Keywords : Type
Triglycerides effect on the levels of low density lipoprotein and high density lipoprotein in type 2 diabetic patients.
The Medical Journal of Basrah University,
2017, Volume 35, Issue 1, Pages 31-38
Background: Type 2 Diabetes mellitus is a worldwide disease with the recent changes in life styles is associated with increasing complications and hyperlipidemia is hallmark risk factor for most complications.
Objective: To evaluate the effect of triglycerides on the levels of other lipid type’s mainly low density lipoprotein cholesterol and high density lipoprotein cholesterol in type 2 diabetic patients.
Patients and method: From three hundred type 2 diabetic patients who consulted Diabetic and Endocrine Center in Al-Mawani General Hospital complaining from symptoms of diabetes over the period from January 2013 to July 2014, two hundred sixty six patients were eligible for this study. One hundred sixty four (61.7%) patients were males and one hundred two patients (37.3%) were females, their mean age was 50.57±9.28years. All patients were subjected to a thorough history and physical examination including their height, weight and body mass index were calculated, blood pressure was measured and fasting blood sample tested for blood sugar, glycosylated hemoglobin and lipid profile.
Results: level of low density lipoprotein lipid was greatly changed by level of triglyceride with mean difference ranges from (-0.05745 to 0.60150*) in patients with normal triglyceride and very high triglyceride with confidence interval (CI/ -0.6517 to 0.5368) in low and (CI/0.00441 to 0.1986) in patients with very high triglyceride. While the mean difference for Non high density lipoprotein ranges from ( -0.55268 to -0.53312 ) and the value of confidence interval was ( CI/-01.1761 to 0.0707) and ( CI/ -01.15950 to 0.0933) between low and very high triglyceride levels The high density lipoprotein closely related in a parallel direction to level of triglyceride with mean difference ranges from (-0.01095 to -0.01942) with confidence interval (CI/ -0.2150 to 0.1931) and (CI/-0.2245 to 0.1856) between low and very high triglyceride type group.
Conclusion: Triglycerides which is frequently elevated in type 2 diabetic patients significantly influence the levels of low density lipoproteins but not high density lipoprotein and was reverse of the first and parallel levels of the second respectively. This lead to underestimation of atherogenic lipid or overestimation of the protective lipid respectively in type 2 diabetic patients.
The Medical Journal of Basrah University,
2015, Volume 33, Issue 1, Pages 17-23
Background: Hypoglycemia is one of the most common side effect of insulin treatment, it affect liver and can potentiate ketoconazole toxicity.
Objectives: To measure effect of ketoconazole on liver enzymes, hypoglycemic oxidative stress and to evaluate if N-acetylcysteine, can modulate this effect.
Methods: Thirty five male rabbits were randomly divided into five groups:
Group 1: (control group), Group 2:( ketoconazole), Group 3: (insulin), Group 4: ( ketoconazole+ insulin), Groups 5: (ketoconazole + insulin + N-Acetyl cysteine). Animals were sacrificed at day 3. Blood collected for measurement of liver enzymes, and total bilirubin. Malondialdehyde and glutathione were measured in serum and liver.
Results: Ketoconazole increased serum and liver malondialdehyde, 0.594 ± 0.17 and 4614.49 ± 1288.00 nmol/gm. Increased aspartate aminotransferase 38.19 ± 17.29 and alkaline phosphatase 29.29 ± 10.2 U/L. Insulin increased serum malondialdehyde 0.522 ± 0.19, alkaline phosphatase 15.77 ± 6.12 U/L and bilirubin 0.56 ± 0.26 mg/dl. Ketoconazole + insulin, increased serum malondialdehyde 0.850 ± 0.16 µmol/l and bilirubin 0.77 ± 0.55 mg/dl. Ketoconazole + insulin increased serum malondialdehyde 0.850 ± 0.16 µmol/l, aspartate amino transferase 54.35 ± 18.34 U/L, alanine amino transferase, 34.74 ± 11.08 U/L, alkaline pohospahtase 30.81 ± 12.4 U/L and bilirubin 2.51 ± 1.55 mg/dl. N-acetylcysteine reduced aspartate aminotransferase 28.12 ± 22.21 U/L, alkaline phosphatase 11.81 ± 3.03 IU/L) and bilirubin 0.39 ± 0.18 mg/dl
Conclusion: Hypoglycemia caused hepatotoxicity and oxidative stress and potentiates the toxicity of ketoconazole. N-acetylcysteine partly reverse this hepatotoxicity.