Saudi Arabia is a country with high prevalence of diabetes, uncontrolled diabetes, and diabetes-related complications. Poor glycemic control is multifactorial and could be explained in part by physician and patient reluctance toward insulin or insulin inertia. This study aimed to address physician barriers toward insulin therapy in primary care settings. It included 288 physicians from 168 primary healthcare centers (PHC) in the Jazan region of Saudi Arabia. Participants responded to questionnaire investigating physicians’ attitude and barriers to insulin initiation and intensification in PHCs. In physician opinion, the most common barriers among their patients were fear of injection, lack of patient education, fear of hypoglycemia, and difficult administration. Physicians were reluctant to initiate insulin for T2D patients mostly due to patient non-adherence to blood sugar measurement, non-adherence to appointment or treatment, elderly patients, or due to patient refusal. Physicians’ fear of hypoglycemia, lack of staff for patient education, and lack of updated knowledge were the primary clinician-related barriers. Exaggerated fears of insulin side effects, patient non-adherence, limited staff for patient’s education, patient refusal, and inadequate consultation time were the main barriers to insulin acceptance and prescription.

Background and Objectives: The prevalence of disordered eating behaviors (DEBs) in type 1 diabetes (T1D) has been studied globally; however, data from Saudi Arabia and Arab-speaking countries are scarce. This study aimed to measure the prevalence of DEBs and associated clinical characteristics in adolescents and young adults with T1D, and the impact of DEBs on glycemic parameters. Materials and Methods: A total of 265 adolescents and young adults with T1D (aged 12–25 years) were recruited randomly from the registry at the Jazan Endocrinology and Diabetes Center, Saudi Arabia. Participants completed the Diabetes Eating Problem Survey–Revised (DEPS-R) questionnaire. Other measures included hemoglobin A1c (HbA1c) in addition to sociodemographic, anthropometric, and clinical data. Results: The prevalence of DEBs among T1D was 27.2%. Females (32.5%) had a higher proportion of DEBs than males (18.6%) (p = 0.01). About 27% of the participants reported insulin restriction. A history of hospital admission in the previous 6 months due to DKA and frequent hypoglycemia was more frequently reported in T1D participants with DEBs compared to those without (p = 0.03). Participants with DEBs had higher HbA1c and higher BMI compared to those without DEBs. Conclusions: Adolescents and young adults with T1D with disordered eating and insulin restriction have higher glycated hemoglobin, and are at higher risk of DKA. Routine screening for DEBs should be an essential element in diabetes care, especially among highly vulnerable groups.

Background and Objectives: The link between celiac disease (CD) and type 1 diabetes (T1D) has been well-documented in the medical literature and is thought to be due to a shared genetic predisposition in addition to environmental triggers. This study aimed to determine the seroprevalence and biopsy-proven CD (PBCD) prevalence in individuals with T1D from Saudi Arabia and identify their clinical characteristics and the impact on glycemic control. Materials and Methods: A total of 969 children and adolescents with confirmed T1D were investigated. Prospective and retrospective data were collected to include clinical, anthropometric, and biochemical data. Total IgA and anti-TTG-IgA antibodies were screened to detect seropositive cases. Upper intestinal endoscopy and biopsy were performed to find BPCD. Results: The seroprevalence of CD was 14.6% (141/969), while BPCD prevalence was 7.5%. Females had a higher prevalence than males: 17.8% vs. 9.8%, p < 0.001. The CD group had lower HbA1c and more frequent hypoglycemia than the seronegative group. Conclusions: This study highlighted the high prevalence of CD in T1D Saudi patients. CD has multiple effects on glycemic control, growth, and puberty in children and adolescents with T1D. We emphasize the importance of early screening for CD at the time of diabetes diagnosis and periodically after that or if any atypical features present, especially anemia, growth delay, underweight, or frequent hypoglycemia.

Disordered eating behaviors (DEBs) in type 1 diabetes (T1D) have been studied globally in different age groups. However, there is no validated diabetes-specific questionnaire in the Arabic language for the screening of DEBs. This study aimed to translate the Diabetes Eating Problem Survey–Revised scale (DEPS-R) into the Arabic language and study its psychometric properties in adolescents with T1D. We adopted the forward–backward procedure to translate the DEPS-R questionnaire into Arabic. The validation study enrolled 258 Saudi adolescents with T1D aged 12–18 years who completed the Arabic DEPS-R questionnaire and the EAT-26. The Arabic DEPS-R showed good construct validity and reliability (Cronbach’s alpha = 0.86). The factor analysis revealed a three-factor structure of DEPS-R which explains 54.4 % of the variance. In total, 30.6% of the participants are at high risk for DEBs (DEPS-R score ≥ 20). The psychometric properties of the Arabic DEPS-R are satisfactory, consistent with the original scale and translations in other languages. These results support the validity of the Arabic DEPS-R for assessment of DEBs in the T1D Arabic population.

Background: Various reports described new-onset diabetes during or after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in patients with no previous history of diabetes or glucocorticoid use. Further, SARS-CoV-2 could increase the risk of diabetes, including diabetic ketoacidosis (DKA). However, data on the relationship between new-onset diabetes and COVID-19 are still limited in our region. Thus, we aimed in this study to evaluate the association between new-onset diabetes and DKA in patients with COVID-19. Methods: A retrospective, cross-sectional study was conducted at a diabetic center in Jazan province, Saudi Arabia, between 2020 and 2021. Demographic data, COVID-19 status, and DKA incidence were collected and verified manually from diabetic patients’ medical records. Data were analyzed using a t-test and chi-square test. Results: We included 54 diabetic patients diagnosed during the COVID-19 pandemic, with a median age of 17 years. The majority of patients were females (57.4%). About 38.8% were diagnosed with COVID-19, and 16.6% reported having DKA. About 33.3% of the patients who experienced DKA reported being COVID-19-positive. However, only 6% of patients who denied contracting SARS-CoV-2 developed DKA (p-value = 0.020). Conclusions: Patients with newly diagnosed diabetes due to COVID-19 seem at a higher risk of developing DKA. Further epidemiological and molecular studies are required for a better understanding of the correlation between DKA in patients with diabetes and COVID-19.

Familial partial lipodystrophies (FPLDs) are very rare inherited disorders characterized by partial loss of adipose tissue from the upper and lower extremities. At least seven subtypes of FPLD have been identified and are mostly dominantly inherited. FPLD type 3 is caused by mutations in the PPARγ gene, which encodes for the protein peroxisome proliferator-activated receptor gamma (PPARγ). We identified a Saudi female with PFLD3 presented with partial lipoatrophy, uncontrolled diabetes, severe hypertriglyceridemia, and recurrent pancreatitis. The clinical and biochemical findings in this proband were described before and after treatment with Pioglitazone in addition to the conventional treatment. DNA extraction and whole exome sequencing (WES) were performed to detect the variant. The mutant gene was subjected to Sanger analysis to confirm the results. We applied five specific computational prediction tools to assess the pathogenicity of variation, namely the MT, DANN, CADD, BayesDel, and fitCons tools. We assessed protein modeling and stability with the AlphaFold-generated structures for both wild-type and mutant proteins. Finally, we conducted molecular docking using the AutoDock Vina virtual docking. Upon whole exome sequencing, a c.1024C>T p.(Gln342Ter) missense mutation was detected in the PPARγ gene associated with FPLD3. This variant is a novel mutation that has not been described in all genome databases. Sanger analysis confirmed the heterogenicity and pathogenicity of this variant. All five computational prediction tools indicate that this variant is considered highly pathogenic. Our patient showed a dramatic response to Pioglitazone, a synthetic PPARγ agonist. From structural modeling, we found that the enhanced binding affinity of the mutant PPARγ protein to Pioglitazone likely improves the activation of PPARγ, enhancing its transcriptional activity and resulting in better clinical outcomes. These findings extend the spectrum of PPARγ mutations responsible for FPLD3 and highlight the potential for personalized treatment strategies based on genetic mutations.