Published online Jun 5, 2026. doi: 10.4331/wjbc.v17.i2.118440
Revised: February 3, 2026
Accepted: May 21, 2026
Published online: June 5, 2026
Processing time: 154 Days and 16.3 Hours
Oxidative stress has been suggested to play a role in the pathogenesis of type 2 diabetes mellitus (T2DM) and development of complications by altering antio
To evaluate the levels of malondialdehyde (MDA) - a marker of lipid peroxidation and catalase (CAT) - an antioxidant enzyme in patients with T2DM categorized by glycemic control, and to compare these levels with those of apparently healthy individuals in Buea, Cameroon.
A hospital-based case-control study was conducted at Buea Regional Hospital from January 2024 to June 2024 involving patients with T2DM and age-matched healthy controls. Socio-demographic, clinical and anthropometric data were collected using a structured questionnaire. Levels of glucose, lipid profile, CAT and MDA were de
A total of 192 participants (96 patients with T2DM and 96 healthy controls) were recruited in this study. The mean age of the participants was were 47.97 ± 10.3 years with most being males (62.5%). CAT activity and high-density lipoprotein cholesterol levels were higher in control subjects (P < 0.05). The majority of patients with T2DM (80.2%) had a poor glycemic control. CAT activity was lower and MDA was significantly higher in patients with T2DM with poor glycemic control (P < 0.001). Glycated hemoglobin showed a significantly strong positive correlation with MDA levels (r = 0.846, P < 0.001) and a significantly strong negative correlation with CAT activity (r = -0.567, P < 0.001). Additionally, there was a significant negative correlation between CAT activity and MDA (r = -0.568, P < 0.001).
The results of this study indicated a significantly higher level of MDA and lower CAT activity in patients with T2DM compared to apparently healthy age-matched and sex-matched controls. Increased lipid peroxidation and decrease antioxidant enzyme activity were associated with poor glycemic control. The correlation between lipid peroxidation, antioxidant activity, and glycemic control highlights the role of oxidative stress in the pathophy
Core Tip: Hyperglycemia in type 2 diabetes mellitus (T2DM) generates free radicals which reduce antioxidant enzyme activities leading to oxidative stress. The influence of glycemic control on enhanced free-radical activity is poorly under
- Citation: Ojong EW, Nyake Mbu Akime LB, Tambe AB, Seukep AJ, Ofon EA, Akwa TC, Sawah CN. Glycemic status, antioxidant enzyme and lipid peroxidation among patients with diabetes mellitus in Buea Regional Hospital in Cameroon. World J Biol Chem 2026; 17(2): 118440
- URL: https://www.wjgnet.com/1949-8454/full/v17/i2/118440.htm
- DOI: https://dx.doi.org/10.4331/wjbc.v17.i2.118440
Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by chronic hyperglycemia and insufficient insulin action[1]. Nearly half a billion people worldwide are living with T2DM, with low-income and middle-income countries reporting the highest morbidity, mortality, and economic costs[2]. As of 2024, approximately 589 million adults (aged 20-79) are living with diabetes, representing roughly 1 in 9 adults[3]. This figure is expected to reach 853 million by 2050. Roughly 40%-50% of adults living with diabetes worldwide are unaware of their condition[3]. Africa currently has the lowest prevalence (4.5%) but is projected to see the most substantial increase (129%) by 2045. In 2024, diabetes was responsible for an estimated 3.4 million deaths. Diabetes is a leading cause of blindness, kidney failure, heart attacks, stroke, and lower limb amputations[3]. T2DM is managed by blood glucose measurement, lifestyle changes and use of oral or injectable medications[3]. Glycemic control is assessed by glycated hemoglobin (HbA1c), fasting blood glucose or a combination of both markers[3]. Maintaining optimal glycemic control is recommended as it delays or prevents the onset of debilitating diabetic complications such as nephropathy, retinopathy and cardiovascular diseases[3]. The cut-off points for defining good glycemic control depends on the guideline used.
Hyperglycemia in patients with T2DM increases free radical production and impairs the endogenous antioxidant defense system[4]. The excess synthesis and insufficient scavenging of free radicals such as reactive nitrogen species and reactive oxygen species (ROS) lead to oxidative stress[5]. Free radical formation in diabetes by non-enzymatic glycation of proteins, glucose oxidation and increased lipid peroxidation induces oxidative stress which damages antioxidant enzymes, cellular machinery and promotes increased insulin resistance[6]. Oxidative stress and increased levels of lipid peroxidation products like malondialdehyde (MDA) in patients with T2DM lead to the development of diabetic complications, vascular diseases and increased mortality[7]. As a stable secondary product of lipid peroxidation, MDA serves as a widely utilized biomarker for assessing oxidative stress; consequently, numerous studies suggest that elevated circulating MDA levels may function as a predictive marker for the development of diabetic complications[8,9]. Both enzymatic and non-enzymatic anti-oxidant defense systems in the human body combat oxidative stress[9]. Key antioxidant enzymes include superoxide dismutase, glutathione peroxidase and catalase (CAT). CAT acts as a regulator of hydrogen peroxide metabolism that can, in excess, cause serious damage to lipids, ribonucleic acid and deoxyribonucleic acid[8].
2H2O2 → 2H2O + O2, this reaction occurs in two stages involving the enzyme’s heme group: Enz(FeIII) + H2O2 → Compound I(FeIV = O•) + H2O (equation 1). Compound I (FeIV = O•) + H2O2 → Enz(FeIII) + H2O + O2 (equation 2).
CAT deficiency leads to production of excess ROS in beta cells of the pancreas causing their dysfunction and ultimately diabetes. Over the past decade, there has been substantial interest in the role of oxidative stress in diabetogenesis, development of diabetic complications, atherosclerosis and associated cardiovascular diseases[10]. Although increased levels of lipid peroxidation, as a consequence of free radical activity, have been reported in both type 1 and type 2 diabetes with vascular complications[11-13]; some studies failed to detect any significant elevation in lipid peroxidation in patients with diabetes[14], likely owing to the heterogeneity of the patient population. Few studies have attempted to describe the differences in plasma lipid peroxidation and antioxidant enzymes activities between patients with T2DM and healthy control groups[15,16]. Thus, the aim of this study was to evaluate the levels of MDA - measured as thiobarbituric acid reactive substances and activity of the antioxidant enzyme CAT in patients with T2DM with different glycemic status at the Buea Regional Hospital, South Western Cameroon and to compare these findings with healthy subjects. Effective diabetes management requires a multifaceted approach that combines strict blood sugar control with antioxidant support - achieved through diet, lifestyle, and supplementation - to prevent long-term tissue damage caused by oxidative stress.
A hospital-based case-control study was conducted from January 2024 to June 2024 at Buea Regional Hospital in the South West Region, Cameroon. Patients with T2DM and age and sex-matched healthy controls were recruited.
Patients with T2DM defined by the World Health Organization (WHO) criteria[17] enrolled at the diabetic center of the Buea Regional Hospital. Patients with T2DM aged > 21 years who provided written informed consent were recruited. Control individuals, consisting of patient caregivers confirmed by a medical doctor to be in stable health at the time of enrollment, who gave written informed consent were also included.
Patients with T2DM receiving treatment for chronic infections, kidney disease, cardiovascular disease, liver disease, lipid and thyroid disorders were excluded. Exclusion criteria for controls included, smokers, pregnant or lactating women, individuals on medications or supplements that may affect lipid peroxidation such as antioxidant therapy, statins, or omega-3 fatty acids. Controls who had chronic diseases that may affect lipid peroxidation, such as liver disease, kidney disease, or cancer were also excluded. None of the study subjects had received trace element supplementation in the previous 2-3 months.
A structured questionnaire was used to collect information on participants’ socio-demographic characteristics, clinical history, and physical examination. Participants’ heights and body weight were measured and recorded to the nearest 0.1 cm and 0.1 kg respectively, using a portable stadiometer (Seca GmbH & Co. KG, Hamburg, Germany) and a calibrated scale (Seca GmbH & Co. KG, CA, United States). Body mass index was calculated using the formula weight (kg) divided by the square of height (m2). With the aid of a mercury sphygmomanometer (OMRON Healthcare, Tokyo, Japan), systolic blood pressure and diastolic blood pressure were measured thrice following a 10-minute rest, and the average of these readings was recorded.
After an overnight fast of 8 hours to 14 hours, about 5 mL of venous blood samples were drawn from the antecubital vein of each participant following aseptic techniques. The blood was dispensed into fluoride oxalate tubes, ethylene diamine tetra-acetic acid tubes and dry tubes. Samples were centrifuged at 3000 rpm for 5 minutes to separate plasma and serum. The plasma obtained in the fluoride oxalate tube was used to measure fasting plasma glucose concentration by the glucose oxidase method using kits provided by Biolabo S.A.S (Maizy, France). Serum was used for the measurement of total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) by enzymatic colorimetric methods using the Chem Enzyme, Co kit (Codexis, CA, United States). MDA was measured as thiobarbituric acid reactive substances using the method described by Rael et al[16]. All biochemical analyses were performed on a semi-automated chemistry analyzer (RA50. Ames Bayer Diagnostics India, Mumbai, India). T2DM was defined based on the WHO criteria [fasting plasma glucose values ≥ 7.0 mmol/L (126 mg/dL)], 2-hour post-load plasma glucose ≥ 11.1 mmol/L (200 mg/dL), HbA1c ≥ 6.5% (48 mmol/mol); or random blood glucose ≥ 11.1 mmol/L (200 mg/dL) in the presence of signs and symptoms considered related to diabetes[17]. Blood collected in ethylene diamine tetra-acetic acid tubes was used to determine HbA1c by an ion exchange high performance liquid chromatography method, using kit supplied by LabCare Diagnostics India Pvt. Ltd (LabCare Diagnostics, Gujarat, India). Good glycemic control was defined as HbA1c < 7 and poor glycemic control when HbA1c > 7 in accordance with WHO reco
This study was approved by the Institutional Review Board of the Faculty of Health Sciences, University of Buea (Approval No. 2024/2425-02/UB/SG/IRB/FHS). After assessment of the research protocol, questionnaire, participants’ information leaflet and consent form. Further permission was obtained from the Regional Delegation of Public Health, Buea, South West Region Cameroon (No. P42/MPH//SWR/RDPH/CBPT/613/518) and from the Internal Review Board of the Regional Hospital Buea (No. MPH/SWRDPH/BRH/IRB). Voluntary and written informed consent was obtained from the study participants before recruitment into the study.
Data were analyzed using the Statistical Package for Social Sciences software version 26.0 (SPSS, Chicago, IL, United States). Data analysis was performed using both descriptive and inferential statistics. The n (%) were used to report categorical variables, and means ± SD to report continuous variables. The Kolmogorov-Smirnov and Shapiro-Wilk tests were performed to test data normality. Differences between categorical variables were assessed using the χ2 or Fisher’s exact test as appropriate. In addition, bivariate logistic regression model was used to examine the association between independent variables and lipid peroxidation. Group differences for measured biochemical parameters were compared using the independent samples t-test. The level of significance was set at 0.05 at 95% confidence interval.
The majority of the participants were males (62.5%) with an equal distribution in the diabetic group and control group. Furthermore, approximately half of the participants (49.5%) lived in semi-urban areas. while 57.3% were single. Furthermore, less than half of the participants (40.1%) were unemployed comprising 47.9% selected in the control group and 32.3% in the diabetic group (Table 1).
| Characteristics | Total (n = 192) | T2DM (n = 96) | Control (n = 96) |
| Age group (years) | |||
| 30-44 | 27 (14.1) | 11 (11.5) | 16 (16.7) |
| 45-59 | 64 (33.3) | 34 (35.4) | 30 (31.3) |
| ≥ 60 | 101 (52.6) | 51 (53.1) | 50 (52.0) |
| Gender | |||
| Female | 72 (37.5) | 36 (37.5) | 36 (37.5) |
| Male | 120 (62.5) | 60 (62.5) | 60 (62.5) |
| Educational status | |||
| No formal | 18 (9.4) | 10 (10.4) | 8 (8.3) |
| Primary | 75 (39.1) | 38 (39.6) | 37 (38.5) |
| Secondary | 70 (36.5) | 32 (33.3) | 38 (39.6) |
| Tertiary | 29 (15.1) | 16 (16.7) | 13 (13.5) |
| Residence | |||
| Rural | 36 (18.8) | 15 (15.6) | 21 (21.9) |
| Semi-urban | 95 (49.5) | 35 (36.5) | 60 (62.5) |
| Urban | 61 (31.8) | 46 (47.9) | 15 (15.6) |
| Marital status | |||
| Married | 17 (8.9) | 13 (13.5) | 4 (4.2) |
| Single | 110 (57.3) | 51 (53.1) | 59 (61.5) |
| Separated | 65 (33.9) | 32 (33.3) | 33 (34.4) |
| Occupation | |||
| Unemployment | 77 (40.1) | 31 (32.3) | 46 (47.9) |
| Self-employment | 73 (38.0) | 33 (34.4) | 40 (41.7) |
| Formal employed | 42 (21.9) | 32 (33.3) | 10 (10.4) |
The body mass index, HbA1c, TC, TG, LDL-C, MDA and fasting plasma glucose of patients with T2DM were significantly higher than those in the control group individuals (P < 0.05). However, the mean HDL-C was significantly lower in patients with T2DM (44.04 ± 11.29 mg/dL) compared to controls (56.98 ± 5.57 mg/dL; P < 0.001). CAT activity of controls was significantly higher in comparison with patients with T2DM (P = 0.04). Other measured parameters did not show significant differences between the two groups (Table 2).
| Variable | T2DM (n = 96) | Control (n = 96) | t test | P value |
| Weight (kg) | 76.29 ± 16.3 | 75.2 ± 14.3 | 1.70 | 0.34 |
| Height (m) | 1.61 ± 0.1 | 1.43 ± 2.1 | 0.45 | 0.55 |
| BMI (kg/m2) | 29.45 ± 6.6 | 27.38 ± 5.8 | 2.30 | 0.023 |
| WC (cm) | 101.27 ± 18.3 | 98.23 ± 15.6 | 0.32 | 0.64 |
| SBP (mm/Hg) | 126 ± 24.1 | 119 ± 14.2 | 0.03 | 0.99 |
| DBP (mm/Hg) | 84.34 ± 1.4 | 81.29 ± 3.6 | 0.33 | 0.32 |
| HbA1c (%) | 7.65 ± 0.85 | 4.83 ± 0.51 | 27.80 | < 0.001 |
| HDL-C (mg/dL) | 44.04 ± 11.29 | 56.98 ± 5.57 | -10.00 | < 0.001 |
| LDL-C (mg/dL) | 130.08 ± 14.98 | 120.9 ± 9.91 | 16.00 | < 0.001 |
| TG (mg/dL) | 138.60 ± 25.14 | 107.42 ± 11.25 | 11.40 | < 0.001 |
| TC (mg/dL) | 200.13 ± 15.15 | 175.85 ± 9.66 | 13.30 | < 0.001 |
| MDA (nmol/mL) | 1.45 ± 0.62 | 0.75 ± 0.26 | 10.03 | < 0.001 |
| FPG (mg/dL) | 181.37 ± 89.23 | 89.00 ± 80.00 | 10.03 | < 0.001 |
| CAT (U/L) | 49.23 ± 13.17 | 58 ± 14.23 | 12.20 | 0.04 |
Only 19 (19.8%) of patients with T2DM had good glycemic control while the majority of them 77 (80.2%) had poor glycemic control.
Patients with T2DM with good glycemic control had significantly lower (P < 0.001) HbA1c percentage (6.40 ± 0.38) compared to those with poor control (8.02% ± 0.67%). Similarly, mean LDL-C, TG, TC, and MDA concentrations were significantly lower (P < 0.05) in patients with good glycemic control. HDL-C levels were higher in patients with good glycemic control (58.69 ± 4.78 mg/dL) compared to the poorly controlled group (39.98 ± 9.27 mg/dL; P < 0.001). Furthermore, the mean CAT activity was significantly higher (P < 0.01) in the patients with good glycemic control (54.58 ± 17.19 U/L) than in those with poor glycemic control (33.26 ± 12.06 U/L; Table 3).
| Parameter | Good glycemic control (n = 19) | Poor glycemic control (n = 77) | t test | P value |
| HbA1c (%) | 6.40 ± 0.38 | 8.02 ± 0.67 | -9.1 | < 0.001 |
| HDL-C (mg/dL) | 58.69 ± 4.78 | 39.98 ± 9.27 | 7.7 | < 0.001 |
| LDL-C (mg/dL) | 107.06 ± 6.04 | 136.60 ± 11.42 | -9.9 | < 0.001 |
| TG (mg/dL) | 102.25 ± 12.60 | 145.08 ± 20.52 | -7.8 | < 0.001 |
| TC (mg/dL) | 184.88 ± 6.87 | 204.06 ± 16.14 | -4.6 | < 0.001 |
| MDA (nmol/mL) | 0.78 ± 0.14 | 1.61 ± 0.58 | -6.0 | < 0.001 |
| Catalases (U/L) | 54.58 ± 17.19 | 33.26 ± 12.06 | -6.3 | < 0.001 |
There was a significant strong positive correlation between HbA1c and MDA (r = 0.846, P < 0.001) and a significant strong negative correlation between HbA1c and CAT activity (r = -0.567, P < 0.001). Also, there was a significant strong negative correlation between CAT levels and MDA (r = -0.568, P < 0.001; Table 4).
| HbA1c (%) | MDA | FPG | Catalase | |||||
| r | P value | r | P value | r | P value | r | P value | |
| HbA1c (%) | 1 | |||||||
| MDA (nmol/mL) | 0.846 | < 0.001 | 1 | |||||
| FPG (mg/dL) | -0.129 | 0.21 | -0.123 | 0.233 | 1 | |||
| Catalase (U/L) | -0.567 | < 0.001 | -0.568 | < 0.001 | 0.08 | 0.437 | 1 | |
There was a significant association between CAT activity and MDA levels of patients with T2DM (P = 0.001). Also, glycemic status amongst patients with T2DM showed significant association with CAT activity (P = 0.002; Table 5).
| Characteristics | Catalase activity | χ2 test | P value | |
| Low | Normal | |||
| MDA | 10.48 | 0.001 | ||
| Normal | 5 (18.5) | 22 (81.5) | ||
| Abnormal (high) | 38 (55.1) | 31 (44.9) | ||
| Diabetes control (HbA1c concentration) | 5.398 | 0.002 | ||
| Good control | 4 (21.1) | 15 (78.9) | ||
| Poor control | 39 (50.6) | 38 (49.4) | ||
The current study demonstrates that patients with T2DM at Buea Regional Hospital are more prone to lipid peroxidation compared to apparently healthy controls as indicated by elevated levels of MDA. A similar observation was made by Okoduwa et al[19], who reported that lipid peroxidation is high in patients with T2DM compared to controls.
A study by Rani and Mythili[20] reported that MDA levels were significantly higher in patients with T2DM compared to controls. Similarly, Karadsheh et al[21], observed that MDA levels were significantly increased by 28%-41% in patients with diabetes mellitus, then in non-diabetic’s subjects. A systematic review and meta-analysis of 21 previous studies, based on the random-effects model of meta-analysis, reported significantly higher levels of serum MDA in patients with T2DM relative to control subjects[22]. Hyperglycemia is a widely known cause of enhanced plasma free radical concentrations[23]. The relationship between oxidative stress and diabetes mellitus is a complex, bidirectional phenomenon where chronic hyperglycemia induces the production of reactive species, which in turn impairs insulin signaling and accelerates systemic complications[28]. There are four known biochemical pathways by which hyperglycemia - induced free radical synthesis occurs, namely; increased glycolysis, intercellular activation of sorbitol (polyol) pathway, autooxidation of glucose and non-enzymatic protein glycation[24-27]. Griesmacher et al[28] reported increased lipid peroxi
According to the current study, significantly higher levels of MDA were observed in patients with T2DM who had poor glycemic control compared to those with good glycemic control. Levels of HbA1c were also positively correlated with levels of MDA. This finding corroborates the results of a study conducted at the First Affiliated Hospital of Xiamen University, China[30]. This finding suggests, that poorly regulated T2DM in the long-term leads to the release of ROS, which then induce oxidative stress. Hence, keeping blood glucose levels in check is imperative for preventing and limiting further complications in T2DM patients. A study correlating glycemic control with salivary oxidative markers in subjects with prediabetes and diabetes, and sex-matched normoglycemic individuals[31], reported that salivary MDA levels were significantly higher in individuals with diabetes compared to both the prediabetic and control groups. Findings from this study[31] suggest that while oxidative stress markers like MDA are elevated in diabetes, their correlation with glycemic control may not be as robust as previously thought, indicating the complexity of the rela
The current study also reports a significant association between CAT activity and glycemic control with patients with poor glycemic control having lower CAT activity compared to those with good control. Rodríguez-Carrizalez et al[32], reported that erythrocyte CAT activity increases in patients with T2DM compared to controls. Okoduwa et al[19], reported significant decreases in CAT activities in patients with T2DM and hypertensives compared to controls. The observation in CAT activity of the current study contradicts the finding of Ali et al[33], who found no significant difference in CAT between patients with T2DM and controls. Decreased CAT activity has also been reported in patients with T2DM with diabetic retinopathy[34]. The inverse relationship between CAT and HbA1c is driven by non-enzymatic glycation of the enzyme itself, the inhibitory effects of superoxide radicals, and the exhaustion of antioxidant defenses under chronic hyperglycemic stress[34].
We acknowledge that the single-center nature of the study, conducted only at Buea Regional Hospital, limits the generalizability of the findings to the broader type 2 diabetes population in Cameroon. Furthermore, the cross-sectional design of the study cannot establish causal relationships between diabetes mellitus, antioxidant status and lipid peroxidation. Additionally, unmeasured factors such as diet and lifestyle behaviors may have influenced oxidative stress levels and were not fully accounted for. Notwithstanding this limitation, to the best of our knowledge, this study is the first to assess antioxidant enzyme levels and lipid peroxidation of patients with T2DM and healthy control individuals in the Buea Health District, a setting where metabolic research is limited. Its robust case-control design, with an adequate sample size and age-matched controls, strengthens the reliability of the findings and minimizes confounding.
The results of this study found a significantly higher level of MDA and lower CAT activity in patients with T2DM compared to apparently healthy age and sex-matched controls. Furthermore, lipid peroxidation and decrease antioxidant enzyme activity were associated with poor glycemic control. These findings underscore the critical role of oxidative stress in the pathogenesis of T2DM and the paramount importance of maintaining optimal glycemic control in T2DM mana
We thank all patients with T2DM and caregivers at Buea Regional Hospital who consented to participate in this study. We also thank the management of Buea Regional Hospital.
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