Relation between Serum Resistin and Insulin Resistance in Egyptian Type 2 Diabetic Patients
Heba Atef Hussien Ali;
Abstract
Summary and Conclusion
D
iabetes mellitus (DM) is a group of metabolic diseases in which there are high blood sugar levels over a prolonged period. If left untreated, diabetes can cause many complications. Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced.
Resistin is an adipokine that is thought to antagonizes the effect of insulin on glucose metabolism in liver and skeletal muscles, interacts with and reinforces inflammatory pathways, and may promote endothelial cell activation. It may mediate a link between obesity, insulin resistance, metabolic syndrome, type 2 diabetes, and cardiovascular risk. The aim of the present study is to investigate the relationship between levels of serum resistin, obesity and insulin-resistance in type 2 Egyptian diabetic patients.
The study included 84 subjects divided into 4 groups as follows; lean conrtol group (L.C.) includes 21 subjects with body mass index BMI=23.3 ± 1.2, lean diabetic group (L.D.) includes 20 type 2 diabetic patients with BMI=22.2 ± 0.6, obese control group (O.C.) includes 20 obese subjects with BMI ≥ 30, and obese diabetic group (O.D.) includes 23 obese type 2 diabetic patients with BMI ≥ 30.
Results of the present study can be summarized as follows:
Fasting plasma glucose (FPG), glycated heamoglobin (HbA1c), homeostasis model assessment-insulin resistance (HOMA-IR), total cholesterol, triacylglycerols and LDL-C levels showed a highly significant increase (p<0.001) in lean and obese diabetic patients compared to lean controls, while they showed a non significant change in obese controls compared to lean controls.
Insulin, hepatic insulin sensitivity (HIS) and urea levels showed a highly significant decrease (p<0.001) in diabetic subjects compared to lean controls, Moreover, HDL-C levels showed a significant decrease in lean diabetic and obese diabetic subjects (p<0.01& p<0.001, respectively) compared to lean controls. No significant change in the levels of insulin, HIS, urea and HDL-C was recorded in obese control subjects compared to lean controls.
Homeostasis model assessment of β-cell function (HOMA-β) showed a highly significant decrease (p<0.001) in diabetic subjects compared to lean controls. Moreover, a significant decrease (p<0.05) in the level of HOMA-β was also observed in obese controls when compared to lean controls.
Creatinine recorded no significant change in all studied groups compared to lean subjects.
Resistin recorded a highly significant elevation (p<0.001) in obese subjects (O.C. and O.D.) compared to lean control subjects. In addition, a significant increase (p<0.05) was also recorded in the levels of resistin in lean diabetic subjects compared to lean controls.
Meanwhile, on comparing diabetic subjects (lean and obese), the levels of FPG, HbA1c, insulin, HOMA-IR, total cholesterol, LDL-C and resistin showed a significant increase in obese diabetic subjects compared to lean diabetic subjects, (p<0.05) for FPG, insulin, (p<0.01) for HbA1c & (p<0.001) for HOMA-IR, total cholesterol, LDL-C and resistin levels, respectively, HIS showed a significant decrease (p<0.05) in obese diabetic subjects compared to lean diabetics.
Analysis of gender effect on the levels of biochemical parameters revealed that the levels of resistin and LDL-C were significantly increased (p<0.05) & (p<0.01), respectively, in lean diabetic males, but not in females, compared to their matching lean controls. Meanwhile, insulin and HOMA-β levels showed a significant decrease in obese diabetic males (p<0.01), and obese control males (p<0.05), but not in females, compared to their matching lean controls.
Diabetic females (lean and obese) had a significant decrease in HDL-C levels (p<0.05) & (p<0.01), respectively, with no significant difference in their corresponding diabetic males, compared to their matching lean controls.
D
iabetes mellitus (DM) is a group of metabolic diseases in which there are high blood sugar levels over a prolonged period. If left untreated, diabetes can cause many complications. Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced.
Resistin is an adipokine that is thought to antagonizes the effect of insulin on glucose metabolism in liver and skeletal muscles, interacts with and reinforces inflammatory pathways, and may promote endothelial cell activation. It may mediate a link between obesity, insulin resistance, metabolic syndrome, type 2 diabetes, and cardiovascular risk. The aim of the present study is to investigate the relationship between levels of serum resistin, obesity and insulin-resistance in type 2 Egyptian diabetic patients.
The study included 84 subjects divided into 4 groups as follows; lean conrtol group (L.C.) includes 21 subjects with body mass index BMI=23.3 ± 1.2, lean diabetic group (L.D.) includes 20 type 2 diabetic patients with BMI=22.2 ± 0.6, obese control group (O.C.) includes 20 obese subjects with BMI ≥ 30, and obese diabetic group (O.D.) includes 23 obese type 2 diabetic patients with BMI ≥ 30.
Results of the present study can be summarized as follows:
Fasting plasma glucose (FPG), glycated heamoglobin (HbA1c), homeostasis model assessment-insulin resistance (HOMA-IR), total cholesterol, triacylglycerols and LDL-C levels showed a highly significant increase (p<0.001) in lean and obese diabetic patients compared to lean controls, while they showed a non significant change in obese controls compared to lean controls.
Insulin, hepatic insulin sensitivity (HIS) and urea levels showed a highly significant decrease (p<0.001) in diabetic subjects compared to lean controls, Moreover, HDL-C levels showed a significant decrease in lean diabetic and obese diabetic subjects (p<0.01& p<0.001, respectively) compared to lean controls. No significant change in the levels of insulin, HIS, urea and HDL-C was recorded in obese control subjects compared to lean controls.
Homeostasis model assessment of β-cell function (HOMA-β) showed a highly significant decrease (p<0.001) in diabetic subjects compared to lean controls. Moreover, a significant decrease (p<0.05) in the level of HOMA-β was also observed in obese controls when compared to lean controls.
Creatinine recorded no significant change in all studied groups compared to lean subjects.
Resistin recorded a highly significant elevation (p<0.001) in obese subjects (O.C. and O.D.) compared to lean control subjects. In addition, a significant increase (p<0.05) was also recorded in the levels of resistin in lean diabetic subjects compared to lean controls.
Meanwhile, on comparing diabetic subjects (lean and obese), the levels of FPG, HbA1c, insulin, HOMA-IR, total cholesterol, LDL-C and resistin showed a significant increase in obese diabetic subjects compared to lean diabetic subjects, (p<0.05) for FPG, insulin, (p<0.01) for HbA1c & (p<0.001) for HOMA-IR, total cholesterol, LDL-C and resistin levels, respectively, HIS showed a significant decrease (p<0.05) in obese diabetic subjects compared to lean diabetics.
Analysis of gender effect on the levels of biochemical parameters revealed that the levels of resistin and LDL-C were significantly increased (p<0.05) & (p<0.01), respectively, in lean diabetic males, but not in females, compared to their matching lean controls. Meanwhile, insulin and HOMA-β levels showed a significant decrease in obese diabetic males (p<0.01), and obese control males (p<0.05), but not in females, compared to their matching lean controls.
Diabetic females (lean and obese) had a significant decrease in HDL-C levels (p<0.05) & (p<0.01), respectively, with no significant difference in their corresponding diabetic males, compared to their matching lean controls.
Other data
| Title | Relation between Serum Resistin and Insulin Resistance in Egyptian Type 2 Diabetic Patients | Other Titles | العلاقة بين الرزيستين في مصل الدم و مقاومة الإنسولين فى المرضى السكري من النوع الثاني المصريين | Authors | Heba Atef Hussien Ali | Issue Date | 2016 |
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