Current Organizations / Institutes

The organizations/institutes from the scholar's latest article

Previous Organizations / Institutes

The organizations / institutes from the scholar's other articles in the past ten years


Joe Varghese has a total of 11 co-authors. Here are the top co-authors by number of shared publications:


Latest Publications

  • Open Access

    COVID-19 Vaccine Hesitancy among Population in Jazan Region of Saudi Arabia

    by Manal Almalki, Mohammed Kotb Sultan, Mohammed Abbas, Ajiad Alhazmi, Yasser Hassan, Joe Varghese

    COVID-19 vaccine acceptance and refusal vary across countries and among different socio-demographic groups. This study investigates hesitancy related to the COVID-19 vaccine and the associated factors in the rural-community-dominated Jazan Province, Saudi Arabia. A cross-sectional study through an online questionnaire was conducted from February to April 2021 to investigate the extent of vaccine hesitancy related to the COVID-19 vaccine and the associated factors in the Jazan region. A Chi-squared test and post hoc analysis were conducted to analyze the statistical significance of the association between variables. Of the 569 participants who completed the online questionnaire, the majority were males (81.5%) and had a university education (72.6%). Of the participants, more than one-third (36.9%) were hesitant to vaccinate. Concern about adverse side effects following vaccination was the most reported reason for vaccine hesitancy (42.6%), followed by beliefs that the vaccine was unsafe or ineffective (15.5%). The data analysis revealed that people who lived in cities in Jazan Province or those who did not have a family history of COVID-19 infection were more likely to be vaccine hesitant. It is more important than ever to develop and implement community-based strategies to address vaccine hesitancy, especially in rural areas.


  • Open Access

    Insulin resistance and adipose tissue inflammation induced by a high-fat diet are attenuated in the absence of hepcidin

    by Jithu Varghese James, Joe Varghese, Nikhitha Mariya John, Jean-Christophe Deschemin, Sophie Vaulont, Andrew T. McKie, Molly Jacob

    Increased body iron stores and inflammation in adipose tissue have been implicated in the pathogenesis of insulin resistance (IR) and type 2 diabetes mellitus. However, the underlying basis of these associations are unclear. In order to assess this, we studied how IR and associated inflammation in adipose tissue developed in the presence of increased body iron stores. Male hepcidin knock-out ( Hamp1 -/- ) mice, which have increased body iron stores, and wild-type (WT) mice were fed a high-fat diet (HFD) for 12 and 24 weeks. Development of IR and metabolic parameters linked to this, insulin signaling in tissue, and inflammation and iron-related parameters in visceral adipose tissue were studied in these animals. HFD-feeding resulted in impaired glucose tolerance in both genotypes of mice. In response to the HFD for 24 weeks, Hamp1-/- mice gained less body weight and developed less IR than corresponding WT mice. This was associated with less lipid accumulation in the liver and decreased inflammation and lipolysis in the adipose tissue in the knock-out mice, than in the WT animals. Fewer macrophages infiltrated the adipose tissue in the knockout mice than in wild-type mice, with these macrophages exhibiting a predominantly anti-inflammatory (M2-like) phenotype. These observations suggest a novel role of hepcidin (central regulator of systemic iron homeostasis) in the development of inflammation in adipose tissue and insulin resistance, in response to a high-fat diet. CLINICAL PERSPECTIVES: Elevated body iron stores and inflammation in adipose tissue have been implicated in the pathogenesis of insulin resistance (IR) and type 2 diabetes mellitus. However, the underlying molecular mechanisms linking them are unclear. In response to high-fat diet (HFD)-feeding (to induce IR), mice that lacked hepcidin ( Hamp1 -/- ) (and hence had elevated body iron stores) gained less body weight and developed less insulin resistance than wild-type (WT) mice. Inflammation and infiltration of macrophages into adipose tissue of HFD-fed Hamp1 -/- mice were less than in WT mice, with the macrophages exhibiting an anti-inflammatory M2-like phenotype. These findings suggest a novel role of iron and hepcidin in HFD-induced inflammation in adipose tissue and development of insulin resistance. They raise the possibility that modulation of body iron may represent a potential way to inhibit these processes.