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11-07-2006, 06:30 AM
A Viewpoint of Cure Type 2 Diabetes Mellitus(T2DM) Completely: A Report of T2DM and Suppose of Teeterboard for T2DM
Haiwei Sun Dr. //sdfci@yahoo.com.cn
1. Establish the standard of cure of T2DM completely:
I have cited "Five Stages of Evolving β-Cell Dysfunction During Progression to Diabetes" by Gordon C. Weir and Susan Bonner-Weir1. The abstract of this reporte is as follow:
1). Stage 0 of β-Cell Dysfunction:
Stage 0 is all normal in β-cell mass, phenotype, and function. The fasting plasma glucose levels is perfectly normal values of ~4.5 mmol/l.
2). Stage 1 of β-Cell Dysfunction:
Stage 1 is compensation: insulin secretion increases to maintain normoglycemia in the face of insulin resistance and/or decreasing β-cell mass. This stage is characterized by maintenance of differentiated function with intact acute glucose-stimulated insulin secretion (GSIS). The fasting plasma glucose levels increase from perfectly normal values of ~4.5 mmol/l to higher values that might be as low as 5.0mmol/l.
3). Stage 2 of β-Cell Dysfunction:
Stage 2 occurs when glucose levels start to rise, reaching ~5.0 –6.5 mmol/l; this is a stable state of β-cell adaptation with loss of β-cell mass and disruption of function as evidenced by diminished GSIS and β-cell dedifferentiation. The fasting plasma glucose levels is from 5.0 mmol/l to 7.3 mmol/l.
4). Stage 3 of β-Cell Dysfunction:
Stage 3 is a transient unstable period of early decompensation in which glucose levels rise relatively rapidly to the frank diabetes of stage 4. The fasting plasma glucose levels is from 7.3 mmol/l to 16 mmol/l.
5). Stage 4 of β-Cell Dysfunction:
stage 4 is characterized as stable decompensation with more severe β-cell dedifferentiation. The fasting plasma glucose levels is from 16 mmol/l to 20 mmol/l.
6). Stage 5 of β-Cell Dysfunction:
stage 5 is characterized by severe decompensation representing a profound reduction in β-cell mass with progression to ketosis. The fasting plasma glucose levels is >22 mmol/l.
I establish a standard of cure of T2DM completely is that the fasting plasma glucose is lower then 4.5 mmol/l.
2. A report of T2DM:
A patient, Male, 38 years old, Guangdong China, Body height: 1.63M, Body weight: 65KG. Chief Complaint: Polyuria, polydipsia, and unexplained weight loss for 1 month. Accessory examination: Glycosuria: +++, Ketonuria: +++; FBG(Fasting plasma blood-glucose)：16.5mmol/L, P2hBG(Postprandial 2 hours plasma blood-glucose): 26.5mmol/L, HbA1c(glycosylated hemoglobin): 12.9%, Meal-tolerance tests: 0`:6.2/41.8, 30`: 14.1/107, 60`: 17.1/193, 120`: 21.6/944, 180`: 19.6 /1016 ; GAD(glutamic acid decarboxylase autoantibody) IAA(insulin autoantibodies) and ICA(islet cell antibody) are all normal. Plasma ketone bodies: 1.3g/L, Carbon dioxide combining powder: 23mmol/L, Plasma osmotic pressure: 291.3 mOsm/L, nerve conductive velocity-) funduscopy-). Clinical diagnosis: (1). Type 2 Diabetes Mellitus; (2).Diabetic ketosis. Treatment: At the first step, a 11-day insulin pump therapy was given to the patient, then the patient began to receive 20 units of Novolin 30R 30min before breakfast and 18 units before dinner, Novolin 30R has been used 3 months, and combined with Glucophage 500mg qd for 1 month, later the diet should be controlled and physics exercise gaven to the patient. 10 months since the beginning of the insulin pump therapy, the his FBG is 4.2mmol/L, and his P2hBG is 4.6mmol/L. and his body weight is 61KG. I think that the β-Cell function of this patient has moved from stage 4 to stage 0. And his T2DM has cured completely.
[B]3. Suppose of teeterboard for T2DM:
Type 2 diabetes results from a combination of insulin resistance and impaired insulin secretion . There are lots of known factors results insulin resistance and impaired insulin secretion. for example: genetic heterogeneity, multigenic pathogenesis, environmental factors, non-esterified fatty acids, adipose decompensate, mitochondrial dysfunction, oxidative stress, glucotoxicity, lipotoxicity, islet amyloid polypeptide deposits, adipocyte-derived hormones, C-reactive protein, serum retinol binding protein 4, sleep disorder, aging, et al. For a patient of T2DM, when the pathopoiesis ability of these factors enhances, the functin of β-cells become lower and lower, It become from Stage 0 of β-Cell Dysfunction to Stage 5 of β-Cell Dysfunction; Another, Gordon C. Weir and Susan Bonner-Weir reported that movement across stages 1–4 can be in either direction; For example, individuals with treated type 2 diabetes can move from stage 4 to stage 1 or stage 2. But my report of T2DM show that the individual with treated type 2 diabetes can move from stage 4 to stage 0. So, when the pathogenicity of these factors attenuates, the function of β-cells will restore from stage 4 to stage 0. There is a suppose that it is a relation of teeterboard between the pathogenicity of the factors of resulting T2DM and the β-Cell Dysfunction(Figure) . For a individual with treated type 2 diabetes, when the fasting plasma glucose is lower then 4.5mmol/l without any antihyperglycemic drug, I think that this patient of T2DM had been cured completely; and The attack process of T2DM at the first time had been terminated thoroughly, However, because of the swing of teeterboard of T2DM, there would be second-time, third-time and even more-time recurrence in the future. Another, for a individual with treated type 2 diabetes, If his FBG can`t lower then 4.5 mmol/L without any antihyperglycemic drug, I think that first process of his T2DM will not been terminated, and his T2DM will go with his all life.
Referrence:
1. Gordon C. Weir, Susan Bonner-Weir. Five Stages of Evolving β-Cell Dysfunction During Progression to Diabetes. Diabetes 2004; 53 (Suppl. 3):S16-S21.
Figure:
E:\t2dm-p\TeeterboardForT2DM.jpg
If you can`t read the figure, click: http://forums.prevention.com/eve/forums/a/tpc/f/5121004491/m/8081086212
Haiwei Sun Dr. //sdfci@yahoo.com.cn
1. Establish the standard of cure of T2DM completely:
I have cited "Five Stages of Evolving β-Cell Dysfunction During Progression to Diabetes" by Gordon C. Weir and Susan Bonner-Weir1. The abstract of this reporte is as follow:
1). Stage 0 of β-Cell Dysfunction:
Stage 0 is all normal in β-cell mass, phenotype, and function. The fasting plasma glucose levels is perfectly normal values of ~4.5 mmol/l.
2). Stage 1 of β-Cell Dysfunction:
Stage 1 is compensation: insulin secretion increases to maintain normoglycemia in the face of insulin resistance and/or decreasing β-cell mass. This stage is characterized by maintenance of differentiated function with intact acute glucose-stimulated insulin secretion (GSIS). The fasting plasma glucose levels increase from perfectly normal values of ~4.5 mmol/l to higher values that might be as low as 5.0mmol/l.
3). Stage 2 of β-Cell Dysfunction:
Stage 2 occurs when glucose levels start to rise, reaching ~5.0 –6.5 mmol/l; this is a stable state of β-cell adaptation with loss of β-cell mass and disruption of function as evidenced by diminished GSIS and β-cell dedifferentiation. The fasting plasma glucose levels is from 5.0 mmol/l to 7.3 mmol/l.
4). Stage 3 of β-Cell Dysfunction:
Stage 3 is a transient unstable period of early decompensation in which glucose levels rise relatively rapidly to the frank diabetes of stage 4. The fasting plasma glucose levels is from 7.3 mmol/l to 16 mmol/l.
5). Stage 4 of β-Cell Dysfunction:
stage 4 is characterized as stable decompensation with more severe β-cell dedifferentiation. The fasting plasma glucose levels is from 16 mmol/l to 20 mmol/l.
6). Stage 5 of β-Cell Dysfunction:
stage 5 is characterized by severe decompensation representing a profound reduction in β-cell mass with progression to ketosis. The fasting plasma glucose levels is >22 mmol/l.
I establish a standard of cure of T2DM completely is that the fasting plasma glucose is lower then 4.5 mmol/l.
2. A report of T2DM:
A patient, Male, 38 years old, Guangdong China, Body height: 1.63M, Body weight: 65KG. Chief Complaint: Polyuria, polydipsia, and unexplained weight loss for 1 month. Accessory examination: Glycosuria: +++, Ketonuria: +++; FBG(Fasting plasma blood-glucose)：16.5mmol/L, P2hBG(Postprandial 2 hours plasma blood-glucose): 26.5mmol/L, HbA1c(glycosylated hemoglobin): 12.9%, Meal-tolerance tests: 0`:6.2/41.8, 30`: 14.1/107, 60`: 17.1/193, 120`: 21.6/944, 180`: 19.6 /1016 ; GAD(glutamic acid decarboxylase autoantibody) IAA(insulin autoantibodies) and ICA(islet cell antibody) are all normal. Plasma ketone bodies: 1.3g/L, Carbon dioxide combining powder: 23mmol/L, Plasma osmotic pressure: 291.3 mOsm/L, nerve conductive velocity-) funduscopy-). Clinical diagnosis: (1). Type 2 Diabetes Mellitus; (2).Diabetic ketosis. Treatment: At the first step, a 11-day insulin pump therapy was given to the patient, then the patient began to receive 20 units of Novolin 30R 30min before breakfast and 18 units before dinner, Novolin 30R has been used 3 months, and combined with Glucophage 500mg qd for 1 month, later the diet should be controlled and physics exercise gaven to the patient. 10 months since the beginning of the insulin pump therapy, the his FBG is 4.2mmol/L, and his P2hBG is 4.6mmol/L. and his body weight is 61KG. I think that the β-Cell function of this patient has moved from stage 4 to stage 0. And his T2DM has cured completely.
[B]3. Suppose of teeterboard for T2DM:
Type 2 diabetes results from a combination of insulin resistance and impaired insulin secretion . There are lots of known factors results insulin resistance and impaired insulin secretion. for example: genetic heterogeneity, multigenic pathogenesis, environmental factors, non-esterified fatty acids, adipose decompensate, mitochondrial dysfunction, oxidative stress, glucotoxicity, lipotoxicity, islet amyloid polypeptide deposits, adipocyte-derived hormones, C-reactive protein, serum retinol binding protein 4, sleep disorder, aging, et al. For a patient of T2DM, when the pathopoiesis ability of these factors enhances, the functin of β-cells become lower and lower, It become from Stage 0 of β-Cell Dysfunction to Stage 5 of β-Cell Dysfunction; Another, Gordon C. Weir and Susan Bonner-Weir reported that movement across stages 1–4 can be in either direction; For example, individuals with treated type 2 diabetes can move from stage 4 to stage 1 or stage 2. But my report of T2DM show that the individual with treated type 2 diabetes can move from stage 4 to stage 0. So, when the pathogenicity of these factors attenuates, the function of β-cells will restore from stage 4 to stage 0. There is a suppose that it is a relation of teeterboard between the pathogenicity of the factors of resulting T2DM and the β-Cell Dysfunction(Figure) . For a individual with treated type 2 diabetes, when the fasting plasma glucose is lower then 4.5mmol/l without any antihyperglycemic drug, I think that this patient of T2DM had been cured completely; and The attack process of T2DM at the first time had been terminated thoroughly, However, because of the swing of teeterboard of T2DM, there would be second-time, third-time and even more-time recurrence in the future. Another, for a individual with treated type 2 diabetes, If his FBG can`t lower then 4.5 mmol/L without any antihyperglycemic drug, I think that first process of his T2DM will not been terminated, and his T2DM will go with his all life.
Referrence:
1. Gordon C. Weir, Susan Bonner-Weir. Five Stages of Evolving β-Cell Dysfunction During Progression to Diabetes. Diabetes 2004; 53 (Suppl. 3):S16-S21.
Figure:
E:\t2dm-p\TeeterboardForT2DM.jpg
If you can`t read the figure, click: http://forums.prevention.com/eve/forums/a/tpc/f/5121004491/m/8081086212