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Proper Management Of Diabetes Slow Down the Atherosclerosis
Diabetes is a group of metabolic diseases in which a person has high blood sugar, either because the body does not produce enough insulin, or because cells do not respond to the insulin that is produced. This high blood sugar produces the classical symptoms of polyuria (frequent urination), polydipsia (increased thirst) and polyphagia (increased hunger).
Diabetes mellitus affects about 100 million persons worldwide. Five to ten percent have type 1 (formerly known as insulin-dependent) and 90% to 95% have type 2 (non–insulin-dependent) diabetes mellitus. It is likely that the incidence of type 2 diabetes will rise as a consequence of lifestyle patterns contributing to obesity. Cardiovascular physicians are encountering many of these patients because vascular diseases are the principal causes of death and disability in people with diabetes. The macrovascular manifestations include atherosclerosis and medial calcification. The microvascular consequences, retinopathy and nephropathy, are major causes of blindness and end-stage renal failure.
Diabetes and Vessels Thickening
Diabetes contributes to abnormalities in endothelial and vascular smooth muscle cell function in several ways, those lead to thrombosis, contribute to atherosclerosis and its complications.
Hyperglycemia decreased the endothelium-derived NO. When normal aortic rings are incubated in a hyperglycemic milieu, endothelium-dependent relaxation is impaired. Similarly, endothelium-dependent vasodilation is reduced in healthy subjects during hyperglycemic clamping. In simple words, in poorly controlled diabetes the vessels don't have good relaxation.
Circulating levels of free fatty acids are elevated in diabetes because of their excess liberation from adipose tissue and diminished uptake by skeletal muscle. Free fatty acids may impair endothelial function through several mechanisms, including increased production of oxygen-derived free radicals, and exacerbation of dyslipidemia. The liver responds to free fatty acid flux by increasing very-low-density lipoprotein production and cholesteryl ester synthesis. This increased production of triglyceride-rich proteins and the diminished clearance by lipoprotein lipase results in hypertriglyceridemia, which is typically observed in diabetes. Elevated triglyceride concentrations lower HDL by promoting cholesterol transport from HDL to very-low-density lipoprotein. These abnormalities change LDL morphology, increasing the amount of the more atherogenic, small, dense LDL. Both hypertriglyceridemia and low HDL have been associated with endothelial dysfunction
In simple words, there is accelerated thickening of the vessels in diabetes patient.
Platelet function is impaired in diabetes, thus lead to thrombosis and coagulation process.
Things to Know
We already know that diabetes patients have an accelerated process of vessels degeneration compare to normal person. But, does the proper management of diabetes can slow down that process to normal rate, thus can improve the quality of life.
On January 2011, American Diabetes Association has published their result of the trial about long-term intensive treatment of diabetes on progression of atherosclerosis. The results support the early initiation and continued maintenance of intensive diabetes management in type 1 diabetes to retard atherosclerosis.
The incidence of cardiovascular events in patients with type 1 diabetes is high for their age, with a prevalence of cardiovascular disease similar to that in nondiabetic individuals who are 10 to 20 years older. Patients with type 1 diabetes have increased levels of subclinical cardiovascular disease, as measured by carotid intima-media thickness (IMT), a measure of atherosclerosis. Carotid IMT is increased in children, adolescents, and adults with type 1 diabetes compared with those without diabetes.
Intensive diabetes therapy aimed at achieving glycemic control as close to the nondiabetic range as safely possible reduced the rate of microvascular complications. A trend favoring the intensive treatment group regarding macrovascular disease prompted the addition of examinations to study earlier signs of cardiovascular disease during the long-term (12 years) observational follow-up.
From Initial report, an intensive diabetes therapy did not appear to influence carotid vessel thickness when measured in the first year of the follow up, at a time when the measurements were not significantly different from those of age-matched and gender-matched nondiabetic individuals.
While the vessel thickness measurement at year 6 demonstrated that the progression of carotid vessel thickness was reduced in the intensive compared with the conventional treatment group, despite comparable A1C levels. These findings suggested that a durable effect of the differences in metabolic control during the trial might play a role in atherosclerosis, as has been shown for microvascular complications of diabetes (“metabolic memory”). The duration of this effect on atherosclerosis is unknown.
From the trial, we can see that long-term blood sugar control with proper management can slow down the progression of atherosclerosis or vessels degeneration. This is important in order to reduce the incidence diabetes related complications.
Eventhough diabetes can't be cure, but it can be controlled. Achieving the control blood glucose at desire level is important to slow down the degeneration process of the vessels.
Diabetes and Vessels Thickening
Diabetes contributes to abnormalities in endothelial and vascular smooth muscle cell function in several ways, those lead to thrombosis, contribute to atherosclerosis and its complications.
Hyperglycemia decreased the endothelium-derived NO. When normal aortic rings are incubated in a hyperglycemic milieu, endothelium-dependent relaxation is impaired. Similarly, endothelium-dependent vasodilation is reduced in healthy subjects during hyperglycemic clamping. In simple words, in poorly controlled diabetes the vessels don't have good relaxation.
Circulating levels of free fatty acids are elevated in diabetes because of their excess liberation from adipose tissue and diminished uptake by skeletal muscle. Free fatty acids may impair endothelial function through several mechanisms, including increased production of oxygen-derived free radicals, and exacerbation of dyslipidemia. The liver responds to free fatty acid flux by increasing very-low-density lipoprotein production and cholesteryl ester synthesis. This increased production of triglyceride-rich proteins and the diminished clearance by lipoprotein lipase results in hypertriglyceridemia, which is typically observed in diabetes. Elevated triglyceride concentrations lower HDL by promoting cholesterol transport from HDL to very-low-density lipoprotein. These abnormalities change LDL morphology, increasing the amount of the more atherogenic, small, dense LDL. Both hypertriglyceridemia and low HDL have been associated with endothelial dysfunction
In simple words, there is accelerated thickening of the vessels in diabetes patient.
Platelet function is impaired in diabetes, thus lead to thrombosis and coagulation process.
Things to Know
We already know that diabetes patients have an accelerated process of vessels degeneration compare to normal person. But, does the proper management of diabetes can slow down that process to normal rate, thus can improve the quality of life.
On January 2011, American Diabetes Association has published their result of the trial about long-term intensive treatment of diabetes on progression of atherosclerosis. The results support the early initiation and continued maintenance of intensive diabetes management in type 1 diabetes to retard atherosclerosis.
The incidence of cardiovascular events in patients with type 1 diabetes is high for their age, with a prevalence of cardiovascular disease similar to that in nondiabetic individuals who are 10 to 20 years older. Patients with type 1 diabetes have increased levels of subclinical cardiovascular disease, as measured by carotid intima-media thickness (IMT), a measure of atherosclerosis. Carotid IMT is increased in children, adolescents, and adults with type 1 diabetes compared with those without diabetes.
Intensive diabetes therapy aimed at achieving glycemic control as close to the nondiabetic range as safely possible reduced the rate of microvascular complications. A trend favoring the intensive treatment group regarding macrovascular disease prompted the addition of examinations to study earlier signs of cardiovascular disease during the long-term (12 years) observational follow-up.
From Initial report, an intensive diabetes therapy did not appear to influence carotid vessel thickness when measured in the first year of the follow up, at a time when the measurements were not significantly different from those of age-matched and gender-matched nondiabetic individuals.
While the vessel thickness measurement at year 6 demonstrated that the progression of carotid vessel thickness was reduced in the intensive compared with the conventional treatment group, despite comparable A1C levels. These findings suggested that a durable effect of the differences in metabolic control during the trial might play a role in atherosclerosis, as has been shown for microvascular complications of diabetes (“metabolic memory”). The duration of this effect on atherosclerosis is unknown.
From the trial, we can see that long-term blood sugar control with proper management can slow down the progression of atherosclerosis or vessels degeneration. This is important in order to reduce the incidence diabetes related complications.
Eventhough diabetes can't be cure, but it can be controlled. Achieving the control blood glucose at desire level is important to slow down the degeneration process of the vessels.
