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A cross sectional comparative study was performed in Owerri metropolis to evaluate the serum electrolyte and lipid profile among type 2 diabetic patient and non diabetics. A total of 60 subjects within age range 40-69 years were selected and grouped as diabetics and non diabetics (control) with 30 cases in each. Fasting serum lipid profile, glucose and electrolyte were measured using enzymatic kits. Data were compared between diabetics and control and analyzed statistically by student independent t-test. The results show that total cholesterol was significantly (p<0.05) higher in diabetics (216.00 ± 11.67mg/dl) than Control (181.57 ± 12.94mg/dl). Mean serum TG level was significantly (p˂ 0.05) higher in diabetics (149.27 ± 21.82mg/dl) than Control (113.80 ± 11.18mg/dl). The group means of High Density Lipoprotein Cholesterol (HDLC) shows a lower level of concentration in Diabetics (33.30 ± 4.56mg/dl) than Control(44.33 ± 6.72mg/dl); and this difference is statistically significant. Statistical analysis of the Low Density Lipoprotein Cholesterol (LDLC) shows a higher level in diabetics (152.87 ± 13.05mg/dl) than Control (114.47 ±13.47mg/dl). This difference is statistically significant. Comparism of Glucose values of both groups shows a statistical significant (p<0.05) increase in diabetics (192.03±25.35mg/dl) than Control (78.07 ± 7.84mg/dl). Sodium and potassium level of diabetics (130.53 ±3.83mmol/l, 3.21±0.25mmol/l) are significantly (P<0.05) reduced than the control (138.77± 3.07mmol/l, 4.05± 0.27). Bicarbonate values of the diabetics (22.10±2.6mmol/l) are non significantly (p>0.05) reduced than that of the control (25.57 ±1.57mmol/l). Chloride values of the diabetics (109.37±4.06mmol/l) are significantly higher than that of the control (101.10±2.58mmol/l). It may be concluded that lipid abnormalities and electrolyte imbalance contribute towards complications observed in diabetes.   








Diabetes mellitus is a group of metabolic disorders that is characterized by elevated levels of glucose in blood (hyperglycemia) and insufficiency in production or action of insulin produced by the pancreas inside the body (Maritim et al., 2013). Insulin is a protein (hormone) synthesized in beta cells of pancreas in response to various stimuli such as glucose, sulphonylureas, and arginine however glucose is the major determinant (Joshi et al., 2007). Long term elevation in blood glucose levels is associated with macro- and micro-vascular complications leading to heart diseases, stroke, blindness and kidney diseases (Loghmani, 2015). Sidewise to hyperglycemia, there are several other factors that play great role in pathogenesis of diabetes such as hyperlipidemia and oxidative stress leading to high risk of complications (Kangralkar et al., 2010).

Type 2 diabetes mellitus is a multifactorial disease characterized by chronic hyperglycemia, altered insulin secretion, and insulin resistance – a state of diminished responsiveness to normal concentrations of circulating insulin (Landas and Goldstein, 2008). T2DM is also defined by impaired glucose tolerance (IGT) that results from islet β-cell dysfunction, followed by insulin deficiency in skeletal muscle, liver, and adipose tissues (Radami et al., 2010). In individuals with IGT, the development of T2DM is governed by genetic predisposition and environmental variables (a hypercaloric diet and the consequent visceral obesity or increased adiposity in liver and muscle tissues) and host-related factors (age, imbalances in oxidative stress, and inflammatory responses) (Pickup et al., 2014). Clinical complications of T2DM include both microvascular diseases (eg, retinopathy, nephropathy, and neuropathy) and macrovascular complications (eg, myocardial infarction, peripheral vascular disease, and stroke). The macrovascular diseases are considered to be the leading cause of mortality among diabetics (Johanson et al., 2015).

Dyslipidemia is elevation of plasma cholesterol, triglycerides (TGs), or both, or a low high-density lipoprotein level that contributes to the development of atherosclerosis of which causes may be primary (genetic) or secondary and diagnosed by measuring plasma levels of total cholesterol, TGs, and individual lipoproteins. It is traditionally classified by patterns of elevation in lipids and lipoproteins. Dyslipidaemia is a well-recognized and modifiable risk factor that should be identified early to institute aggressive cardiovascular preventive management (Keech et al., 2013). The most typical lipoprotein pattern in diabetes, also known as diabetic dyslipidemia or atherogenic dyslipidemia consists of moderate elevation in triglyceride levels, low HDL cholesterol values, and small dense LDL particles (Smith et al., 2008). Type 2 DM is associated with a marked increased risk of cardiovascular disease (CVD). Thus the management of diabetic dyslipidaemia is a key approach in preventing CVD in individuals with Type 2 DM.


Dyslipidemia using World Health Organization (WHO) criteria [serum triglyceride- 150-400 mg/dL (1.7-4.5 mmol/L), total cholesterol (TC) > 200 mg/dL (>5.2 mmol/L), low-density lipoprotein (LDL)-cholesterol (LDL-C) > 135 mg/dL (>3.5 mmol/L), high-density lipoprotein (HDL)-cholesterol (HDL-C) < 35 mg/dL (<0.9 mmol/L) in men or <40 mg/dL (<1.0 mmol/L) in women, and a ratio of total cholesterol to HDL-cholesterol > 5] has been identified as a risk factor in the development of micro- and macrovascular complications in diabetic patients including diabetic nephropathy (WHO, 2014).


Electrolytes are the smallest of chemicals that are important for the cells in the body to function and allow the body to work. Electrolytes regulate our nerve and muscle function, our body’s hydration, blood pH, blood pressure, and the rebuilding of damaged tissue. In our bodies, electrolytes include sodium (Na+), potassium (K+), calcium (Ca2+), bicarbonate (HCO3), magnesium (Mg2+), chloride (C1), and hydrogen phosphate (HPO42-). Various mechanisms exist in our body that keeps the concentrations of electrolytes under strict control.


Diabetic nephropathy is one of the complications of diabetes mellitus, which ultimately leads to renal failure and renal failure is a cause of electrolyte imbalance among hospitalized diabetic patients; other causes are diarrhea, vomiting, diuretic use and chronic laxative use. The most common electrolyte imbalance is hyponatraemia, others are hypokalaemia, hypomagnesaemia and hyperkalaemia (Haque et al., 2012).


Hyponatraemia, defined as a plasma sodium concentration <130 mmol/L, usually reflect a hypotonic state. However, plasma osmolality may be normal or increased in some cases of hyponatraemia. Hypertonic hyponatraemia is usually due to hyperglycemia. Relative insulin deficiency causes myocyte to become impermeable to glucose. Therefore, during poorly controlled diabetes mellitus, glucose is an effective osmole and draws water from muscle cells resulting in hyponatraemia. Isotonic hyponatraemia may occur in conditions like hyperlipidemia and hyperproteinemia. In general, hypotonic hyponatraemia occurs due either to a primary Na+ loss (secondary water gain) like sweating, burns, gastrointestinal loss: vomiting, diarrhea; renal loss: diuretics, hypoaldosteronism, saltwasting nephropathy; or due to a primary water gain (secondary Na+ loss), hypothyroidism, primary polydipsia; or due to a primary Na+ gain (exceeded by secondary water gain) like heart failure, hepatic cirrhosis, nephritic syndrome. It is important to note that diuretic-induced hyponatraemia is almost always due to thiazide diuretics and cerebral salt wasting after neurosurgery are also the cause of hyponatraemia (Braunwald et al., 2005). Hypernatraemia can occur in hyperglycaemic hyperosmolar state. Potassium is the principal intracellular cation and maintenance of the distribution of potassium between the intracellular and the extracellular compartments relies on several homeostatic mechanisms; when these mechanisms are perturbed, hypokalemia or hyperkalemia may occur (Kimberley, 2005). Hypokalemia, defined as a plasma K+ concentration <3.5 mmol/L, may result from one or more of the followings: decreased net intake like starvation; shift into cells like metabolic alkalosis, insulin, total parenteral nutrition; and increased net loss like diarrhea, sweating, renal loss: diuretics, primary and secondary hyperaldosteronism. Diminished intake is seldom the sole cause of K+ depletion since urinary excretion can be effectively decreased to <15 mmol/day as a result of net K+ reabsorption in the distal nephron. However, dietary K+ restriction may exacerbate the hypokalemia secondary to increased gastrointestinal or renal loss (Braunwald et al., 2005). Hyperkalemia, defined as a plasma K+ concentration >5.3 mmol/L, occurs as a result of either K+ release from cells or decreased renal loss. Increased K+ intake is rarely the sole cause of hyperkalemia since the phenomenon of potassium adaptation ensures rapid K+ excretion in response to increase in dietary consumption. Iatrogenic hyperkalemia may result from overzealous parenteral K+ replacement or in patients with renal insufficiency. Metabolic acidosis, with the exception of those due to the accumulation of organic anions, can be associated with mild hyperkalemia resulting from intracellular buffering of H+. Insulin deficiency and hypertonicity (e.g., hyperglycemia) promote K+ shift from the ICF to the ECF. The severity of exercise induced hyperkalemia is related to the degree of exertion. It is due to release of K+ from muscles and is usually rapidly reversible. Severe digitalis toxicity and treatment with beta blockers may contribute to the elevation in plasma K+ concentration. Other drugs like angiotensin receptor inhibitors (ACE inhibitors), angiotensin receptor blocker (ARBs) and spironolactone are often responsible for hyperkalaemia. Pseudohyperkalemia represents an artificially elevated plasma K+ concentration due to K+ movement out of cells immediately prior to or following venepuncture. Contributing factors include prolonged use of a tourniquet with or without repeated fist clenching, hemolysis, and marked leukocytosis or thrombocytosis. Intravascular hemolysis, tumor lysis syndrome, and rhabdomyolysis all lead to K+ release from cells as a result of tissue breakdown. Magnesium is the major intracellular divalent cation that forms a key complex with ATP and is an important cofactor for a wide range of enzymes, transporters, and nucleic acids required for normal cellular function, replication, and energy metabolism. The concentration of magnesium in serum is closely regulated within the range of 0.7–1.0 mmol/L.

Magnesium deficit is associated with several acute and chronic illness, of major concern is the association of hypomagnesaemia with cardiovascular problems, such as myocardial infarction, hypertension and congestive heart failure. In addition, evidence is mounting regarding the relationship between Type 2 Diabetes Mellitus, and magnesium deficit. Hypomagnesaemia can result from intestinal malabsorption; protracted vomiting, diarrhea, or intestinal drainage; defective renal tubular magnesium reabsorption; or rapid shift of magnesium from the ECF into cells, bone, or third spaces. Dietary magnesium deficiency is unlikely except possibly in the setting of alcoholism (Haque et al., 2012).













Diabetes mellitus a problem of glucose metabolism is associated with a lot of microvascular and macrovascular disorders. It is a global concern for its increase in endemicity is quite alarming. Type 2 diabetes mellitus pathogenesis has been linked with a lot of environmental factors and some metabolic disorders. So many research have been carried out linking its association with dyslipidaemia and. Also its association with electrolyte imbalance has been studied but there is scarcity of this research being done in Nigeria. Therefore this research is carried out to evaluate the level of lipid parameters and electrolyte in type 2 diabetes in Owerri.


AIM: To estimate the levels of lipid profile and electrolyte parameters in type 2 diabetes mellitus individuals.


  1. To determine the levels of total cholesterol, high density lipoprotein cholesterol, triglyceride and low density lipoprotein cholesterol, in type 2 diabetes mellitus individuals.
  2. To evaluate the levels of potassium, sodium, chloride and bicarbonate in type 2 diabetes mellitus individuals.



HO There is no change in the levels of total cholesterol, high density lipoprotein cholesterol, triglyceride and low density lipoprotein cholesterol, in type 2 diabetes mellitus individuals.

H1 There is change in the levels of total cholesterol, high density lipoprotein cholesterol, triglyceride and low density lipoprotein cholesterol, in type 2 diabetes mellitus individuals.

Ho There is no change in the levels of potassium, sodium, chloride and bicarbonate in type 2 diabetes mellitus individuals.

H1 There is change in the levels of potassium, sodium, chloride and bicarbonate in type 2 diabetes mellitus individuals.









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