Significance of glycaemic control in type 1 diabetes

Diabetes mellitus is accompanied with drastic hormonal and metabolic alterations. In uncontrolled diabetes, these disturbances worsen the condition leading to development of life threatening complications. Present study was planned to compare hormonal and metabolic disturbances in controlled and uncontrolled type 1 diabetes [T1D]. This retrospective, analytical case control study was carried out from Jan 2004 to July 2007. Sample size was 60, divided into 3 groups: Non-diabetic control [group A], controlled T1D [group B] and uncontrolled T1D [group C]. Uncontrolled type 1 diabetics when compared with control group, presented with significant hyperglycaemia [p<0.001], hypoinsulinemia [p<0.001], hyperglucagonemia [p<0.01], raised BMI [p<0.05], hyponatremia [p<0.01], hyperkalemia [p<0.01], acidemia [p<0.05], high arterial Pco2 [p<0.05], low plasma HCO3 - [p<0.05], raised plasma triglyceride, LDL Cholesterol and total cholesterol level [p<0.01] but low HDL cholesterol [p<0.05]. On similar comparison controlled type 1 diabetics showed significant hyperglycaemia [p<0.001] and hypoinsulinemia [p<0.05]. Regular assessment, monitoring and control of T1D has positive impact in preventing development of diabetic dyslipidemia and other hormonal and metabolic derangements which, if left uncontrolled can lead to life threatening diabetic complications

Assessment of metabolic derangements in diabetes and associated hyperglycemic emergencies

To assess and compare the plasma insulin level and pre-treatment metabolic and acid base status findings in patients with uncontrolled TIDM, uncontrolled T2DM, DKA and HHS with healthy non-diabetic subjects. A retrospective analytical study. This study was conducted at the Army Medical College, Rawalpindi during the period from 2004 to 2006. This study was conducted on TIDM, T2DM, DKA and HHS patients and monitored insulin level, plasma osmolatily, serum electrolytes and arterial blood gases levels revealed that the clinical records and data confirmed and described each event and its likely causes. Ketoacidosis was frequently seen among persons with type 1 diabetes with marked hypoinsulinemia, hyperkalemia and acidosis. Hyperinsulinemia, acidosis and hyperosmolality were the significant finding in HHS. The observed association between insulin level and pretreatment metabolic and acid based derangements were statistically highly significant

High incidence of dyslipidemia in obese type 2 diabetics

To ascertain the effect of Body Mass Index [BMI] on plasma lipid profile in type 2 diabetes mellitus [T2DM]. Comparative, observational study Army Medical College, Rawalpindi from Jan 2007- June 2010. Sample size was 60, subdivided in to two groups. Group 1 comprising on 30 type 2 diabetics with BMI /=28. Blood glucose, HbA[1c] plasma cholesterol and triglyceride levels were determined. Group 1 consisted of 56% males and 44% females, whereas Group 2 had 54% males and 46% females. Mean age to develop T2DM for group 1 was 44.60 +/- 1.22 years and for group 2 was 42.13 +/- 0.86 years. BMI of group 1 was 20.29 +/- 0.56 and Group 2 was 28.95 +/- 0.26. Mean plasma cholesterol and plasma triglyceride levels of group 2 diabetics were significantly higher [p< 0.001] as compared with group 1 non obese diabetics. Whereas, mean plasma glucose [p< 0.01] and Glycosylated hemoglobin [p< 0.05] of group 2 diabetics were significantly higher as compared with group 1 non obese diabetics Dyslipidemia was more marked in obese type 2 diabetics. Whereas diabetics with low BMI had plasma lipid profile within normal range

Mitochondrial tRNA [Leu[UUR] gene mutation and maternally inherited diabetes mellitus in Pakistani population

Maternally Inherited Diabetes Mellitus and Deafness [MIDD] occurs due to the mutations in mitochondrial DNA [mtDNA]. The most common heteroplasmic point mutation reported, is in the tRNA [Leu[UUR] gene, i.e., A3243G, accompanied with deafness. The objectives of the present study were to determine whether the cause of MIDD in selected Pakistani population, is also the mutation of A3243G in mitochondrial tRNA [Leu[UUR] gene or not, and is there any genotype-phenotype correlation for the MIDD in this population. The present study was conducted in the Department of Biochemistry and Molecular Biology, Army Medical College, Rawalpindi, Pakistan, during the period November 2005 to November 2007. The patients and control subjects were randomly selected from the two cities; Rawalpindi and Multan [both rural and urban areas] and were divided into three groups. [1] Fifty patients with T2DM and maternal history with feature [s] of MIDD. [2] Fifty non-diabetic first-degree relatives of patients with T2DM. [3] Fifty non-diabetic controls with no maternal history of T2DM. The patients and control subjects were scanned for the detection of potential mutations in mitochondrial DNA tRNA [Leu[UUR] gene [np 3035-3456, 422 bp fragment]. On the basis of a polymerase chain reaction, electrophoresis and mtDNA sequencing along with insulin dependence, degree of deafness in patients and subjects, it is proved that there is no A-to-G mutation at np 3243 of mitochondrial leucine tRNA gene in any of the groups studied. Conclusion: It is concluded that in the Pakistani population, selected for the present study, the MIDD is not due to A3243G mutation in mitochondrial tRNA [Leu[UUR] gene

Insulin and glucagon ratio in the patho-physiology of diabetic ketoacidosis and hyperosmolar hyperglycemic non-ketotic diabetes

To assess the role of insulin / glucagon ratio in pathophysiology of diabetic ketoacidosis and hyperosmolar hyperglycemic non-ketotic diabetes. Case control, analytical study. Military Hospital, Rawalpindi from September 2003 to August 2004. The study included 7 patients with diabetic ketoacidosis, 3 patients with hyperosmolar hyperglycemic non-ketotic diabetes, 8 patients with uncontrolled type 1 diabetes mellitus and 12 patients with uncontrolled type 2 diabetes mellitus. Twenty non-diabetic persons having blood glucose level less than 6 mmol/L were selected as control group. Patients' detailed history was taken and general physical examination was done. Plasma samples of all the patients and control subjects were assayed for plasma glucose, glycosylated hemoglobin, plasma insulin and glucagon levels. Presence or absence of ketone bodies in urine was also determined. Seven patients with diabetic ketoacidosis, 3 females and 4 males, were found to be hyperglycemic [p < 0.001], hypoinsulinemic [p < 0.05] and hyperglucagonemic [p < 0.001] as compared to control group. Three patients with hyperosmolar hyperglycemic non-ketotic diabetes, 1 male and 2 females, were hyperglycemic [p < 0.001]. Eight patients with uncontrolled type I diabetes mellitus, 6 males and 2 females, were having hyperglycemia [p< 0.001] along with hyperglucagonemia [p < 0.001]. Twelve patients with uncontrolled type 2 diabetes mellitus, 6 males and 6 females, were found to be hyperglycemic [p < 0.001] and hyperinsulinemic [p < 0.001] as compared to control group. The insulin / glucagon ratio was found to be 1: 0.9 in diabetic ketoacidosis, 1: 0.15 in hyperosmolar hyperglycemic non-ketotic diabetes, 1: 0.24 in type 1 diabetics, 1: 0.08 in type 2 diabetics, and 1: 0.1 in the control group. It was concluded that if insulin / glucagon ratio in type 2 diabetics reduces to 1: 0.9 then these patients may develop ketoacidosis instead of hyperosmolar hyperglycemic non ketotic diabetes. Hence, it is the balance and interplay of insulin and glucagon which predicts the type of acute hyperglycemic emergencies [diabetic ketoacidosis and hyperosmolar hyperglycemic non-ketotic diabetes] being observed in diabetic patients and not the type of diabetes mellitus