The prevalence of diabetes in 2021 had been reported to be about 537 million people and is expected to rise to 783 million in 2045 worldwide [¹]. A conjugation of demographic and economic changes, with the association of large shifts in physical activity and dietary patterns, are properly considered a primary driver for the rise in diabetes in low- and middle-income countries [²]. Diabetes mellitus (DM) is a chronic disease causing insulin action resistance that leads to prolonged hyperglycemia besides metabolic disorders of lipids and protein [³]. Type 2 diabetes (T2DM), the most common type of DM, is characterized by an insulin resistance state that leads to a progressive decrease of adequate insulin secretion from \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\beta$\end{document}β-cells [⁴]. Many results show increased levels of Homeostatic Model Assessment-Insulin Resistance HOMA-IR and fasting serum glucose FSG in patients with diabetes when compared to non-diabetics [⁵]. Although an individual’s susceptibility to T2DM is determined by genetic predisposition, which is related to more than 88 genetic loci involved in susceptibility to T2DM [⁴], the increase in obesity, a sedentary lifestyle, industrialization, and energy-dense diets are responsible for making T2DM a widespread state [⁶]. Adiponectin was first described in 1995; it is a 30 kDa peptide generated in adipose tissues [⁷] exclusively produced by adipose tissue. Also, it is produced from skeletal muscles, cardiomyocytes, and endothelial cells [⁸]. The normal plasma level of 5–30 micrograms/ml [⁹]. There is a similarity between Adiponectin and Insulin in their effect on the liver and muscles concerning glucose metabolism, as shown in . CRP is a 206-amino acid [¹⁰]. C-reactive protein (CRP) estimation is considered a marker for systemic inflammation [¹¹]This study aims to estimate the serum levels of Adiponectin in relation to insulin, high-sensitivity C-reactive protein (hs-CRP), fasting serum glucose, and HOMA-IR in patients with T2DM compared with apparently healthy controls.

This study compared two groups: 45 patients with T2DM and 39 healthy controls. The T2DM patients were primarily middle-aged, with a mean age of 52.1 years (SD = 10.375), while the control group was younger, averaging 33.3 years (SD = 5.488), indicating a statistically significant age difference (p < 0.0001) . The analysis of body metrics showed that patients with T2DM had a higher mean weight of 83.088 kg (SD = 11.925) compared to 77.384 kg (SD = 14.401) in controls, with marginal statistical significance (p = 0.0502). However, the average height was comparable between groups—1.669 meters (SD = 0.095) for diabetics and 1.675 meters (SD = 0.089) for controls, which did not differ significantly (p = 0.7387) .

The biochemical profile revealed that FSG, hs-CRP, and HOMA-IR levels were significantly higher in the diabetic group (p < 0.05), while levels of fasting insulin and adiponectin were significantly lower compared to controls. Specifically, adiponectin levels were notably lower in T2DM patients at 14.848 µg/ml (SD = 7.790) versus 30.887 µg/ml (SD = 9.780) in controls (p < 0.0001) .

In addition, significant negative correlations were identified between adiponectin levels and both weight (r = -0.683, p = 0.001) and height (r = -0.740, p = 0.001) in the control group, underscoring the inverse relationship between adiponectin and body measurements in a healthy population .

The significantly (P<0.05) higher FSG, hs-CRP, and HOMA-IR levels in patients with diabetes compared to the controls may be explained by the hyperglycemia during type 2 diabetes participation in the inflammation process, which agrees with Wu et al. [¹⁵]This inflammation could lead to two effects: insulin resistance, as was found in Asimakidou et al. [¹⁶], and the significant (P<0.05) lowered adiponectin level, as agreed with El-Araby et al. [¹⁷]. The significantly (P<0.05) lowered level of insulin secretion in patients with diabetes could result from prolonged time exposure to the disease, which promotes hypo-insulinemia and hyperglycemia as \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\beta$\end{document}β-cells will be exhausted with time, agreeing with (Faraj et al.;2020) [¹⁸]Besides, people with diabetes age more than controls, as aging can cause a gradual loss of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\beta$\end{document}β-cell mass, which agrees with Nasteska et al. [¹⁹].

The significant (P<0.05) higher adiponectin level with concurrent significant (P<0.05) higher insulin level in controls as compared to people with diabetes may come from the effect of adiponectin in increasing insulin sensitivity, which agrees with Wu et al. [²⁰]. The significant (P<0.05) low levels of each of FSG, HOMA-IR, and hs-CRP in controls as compared to diabetics might be due to the anti-inflammatory effect of adiponectin, agreeing with Shimizu et al. [²¹]. It regulates glucose metabolism as adiponectin enhances glucose uptake in adipose and muscle tissues, as with Guo L et al [¹³]. The significant (P<0.05) negative correlation between adiponectin and weight with the concurrent significant (p<0.05) lower weight value in controls compared to diabetics could be a result of adiponectin’s influence in enhancing fatty acid oxidation [²²], the same was found in Lara-Guzmán et al.[²³]. The significant (P<0.05) negative correlation between adiponectin and height was also found by Norton et al., and they explained it on a genetic base [24] while disagreeing with Barnabé et al. [²⁴]. The limited sample size of 84 individuals may restrict the findings’ generalizability to the larger Iraqi population. The sample may not entirely reflect the variety of the entire country. As a result, the findings may not accurately reflect the country’s overall image. Future studies should use bigger, nationally representative samples to improve the external validity of the findings.

Adiponectin can ameliorate diabetes mellitus, insulin resistance, and overweight risks as it can decrease the levels of glucose, hs-CRP, and HOMA-IR and enhance insulin sensitization and fatty acid oxidation, suggesting using adiponectin in the improvement of the risks of these cases. Therefore, a merit investigation is requested to pave the way for this finding.