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 majordeterminant (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 levelthat contributes to the development of atherosclerosis of which causes may be primary (genetic) or secondary anddiagnosed by measuring plasma levels of total cholesterol, TGs, and individual lipoproteins. It is traditionallyclassified by patterns of elevation in lipids and lipoproteins. Dyslipidaemia is a well-recognized and modifiablerisk factor that should be identified early to institute aggressive cardiovascular preventive management (Keech et al., 2013). Themost typical lipoprotein pattern in diabetes, also known as diabetic dyslipidemia or atherogenic dyslipidemiaconsists 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 managementof diabetic dyslipidaemia is a key approach in preventing CVD in individuals with Type 2 DM.


Dyslipidemiausing World Health Organization (WHO) criteria [serumtriglyceride- 150-400 mg/dL (1.7-4.5 mmol/L), totalcholesterol (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 toHDL-cholesterol > 5] has been identified as a risk factor inthe 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 ofthe complications of diabetes mellitus, which ultimatelyleads to renal failure and renal failure is a cause ofelectrolyte imbalance among hospitalized diabeticpatients; other causes are diarrhea, vomiting, diureticuse and chronic laxative use.The most commonelectrolyte imbalance is hyponatraemia, others arehypokalaemia, hypomagnesaemia and hyperkalaemia (Haque et al., 2012).


Hyponatraemia, defined as a plasma sodiumconcentration <130 mmol/L, usually reflect a hypotonicstate. However, plasma osmolality may be normal orincreased in some cases of hyponatraemia. Hypertonic hyponatraemia is usually due to hyperglycemia. Relativeinsulin deficiency causes myocyte to becomeimpermeable to glucose. Therefore, during poorlycontrolled diabetes mellitus, glucose is an effectiveosmole and draws water from muscle cells resulting inhyponatraemia. Isotonic hyponatraemia may occur inconditions like hyperlipidemia and hyperproteinemia.In general, hypotonic hyponatraemia occurs due eitherto a primary Na+ loss (secondary water gain) likesweating, burns, gastrointestinal loss: vomiting,diarrhea; renal loss: diuretics, hypoaldosteronism, saltwastingnephropathy; 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 tonote that diuretic-induced hyponatraemia is almostalways due to thiazide diuretics and cerebral salt wastingafter neurosurgery are also the cause of hyponatraemia (Braunwald et al., 2005). Hypernatraemia can occur in hyperglycaemichyperosmolar state.Potassium is the principal intracellular cation andmaintenance of the distribution of potassium betweenthe intracellular and the extracellular compartmentsrelies on several homeostatic mechanisms; when thesemechanisms are perturbed, hypokalemia orhyperkalemia may occur (Kimberley, 2005). Hypokalemia, defined as aplasma K+ concentration <3.5 mmol/L, may result fromone or more of the followings: decreased net intake likestarvation; 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 effectivelydecreased to <15 mmol/day as a result of net K+reabsorption in the distal nephron. However, dietary K+restriction may exacerbate the hypokalemia secondaryto 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+ releasefrom cells or decreased renal loss. Increased K+ intakeis rarely the sole cause of hyperkalemia since thephenomenon of potassium adaptationensures rapid K+excretion in response to increase in dietary consumption.Iatrogenic hyperkalemia may result from overzealousparenteral K+ replacement or in patients with renalinsufficiency. Metabolic acidosis, with the exception ofthose due to the accumulation of organic anions, can beassociated with mild hyperkalemia resulting fromintracellular buffering of H+. Insulin deficiency andhypertonicity (e.g., hyperglycemia) promote K+ shiftfrom the ICF to the ECF. The severity of exerciseinducedhyperkalemia is related to the degree ofexertion. It is due to release of K+ from muscles and isusually rapidly reversible. Severe digitalis toxicity andtreatment with beta blockers may contribute to theelevation in plasma K+ concentration. Other drugs likeangiotensin receptor inhibitors (ACE inhibitors),angiotensin receptor blocker (ARBs) and spironolactoneare often responsible for hyperkalaemia.Pseudohyperkalemiarepresents an artificially elevatedplasma K+ concentration due to K+ movement out ofcells immediately prior to or following venepuncture.Contributing factors include prolonged use of atourniquet with or without repeated fist clenching,hemolysis, and marked leukocytosis or thrombocytosis.Intravascular hemolysis, tumor lysis syndrome, andrhabdomyolysis all lead to K+ release from cells as a result of tissue breakdown. Magnesium is the major intracellular divalent cation thatforms a key complex with ATP and is an importantcofactor for a wide range of enzymes, transporters, andnucleic acids required for normal cellular function,replication, and energy metabolism. The concentrationof magnesium in serum is closely regulated within therange of 0.7–1.0 mmol/L.

Magnesium deficit is associated with several acute andchronic illness, of major concern is the association ofhypomagnesaemia with cardiovascular problems, suchas myocardial infarction, hypertension and congestiveheart failure. In addition, evidence is mounting regardingthe relationship between Type 2 Diabetes Mellitus, andmagnesium deficit. Hypomagnesaemia can result fromintestinal malabsorption; protracted vomiting, diarrhea,or intestinal drainage; defective renal tubular magnesiumreabsorption; or rapid shift of magnesium from the ECFinto cells, bone, or third spaces. Dietary magnesiumdeficiency 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.