







































_____________________________________________________________________________________________________ 
 
*Corresponding author: E-mail: angeayissi04@gmail.com, mondinde@yahoo.com; 
 
Cite as: Ayissi Marie-Ange, Biwole Sida Ghyslaine, Guiedem Elise, Yayah Emerencia Ngah, Jacky Bikio, Emilia Lyonga, 
Martha Messembe, Mispa Yivala Mbanyamsig, and Georges Ikomey. 2025. “Role of Tumour Necrosis Factor-Alpha and 
Adiponectin in Insulin Therapy Failure in Type 2 Diabetic Patients”. Asian Journal of Immunology 8 (1):249–256. 
https://doi.org/10.9734/aji/2025/v8i1176. 

 
 

Asian Journal of Immunology 
 
Volume 8, Issue 1, Page 249-256, 2025; Article no.AJI.146139 
 

 
 

 

 

Role of Tumour Necrosis Factor-Alpha 
and Adiponectin in Insulin Therapy 
Failure in Type 2 Diabetic Patients 

 
Ayissi Marie-Ange a, Biwole Sida Ghyslaine b,  

Guiedem Elise b,c, Yayah Emerencia Ngah d,e, Jacky Bikio b, 
Emilia Lyonga b,f, Martha Messembe b,  

Mispa Yivala Mbanyamsig g and Georges Ikomey a,b,f* 
 

a Catholic University of Central Africa Yaounde, Cameroon. 
b Faculty of Medicine and Biomedical Sciences, University of Yaoundé 1, Cameroon. 
c Siantou Higher School of Health Sciences, Siantou University Institute, Cameroon. 

d Department of Public Health, Faculty of Health Science, Texila American University, Zambia. 
e Regional Hospital Bamenda, Cameroon. 

f Cameroon Centre for the Study and Control of Communicable Diseases (CSCCD), FMBS, 
Cameroon. 

g University of Skövde, Sweden. 
 

Authors’ contributions  
 

This work was carried out in collaboration among all authors. Authors AM-A and GI were responsible for 
development of research concept, recruitment of patients, laboratory analyses, interpretation of results and 

participated in the initial drafting of the manuscript. Authors BSG, GE, YEN were responsible for development of 
research concept, interpretation of results and drafting of manuscript. Authors MM, EL, JB, and MYM contributed 

to the laboratory analyses and drafting of the manuscript. All authors read and approved the final manuscript. 

 
Article Information 

 
DOI: https://doi.org/10.9734/aji/2025/v8i1176  

 
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Received: 18/08/2025 
Published: 03/11/2025 

 
 

Short Research Article 

https://doi.org/10.9734/aji/2025/v8i1176
https://pr.sdiarticle5.com/review-history/146139


 
 
 
 

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250 

 

ABSTRACT 
 

Background: Tumour necrosis factor alpha (TNF-α) and Adiponectin are both Pro and anti-
inflammatory cytokines that play major roles in the pathogenesis and therapeutic management of 
many metabolic diseases.  
Aim: This study aimed at evaluating the role of TNF-α and Adiponectin amongst Insulin-Treatment 
Failure and insulin therapy success in type 2 Diabetic Mellitus subjects using enzyme-linked 
immunosorbent assay (ELISA). 
Methodology: The study was conducted at the Diabetic unit of the Cité verte hospital, Yaounde, 
Cameroon, between February 2023 and March 2024. A case-control study was conducted with 80 
enrolled participants (41 insulin-treated patients with poor glycemic control and 39 patients with 
good glycemic control on insulin. The TNF-α, adiponectin and glycated haemoglobin were 
measured on whole blood specimens using immunoassay techniques. The Graph Pad Prism 5.0 
and EPI Info 7.1. software was used for the analysis of data. 
Results: TNF-α and Glycated haemoglobin (HbAIc) mean levels were higher in insulin-treated 
patients with poor glycemic control (TNF-α: 19.4 ± 8, HbAIc: 35.26 ± 11pg/ml) compared to patients 
with good glycemic control (TNF-α: 17.1 ± 6 pg/ml, HbAIc: 21.5 ± 5 pg/ml) with p < 0.001. The 
Adiponectin mean levels were lower in subjects with treatment failure (5.62 ± 4 pg/ml) compared to 
patients with treatment success (6.33 ± 6 pg/ml), was not statistically significant, p=0.0818. A 
negative correlation was observed between TNF-α and Adiponectin in subjects with treatment 
failure, with r=-0.03, which was not statistically significant, p=-0.08.  
Conclusion: The variation of TNF-alpha and Adiponectin in uncontrolled patients on insulin 
therapy and well-controlled patients could justify their implications in the pathogenesis of type 2 
diabetes. The increased levels of TNF-α, HbAIc, combined with the low levels of adiponectin, could 
be exploited as signalisation biomarkers for monitoring Insulin treatment failure and other metabolic 
dysregulation and inflammation. 

 

 
Keywords: Type 2 diabetes; pro-inflammatory cytokines; insulin-treatment failure; insulin-treatment 

success; adiponectin. 
 

1. INTRODUCTION 
 

"Diabetes mellitus (DM) is a disease 
characterised by the disturbance of glucose 
homeostasis owing to insulin malfunction in the 
target tissues, causing abnormalities in fat, 
protein, and carbohydrate metabolism. The 
principal hallmark of the disease is an elevated 
glucose level in the venous plasma, which is the 
gold standard for the diagnosis of DM. The 
elevation of plasma glucose level is caused by 
absolute insulin deficiency, as in type 1 diabetes 
(T1DM), or increased insulin resistance, as in 
T2DM or both" (Emad-Eldin et al., 2024). "The 
management of insulin-treatment failure (ITF) in 
type 2 diabetes mellitus (T2DM) represents a 
major public health challenge worldwide. Despite 
regular insulin injections, many patients 
experience persistent hyperglycemia, frequent 
hypo- or hyperglycemic episodes, and 
unexplained weight fluctuations. One of the key 
mechanisms underlying these complications is 
chronic low-grade inflammation, which interferes 
with glucose metabolism and pancreatic β-cell 
function" (Beutler & Cerami, 1989; Hotamisligil et 
al., 1993; Hotamisligil, 2000). "Cytokines play a 

central role in this process. Pro-inflammatory 
cytokines such as tumour necrosis factor-alpha 
(TNF-α), interleukin-1β (IL-1β), and interleukin-6 
(IL-6) are consistently elevated in T2DM 
patients" (Chen et al., 2015; Bastard et al., 2002; 
Choi, 2016). "TNF-α, in particular, induces insulin 
resistance by disrupting insulin signalling 
pathways in peripheral tissues and promoting β-
cell apoptosis through oxidative stress and 
endoplasmic reticulum dysfunction" (Lee & Lee, 
2014; Wensveen et al., 2015; Shamsi et al., 
2018). 
 

"Adiponectin, is referred to as AdipoQ, APM1, or 
ACRP30, is composed of 244 amino acids, with 
a molecular weight of around 26 kilodaltons 
(kDa) secreted by white adipose tissue" (Yu et 
al., 2022). "These proteins are encoded by the 
AdipoQ gene and are located on the 
chromosome locus 3q27. They are secreted by 
adipose tissue, exerts protective effects by 
enhancing insulin sensitivity, stimulating lipid 
oxidation, and providing cardiovascular 
protection" (Sajid et al., 2018; Swaroop et al., 
2012; Jeon et al., 2018). "Adiponectin exists in 
various isoforms— low, medium, and high 



 
 
 
 

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251 

 

molecular weight—which exert their effects via 
receptors AdipoR1, AdipoR2, and T-cadherin, 
differentially expressed across tissues and 
immune cells. These distinct isoforms and 
receptor interactions underscore the complexity 
of adiponectin signalling and its broad spectrum 
of physiological effects" (Gianoli et al., 2025; 
Patel et al., 2021).  
 
"However, reduced circulating levels of 
adiponectin are frequently observed in patients 
with obesity and T2DM, which contributes to the 
development of insulin resistance" (Liu et al., 
2016; Matthews et al., 1985). "They cross-talk 
between adipocytes and immune cells, 
particularly macrophages, further aggravate this 
inflammatory state, creating a cycle of metabolic 
inflammation that fuels insulin resistance" (Van 
Dielen et al., 2004; Yudkin et al., 2000; Sartipy & 
Loskutoff, 2003). Glycated haemoglobin (HbA1c) 
is a measurement used for glycaemic control. 
The HbA1c was introduced into clinical use in the 
1980s and subsequently has become a major 
guide for clinical practice.  
 
 Recent studies suggest that "the balance 
between pro-inflammatory cytokines (e.g., TNF-
α) and anti-inflammatory adipokines (e.g., 
adiponectin) may serve as predictive markers for 
insulin therapy outcomes in T2DM" (Morris et al., 
2006; Samad et al., 1997; Swaroop et al., 2012). 
The goal of this study was to evaluate the role of 
TNF-α and Adiponectin amongst Insulin-
Treatment Failure (ITF) and success (ITS) T2DM 
subjects attending the Endocrinology unit of the 
clinical setting in a sub-Saharan African 
population Hospital, Cameroon. 
 

2. MATERIALS AND METHODS 
 

2.1 Study Design 
 
The study was a case-control study with 80 
participants enrolled between February 2023 and 
March 2024. All participants were consecutively 
recruited from the diabetic unit of the Cité verte 
hospital during daily routine consultation. 
 

2.2 Study Population  
 
The study population was made up of 80 diabetic 
patients divided into two groups: a group of 
patients with   Insulin-Treatment Failure (ITF) 
consisting of 41 subjects as the case group and 
a group of 39 people with Insulin-Treatment 
Success (ITS) as the control group. The glycated 
haemoglobin (HbAIc) levels were considered for 

the selection of participants in the study. 
Specimens were aliquoted and stored at −80°C 
until ready to be used. Demographic data and 
clinical information were gathered for each 
participant through a standard questionnaire, 
which covered parameters like age, gender, 
insulin regimen, and duration of insulin treatment. 
 

2.3 Sample Collection and Analysis Site  
 
Five millilitres (5ml) of whole blood were 
collected, transported and analysed at the Centre 
for the Study and Control of Communicable 
Diseases (CSCCD) of the Faculty of Medicine 
and Biomedical Sciences (FMBS), University of 
Yaoundé I, Cameroon. Serum specimens were 
obtained by centrifuging whole blood at 5000 rpm 
for 5 minutes and subsequently stored in cryo-
vals at -20°C. All samples were analysed within 
two months of collection to prevent cytokine 
degradation over time. 
 

2.4 Laboratory Measurements 
 
2.4.1 Measurement of TNF-α and adiponectin 
 
TNF-α and Adiponectin were measured using 
quantitative sandwich Enzyme-linked 
Immunosorbent Assay (ELISA) kits from 
Invitrogen (Thermo Fisher Scientific, USA). A 
solid-phase Immune Enzymatic technique was 
employed on a microtiter plate for the 
quantitative determination of TNF-α and 
Adiponectin in human plasma. Samples were 
analysed according to the manufacturer's 
specifications. The absorbance was read using a 
spectrophotometer (Biotech ELx800, USA) set at 
a dual wavelength of 450-550 nm, with each 
sample run in duplicate. The concentration of 
both cytokines was determined by extrapolating 
the results from a standard curve generated by 
plotting the average absorbance (450-550 nm) 
obtained. 
 

2.4.2 Measurement of glycated haemoglobin 
(HbA1c) using immune turbidimetry 

 

Glycated haemoglobin was measured by 
Immunoturbidimetry using antibodies specific to 
HbA1c.The immunoturbidimetric instrument 
measured the changes in the sample. All the 
procedures as recommended by the 
manufacturer were respected. 
 

2.5 Statistical Analyses 
 

Data were analysed using the Graph Pad PRISM 
5.0 software package (Graph Pad Software Inc., 



 
 
 
 

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252 

 

La Jolla, California, USA) and Epi Info 7.0 
software (Epi Info™). Comparisons between 
TNF-α and Adiponectin within the various groups 
were conducted using the non-parametric 
Student's T-test. The correlations between TNF-
α and Adiponectin were determined using 
Pearson’s correlation coefficient. A significance 
level of p < 0.05 was considered statistically 
significant. 
 

3. RESULTS AND DISCUSSION 
 

3.1 Patient Characteristics 
 

We enrolled 80 diabetic patients, of whom 65 % 
(n= 52) were females and 35 % (n= 28) males. 
Their mean age (± SD) was 56.89 ± 11.08 years. 
Patients were classified into two groups: Insulin 
Treatment Failure 51 %, n= 41, and Insulin 
Treatment Success 49 %, (n= 39). 
 

3.2 Levels of TNF-α  
 

The TNF-alpha levels were higher in ITF subjects 
compared to ITS subjects, with a mean ± SD of -

0.1418±5 pg/ml, and -3.135±4 pg/ml, with p 
≤0.001. The levels of glycated haemoglobin were 
higher in ITF compared to ITS, with a mean of 
9.4 ±8 % and 6.37±6 %. The TNF-alpha levels 
were higher in ITF subjects compared to ITS 
subjects, with a mean ± SD of -0.1418±5                     
pg/ml, and -3.135±4 pg/ml, with p ≤0.001. The 
levels of Adiponectin were lower in ITF                  
subjects compared to ITS subjects, with a mean 
±SD of 5.62±4 pg/ml and 6.332±6 pg/ml, with 
p=0.081. 
 

3.3 Levels of Adiponectin 
 
Adiponectin concentrations varied between 1.60 
and 8.97 pg/ml in ITF subjects, and from 2.252 to 
10.51 pg/ml in ITS subjects (Fig. 2). This                      
study revealed relatively lower levels of 
adiponectin in insulin-treated subjects than in our 
controls, but with a statistically non-significant 
difference (p=0.0818). The levels of glycated 
haemoglobin were higher in ITF compared to 
ITS, with a mean of 9.4 ± 8 % and 6.37±6 % 
respectively. 

 

 
 

Fig. 1. The dot plot illustrates the plasma levels of TNF-α in insulin treatment failure and 
success groups 

 
Table 1. The plasma levels of TNF-Α and ADP in insulin treatment failure and success groups 

 
Variable ADP TNF 

 ITF (Median) 
n=41 

ITS (Median) 
n= 39 

P ITF (Median) n=41 ITS (Median) n=39 P 

Sexe       
Female 5.94 (2.1-7.01) 6.50 (2.25-9.08) 0.79 -1.06 (-4.8 – (-5.31)) -4.83 (-6.17 - 3.15) 0.24 
Male 5.90 (1.60- 8.48) 6.99 (2.5-10.5) 0.46 -0.73 (-4.17- 5.60) -4.51 (-5.95 - 3.38) 0.32 

Age       
[20-40] 5.873 (3.5-7.49) / / -0.8406 (-3.5-5.37) / / 
[41-60] 5.86 (1.60-8.48) 6.36 (2.93-10.5) 0.65 -2.06 (-4.84 - 5.6) -5.17 (-6.18 -  3.38) 0.33 
[61-80] 5.69 (3.7-8.97) 6.99 (2.25-9.08) 0.57 0.71(-3.51 - 4.49) -5.06 (-5.95 - 2.49) 0.27 



 
 
 
 

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253 

 

 
 

Fig. 2. The dot plot illustrates the plasma levels of ADP in insulin treatment failure and success 
groups 

 

 
 

Fig. 3. Association between TNF-α and ADP in the general population study 
 

3.4 Correlation between TNF-alpha and 
Adiponectin 

 
There was a negative correlation between TNF-
alpha and Adiponectin in ITF subjects, with r=-
0.03 but non statistically significant p=-0.08. It is 
understood that within the two populations, for 
concentrations of TNF-alpha that evolve in an 
increasing way, we have concentrations of 
Adiponectin, which evolve in a decreasing Our 
results corroborate those of Chenxiao Liu et al. 
(2016), who found after a meta-analysis that the 
overall risk of T2DM is strongly associated with 
high levels of inflammatory cytokines, including 

TNF-alpha, and low levels of Adiponectin 
Showing that an interaction between 
inflammation and the development of T2 
diabetes  in subjects. 
 

4. DISCUSSION 
 

The results obtained show that the levels of TNF-
alpha are significantly higher in ITF subjects, 
compared to ITS. Among other things, our results 
showed a significant difference between the two 
populations (p≤0.001); with concentrations 
varying between -4.838 and 5.600 pg/ml in ITF 
subjects and -6.170 to 3.379 pg/ml of blood in 
ITS subjects.  



 
 
 
 

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254 

 

This is in line with the results of several scientific 
articles, which have also reported elevated levels 
of TNF-alpha in insulin-treated diabetics. 
According to the study by Shamsi et al. (2018), 
"TNF-alpha is associated with insulin resistance 
in these subjects". In addition, in the study 
conducted by Sajid et al. (2018) on "the role of 
TNF-alpha in the development of insulin 
resistance and the pathogenesis of T2DM, high 
levels of TNF-alpha have been shown to induce 
insulin resistance, which impairs insulin, 
contributing to the development of T2DM". 
Swaroop et al (2012) found "a positive but also 
significant correlation between TNF-alpha and 
HOMA IR (homeostasis assessment method to 
calculate insulin resistance) in T2DM subjects, 
suggesting an involvement of TNF-alpha in the 
development of insulin resistance. It is 
understood that within the two populations, for 
concentrations of TNF-alpha that evolve in an 
increasing way, we have concentrations of 
Adiponectin, which evolve in a decreasing way". 
 
 Our results corroborate those of Chenxiao Liu et 
al. (2016), who found after "a meta-analysis that 
the overall risk of T2DM is strongly associated 
with high levels of inflammatory cytokines, 
including TNF-alpha, and low levels of 
Adiponectin, showing that an interaction between 
inflammation and the development of T2DM". 
The results of this study also support the findings 
of Jeon et al. (2018), who evaluated "the level of 
Adiponectin in subjects with T2DM and healthy 
subjects, reporting a low concentration of 
adiponectin in subjects with type 2 diabetes".  
 
The analyses also showed that there was an 
inverse (r = -0.03) and non-significant (p = 0.82) 
correlation between TNF-alpha and Adiponectin 
ITF subjects. Similarly, there is an inverse 
correlation between TNF-alpha and Adiponectin 
in non-insulin-treated subjects (r= -0.08), but this 
does not remain very significant (p= 0.59). 
 

5. CONCLUSION 
 
The increased levels of TNF-alpha, HbAIc, 
combined with the low levels of adiponectin, 
could be exploited as s ignal isat ion 
biomarkers for monitoring Insulin treatment 
failure and other metabolic dysregulation and 
inflammation. The variation of TNF-alpha and 
Adiponectin in the serum of Treatment Failure 
and non-failure Diabetic patients could justify 
their implications in the pathogenesis of type 2 
diabetes and be a good predictive marker for its 
management. 

CONSENT 
 
All authors declare that written informed consent 
was obtained from the patients (or other 
approved parties) for publication of this study.  
 

ETHICAL APPROVAL  
 
All authors hereby declare that the study was 
conducted in accordance with ethical standards 
approved by the Cameroon National Ethics 
Committee, N° 
2023/0220409/CEIRSH/ESS/MIM, and have 
therefore been performed in accordance with the 
ethical standards laid down in the 1964 
Declaration of Helsinki. 
 

DISCLAIMER (ARTIFICIAL INTELLIGENCE) 
 
Author(s) hereby declare that NO generative AI 
technologies such as Large Language Models 
(ChatGPT, COPILOT, etc) and text-to-image 
generators have been used during writing or 
editing of this manuscript.  
 

ACKNOWLEDGEMENT 
 
The authors thank the staff of the Cite vert 
Hospital and the Centre for the Study and 
Control of Communicable Diseases, Faculty of 
Medicine and Biomedical Sciences, University of 
Yaounde, Cameroon. 
 

COMPETING INTERESTS  
 

Authors have declared that they have no known 
competing financial interests or non-financial 
interests or personal relationships that could 
have appeared to influence the work reported in 
this paper. 

 
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