX: left circumflex coronary artery, RCA: right coronary artery.
Table 2. General characteristics of study subjects.
	      	Controls	T2DM (all)     
N (M / F)		17 (13 / 4)	 34 (27 / 7)
Age (year)		54.9�10.4	 62.1�6.1
BW (kg)		60.7�7.81	 65.2�9.22
HT (cm)		164�11.3	163�8.60
BMI	  		23.4�4.10	 24.5�2.76
SBP (Rest)		129�12.3	139�20.2
DBP (Rest)		76.8�7.34	 79.0�10.5
HR (Rest)		67.1�13.9	 65.2�10.8
RPP (Rest)		8892�1692	9067�1856
SBP (DP)		123�11.7	134�20.6
DBP (DP)		76.4�7.40	71.2�13.2
RPP (DP)		9564�1012  9673�1578
FBS(mmol/L) 	4.82�0.49   9.11�2.22 **
HBA1c (%)	 	5.51�0.23	8.30�1.40 **
TC (mmol/L)		5.01�0.56	4.77�.694
HDL (mmol/L) 	1.46�0.66	1.10�0.27
TG (mmol/L)		1.28�0.45	1.42�0.97
LDL (mmol/L) 	2.99�0.50	2.89�.89
FI (m�U / L)			-	7.29�6.32
Duration of diabetes (M)	-	132�88.5
                                                                                                                                                                                                                                                               N: number of study patients, M: male, F: female, T2DM: type 2 diabetes mellitus, BW: body weight, HT: height, DP: dipyridamole, RPP: rate pressure products, BMI: body mass index, SBP: systolic blood pressure, DBP: diastolic blood pressure, HbA1c: hemoglobin A1c (%), FBS: fasting plasma glucose concentration, TC: total cholesterol, HDL: high density lipoprotein cholesterol, TG: triglycerides, LDL: low density lipoprotein cholesterol. FI: plasma fasting insulin concentration. M; months, ** p<.01 vs controls.
Table 3. Data on MFR, glycemic control, and therapy in patients with T2DM who underwent PET perfusion studies 
0age sex 	Therapies
	    	 (pre / post)
1. 71  M	D&E / D&E
2. 52  F	D&E / A300 mg
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�}gd�ca$d�a$z|�����%�'�:�=�éĩ������'�(�3�4�5�6�8�9�;�<�>�?�A�D�E�F�������������������ϲ����������hB1�h~M�jh~M�Ujh�p0Ujh�p0B*Uph���h�p0h�p0OJQJh�p0B*OJQJo(ph���Uh�p0B*OJQJph���h�p0B*ph���!	 M	D&E / P 0.6 g
4. 58 M	D&E / SU
5. 60  M 	D&E / A 300 g
6. 68 M	 SU / In
7 55 M	D&E / D&E
8. 56 M	SU / In
9. 64 F	 D&E / A 300 mg
10. 62 F	 D&E/D&E
11. 68 M	SU/SU
12. 56 M	 SU/In
13. 69  M	 In / In
14. 57 M	 In / In
15. 66 F	 A 300mg/ A300mg
16. 64 F	 In /In+TRO200mg
17. 64 M	 D&E/D&E
18. 51 M	 D&E/D&E+P 0.6g
19 69 M	In / In + D&E
20. 65M	D&E/ TRO 200 mg
21. 59 M	D&E/ D&E
22. 64 M	 D&E / D&E+SU
23. 63 M	 D&E/D&E 
24. 68 F	 SU/ SU+TRO200mg
25. 55 M	SU /SU
26. 65 M	 D&E/ D&E
27. 56 M	 SU / SU
28. 66 M	SU / SU+TRO200 mg
29. 64 M	D&E/ TRO200mg
30. 48 F	D&E/ D&E								
31. 64M	D&E / TRO200mg
32. 72 F	D&E / D&E 
33 60 M	D&E / D&E
34. 66 M 	D&E / In
MFR ; D: diet therapy, E: exercise therapy, SU: sulfonylurea drugs, A: acarbose, P: poglybose, TRO: troglytazone, In: insulin 
Figure 1



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