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Title : Correlation between HbA1c level and Lipid Profile in Patients with Type 2 Diabetes Mellitus in



Diabetes is becoming a disease of global concern because of its high escalating numbers. The
number of diabetics is expected to increase from 425 million in 2017 to 693 million by 2045. (1) The
leading cause of morbidity and mortality for patients with type 2 diabetes is Cardio Vascular Disease
(CVD). According to American Heart Association, at least 68% of the people with diabetes aged 65 or
older die of heart disease and 16% die of stroke.(2) The overall cardiometabolic risk is driven by a
complex interplay between several non-modifiable (age, gender, genetics), modifiable (hypertension,
hyperlipidemia, hyperglycemia) factors and the components of the metabolic syndrome commonly
associated with type 2 diabetes.(1)
The American Diabetes Association (ADA) estimated that the risk of diabetes related mortality
increased 25% for each 1% increase in HbA1c. It has also been estimated that each percentage point
increase in HbA1c corresponds to a 35% increase in the risk of macrovascular complication and an
18% increase in risk of myocardial infarction. Glycated hemoglobin (HbA1c) is routinely used as a
diagnostic tool for measuring long term glycemic control. In accordance with its function as an
indicator for the mean blood glucose level, HbA1c predicts the risk for the development of diabetic
complication in diabetes patients. (3)
A very common metabolic abnormality associated with diabetes is dyslipidemia, which is
characterized by a spectrum of quantitative and qualitative changes in lipids and lipoproteins. A
common pattern of lipid abnormalities, known as diabetic dyslipidemia, includes hypertriglyceridemia,
reduced high-density lipoprotein (HDL)- cholesterol concentration and a shift towards small dense
lowdensity lipoprotein (LDL). The underlying pathophysiology of diabetic dyslipidemia is complex
and still not well understood. Thus, hyperglycemia alone cannot fully explain the lipid changes. Insulin
resistance is believed to be the main trigger for diabetic dyslipidemia. (4,5)
Hypertriglyceridemia is considered the dominant lipid abnormality in insulin resistance and
plays a pivotal role in determining the characteristic lipid profile of diabetic dyslipidemia. Elevated
triglyceride levels are the result of increased production and decreased clearance of triglyceride-rich
lipoproteins in both fasting and non-fasting states. Increased production of very lowdensity lipoprotein
(VLDL), the main transporter of fasting triglycerides, is a prominent feature of insulin resistance. (6,7)

aiming to stabilize blood glucose levels along with reduction in TG and LDL and to increase HDL. Consequently. (7. Thus. Some of these have shown that all parameters of lipid profile have significant association with glycemic control. the increased hepatic availability of free fatty acids leads to decreased degradation of apoB.8) A few studies have previously tried to find relationship between HbA1c levels and lipid profile in diabetes patients. In the liver. so that the amount of apoB released is largely determined by its rate of degradation. which act as substrates and regulatory factors for VLDL assembly and secretion. which catalyzes the mobilization of free fatty acids from stored triglycerides. thus causing an overproduction of VLDL in insulin resistant states. significantly reduce cardiovascular events and mortality in patients with type 2 diabetes. insulin regulates theamount of circulating free fatty acids. some studies do not report significant correlation between glycemic control and parameters of lipid profile. The production rate of apoB is relatively constant. West Java. which mediates the transfer of triglycerides to nascent apolipoprotein B (apoB). . Early therapeutic interventions. insulin inhibits the transcription of microsomal triglyceride transfer protein. Insulin is involved at all stages of VLDL production and secretion. This problem motivated us to conduct a study about correlation between HbA1c levels and lipid profile in Diabetes patients in Bogor. insulin suppresses lipolysis by inhibiting the activity of hormone sensitive lipase. which depends on the amount of lipidation. the predominant surface protein of VLDL. In adipose tissues. The respondents are regular kohort subjects who had participating in years.13 On the other hand.

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