Objective: The prevalence of diabetes mellitus is known to be increasing rapidly worldwide, but few population-based surveys have been undertaken in Africa or the Middle East. The aims of this study are to report the prevalence of diabetes mellitus and impaired fasting glucose (IFG) in Tunisia, to compare the prevalence to previous studies and to analyse the relationship between diabetes and age, sex, area of residency and body mass index (BMI). Subjects and setting: We have used data from the Tunisian National Nutrition Survey, a cross-sectional health study providing a large nationally representative sample of the Tunisian population including 3729 adults. We used the American Diabetes Association diagnostic criteria to determine the prevalence of diabetes mellitus and IFG. Results: The overall diabetes prevalence was 9.9% (9.5% in men and 10.1 in women) giving age-adjusted prevalence of diabetes of 8.5% (7.3% in men and 9.6% in women).Step-wise logistic regression showed age of more than 40 years, urban residency and high BMI to each be significantly and independently related to diabetes prevalence. The prevalence of diabetes mellitus has more than doubled in Tunisia over a 15-year period. Conclusions: Our study has demonstrated a high prevalence of diabetes in the adult population with a wide difference among the rural and urban areas with an increased prevalence compared to previous studies. The results underline the need to increase public awareness and to emphasize the benefit of lifestyle modification in order to prevent type II diabetes.

Based on the ROC analysis, we suggest a WC of 85 cm for both men and women as appropriate cut-off points to identify central obesity for the purposes of CVD and diabetes-risk detection among Tunisians. WCs of 85 cm in men and 79 cm in women were the most sensitive and specific to identify most subjects with a BMI >/=25 kg/m(2).

In North Africa, overnutrition has dramatically increased with the nutrition transition while micronutrient deficiencies persist, resulting in clustering of opposite types of malnutrition that can present a unique difficulty for public health interventions. We assessed the magnitude of the double burden of malnutrition among urban Moroccan and Tunisian women, as defined by the coexistence of overall or central adiposity and anemia or iron deficiency (ID), and explored the sociodemographic patterning of individual double burden. In cross-sectional surveys representative of the region around the capital city, we randomly selected 811 and 1689 nonpregnant women aged 20-49 y in Morocco and Tunisia, respectively. Four double burdens were analyzed: overweight (body mass index ≥25 kg/m(2)) or increased risk abdominal obesity (waist circumference ≥80 cm) and anemia (blood hemoglobin <120 g/L) or ID (C-reactive protein-corrected serum ferritin <15 μg/L). Adjusted associations with 9 sociodemographic factors were estimated by logistic regression. The prevalence of overweight and ID was 67.0% and 45.2% in Morocco, respectively, and 69.5% and 27.0% in Tunisia, respectively, illustrating the population-level double burden. The coexistence of overall or central adiposity with ID was found in 29.8% and 30.1% of women in Morocco, respectively, and in 18.2% and 18.3% of women in Tunisia, respectively, quite evenly distributed across age, economic, or education groups. Generally, the rare, associated sociodemographic factors varied across the 4 subject-level double burdens and the 2 countries and differed from those usually associated with adiposity, anemia, or ID. Any double burden combining adiposity and anemia or ID should therefore be taken into consideration in all women. This trial was registered at clinicaltrials.gov as NCT01844349.

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In addition to HLA and insulin genes, the costimulatory molecule CTLA-4 gene is a confirmed type 1 diabetes (T1D) susceptibility gene. Previous studies investigated the association of CTLA-4 genetic variants with the risk of T1D, but with inconclusive findings. Here, we tested the contributions of common CTLA-4 gene variants to T1D susceptibility in Tunisian patients and control subjects. The study subjects comprised 228 T1D patients (47.8% females) and 193 unrelated healthy controls (45.6% females). Genotyping for CTLA-4 CT60A/G (rs3087243), ؉49A/G (rs231775), and ؊318C/T (rs5742909) was performed by PCR-restriction fragment length polymorphism (RFLP) analysis. The minor-allele frequencies (MAF) for the three CTLA-4 variants were significantly higher in T1D patients, and significantly higher frequencies of homozygous ؉49G/G and homozygous CT60G/G genotypes were seen in patients, which was confirmed by univariate regression analysis ( Type 1 (insulin-dependent) diabetes (T1D) is the most prevalent form of diabetes in children and young adults and results from autoimmune CD4 ϩ and CD8 ϩ T-cell-directed destruction of insulin-producing pancreatic ␤ islet cells in genetically susceptible individuals (3, 12), leading to irreversible hyperglycemia and related complications (13). There is a strong genetic component to T1D pathogenesis, evidenced by its clustering in families and by the contributions of a number of susceptibility gene variants to its pathogenesis (10,12,29). They include the human leukocyte antigen (HLA) locus, in particular the class II region (DR and DQ), which accounts for 40 to 50% of T1D familial clustering (1, 12, 18), and non-HLA susceptibility loci, several of which were mapped by genome-scanning (11, 29) and/or candidate gene (7, 18, 31) approaches. They include insulin promoter gene variants, which reportedly may modulate immunological tolerance by controlling the expansion of the autoreactive cell pool (26), and the T-cell costimulator cytotoxic T-lymphocyte antigen 4 (CTLA-4) transmembrane glycoprotein, which plays a key role in the fine tuning of T-cell immunity (9,32,33).CTLA-4 is a 40-kDa transmembrane glycoprotein expressed on resting and activated T cells and nonlymphoid cells (33), and along with the related CD28 costimulatory molecule, it regulates T-cell activation (and is itself primarily mediated by engagement of the T-cell receptor [TCR]) but does recognize major histocompatibility complex (MHC)-bound antigenic peptides (9, 33). CTLA-4 negatively regulates T-cell activation and effector function, in part by inhibiting Th1 (interleukin 2 [IL-2] and gamma interferon [IFN-␥]) cytokine production and IL-2 receptor ␣-chain (p55; Tac) expression by engaging antigen-presenting cell (APC)-bound B7