The cross-sectional observational study enrolled 360 participants from clinical cohorts in the Congolese capital and divided them into three groups. Group I comprised 240 patients with isolated type 2 diabetes, Group II included 100 patients with isolated chronic hepatitis C infection, and Group III consisted of 20 patients in whom both diseases were present simultaneously. For every participant, the team measured fasting plasma glucose, fasting insulin, and a panel of inflammatory biomarkers: high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). From the fasting glucose and insulin values, the researchers calculated the homeostatic model assessment of insulin resistance, or HOMA-IR, using the conventional mass-unit formula adjusted for glucose expressed in grams per liter — a technical detail that matters, because inconsistent unit conventions are a well-known source of error in HOMA-IR calculations across studies.

The headline result concerns the corrected median HOMA-IR scores. After strict recalculation of the metabolic parameters, the comorbid Group III recorded a median HOMA-IR of 7.11, significantly higher than the 5.43 observed in the type 2 diabetes group and the 1.98 seen in the chronic hepatitis C group, with a P value below 0.001. To put those numbers in context, a HOMA-IR score of 2.5 is conventionally taken as the threshold above which a person is considered insulin resistant — the state in which the body’s tissues respond poorly to insulin and the pancreas must produce ever-larger amounts of the hormone to keep blood glucose under control. The comorbid patients were not merely above that threshold; they were nearly three times above it.

The frequency of insulin resistance followed the same gradient. Defined as HOMA-IR of at least 2.5, insulin resistance was present in 95.0 percent of the dual-pathology patients, with a 95 percent confidence interval stretching from 75.1 to 99.9 percent — a range so wide precisely because the comorbid group contained only 20 individuals, but a point estimate that leaves little doubt about the direction of the effect. Among patients with type 2 diabetes alone, 84.6 percent were insulin resistant, while only 31.0 percent of those with chronic hepatitis C alone met the criterion. Within the broader hepatitis C clinical sample of 120 patients, type 2 diabetes coexisted in 16.7 percent, or 20 of 120 cases — a proportion that hints at how often the two conditions overlap in routine Congolese clinical practice.

The inflammatory biomarker panel told a parallel story. High-sensitivity C-reactive protein, IL-6, and TNF-α all displayed significant elevation in the presence of dual pathology compared with either condition in isolation. These three molecules are central players in the biology of chronic inflammation. C-reactive protein, produced by the liver in response to inflammatory signals, is one of the most reliable single indicators of low-grade systemic inflammation. IL-6 is a cytokine secreted by immune cells and, notably, by adipose tissue itself, and it acts as a messenger that recruits and activates further inflammatory responses. TNF-α, another pro-inflammatory cytokine, has long been implicated in disrupting insulin signaling pathways, promoting the serine phosphorylation of insulin receptor substrates that impairs the downstream transmission of the insulin signal.

Crucially, the study found that the inflammatory markers demonstrated a strong continuous correlation with HOMA-IR values — meaning that as insulin resistance deepened, the inflammatory burden rose in lockstep across the cohort. This correlation is biologically plausible and, in the view of many metabolic researchers, reflects a genuine mechanistic loop rather than a statistical coincidence. Chronic hepatitis C infection is known to perturb glucose metabolism through direct viral effects on insulin signaling in hepatocytes, while type 2 diabetes is itself characterized by a state of chronic low-grade inflammation driven largely by excess adipose tissue and ectopic fat deposition. When both processes operate in the same patient, the two sources of inflammatory drive can compound, feeding a vicious cycle in which inflammation worsens insulin resistance and insulin resistance, in turn, promotes further inflammation.

The clinical intersection between chronic hepatitis C and type 2 diabetes has been characterized in other regions of the world — studies from Egypt, for instance, have explored insulin receptor genetic variants in patients with both conditions, and research following direct-acting antiviral therapy has shown that clearing the virus can improve glucose metabolism — but Central Africa has remained largely a blank space on this map. The Congolese study is among the first to bring quantitative metabolic and immunological data to bear on the question in a Central African population, where the epidemiology of both diseases differs from that of North America, Europe, or North Africa. Hepatitis C in the region is often acquired through healthcare-associated transmission and remains underdiagnosed, while diabetes is expanding rapidly as urban diets and lifestyles shift.

Statistically, the team handled the comparison with methods appropriate for skewed laboratory data. Because biomarker distributions are rarely normal, inter-group comparisons were executed using Kruskal-Wallis tests — a non-parametric alternative to analysis of variance that compares medians rather than means — followed by Dunn’s post-hoc tests with Bonferroni correction to control for the inflated risk of false positives that arises when multiple pairwise comparisons are performed. The Bonferroni correction, which tightens the significance threshold in proportion to the number of comparisons, is a conservative safeguard, and the fact that the differences survived it strengthens confidence in the reported gradient of insulin resistance across the three groups.

The study’s limitations are worth acknowledging alongside its strengths. The comorbid group contained only 20 participants, which is why the confidence interval around the 95.0 percent estimate of insulin resistance is so broad, and the cross-sectional design means the data can show association but not causation — it cannot determine whether hepatitis C infection accelerates the development of diabetes, whether diabetes worsens the metabolic impact of hepatitis C, or whether both are driven by shared underlying factors such as obesity, diet, or genetic susceptibility. Longitudinal follow-up of dual-pathology patients, ideally with serial measurements of HOMA-IR and inflammatory markers before and after antiviral treatment, would be needed to disentangle the direction of the relationship.

Nevertheless, the practical message for clinicians is clear and urgent. The authors conclude that in this Congolese population, the coexistence of chronic hepatitis C and type 2 diabetes is strongly associated with an aggravated profile of insulin resistance and heightened systemic inflammation compared to either condition alone, and they underscore the need for systematic metabolic surveillance in patients presenting with dual clinical presentations. In concrete terms, that means a patient walking into a Congolese clinic with type 2 diabetes should be screened for hepatitis C, and a patient diagnosed with chronic hepatitis C should have their fasting glucose, fasting insulin, and inflammatory markers checked rather than assumed normal. The research received no specific grant from any funding agency and was approved by the Comité d’Éthique de la Recherche en Sciences de la Santé, the national ethics committee of the Republic of the Congo, with written informed consent obtained from all participants in accordance with the Declaration of Helsinki. As diabetes continues its expansion across sub-Saharan Africa and hepatitis C persists in the shadows of underfunded health systems, studies like this one make the case that the two epidemics can no longer be managed in separate silos — the metabolic consequences of their overlap are simply too severe to ignore.

Subject of Research: coexisting chronic hepatitis C and type 2 diabetes in a Congolese population

Article Title: Association of coexisting chronic hepatitis C and type 2 diabetes with insulin resistance and inflammatory profiles in a Congolese population

Article References: Varret, M. B., Ludmilhia, F. G., Wilson, N. D., Miguel, L., Moukassa, D., & Etienne, N. (2026). Association of coexisting chronic hepatitis C and type 2 diabetes with insulin resistance and inflammatory profiles in a Congolese population. BMC Endocrine Disorders. https://doi.org/10.1186/s12902-026-02643-x

Image Credits: AI Generated

DOI: 10.1186/s12902-026-02643-x

Keywords: hepatitis C, type 2 diabetes, insulin resistance, HOMA-IR, inflammation, Congo, hs-CRP, IL-6, TNF-alpha, Association, coexisting, chronic