Habitual Sleep Deprivation is Associated with Type 2 Diabetes: A Case-Control Study.

OBJECTIVES: It is suggested that a minimum of eight hours of sleep per night is needed for metabolism to work normally. The aim of the study was to determine the association of habitual sleep deprivation and type 2 diabetes mellitus (T2DM). METHODS: We conducted a case-control study comparing patients with T2DM with age and sex matched healthy controls. Standard sleep questionnaires (the Berlin and Epworth Sleepiness Scale) and a weekly diary were used by patients to self-report habitual sleep. RESULTS: A total of 172 diabetics and 188 healthy controls were enrolled in the study. There was a significant difference between T2DM and healthy controls in nocturnal sleep duration (p = 0.033). There was a significant association between nocturnal sleep duration of fewer than six hours and T2DM (χ2 = 14.0; p = 0.0001). There was no significant difference in daytime sleepiness and daytime naps between the T2DM and control groups (p = 0.452; p = 0.581, respectively). CONCLUSIONS: A nocturnal sleep duration < 6 hours is associated with T2DM.

Frequencies of the Arg16Gly, Gln27Glu and Thr164Ile Adrenoceptor ß2 Polymorphisms among Omanis.

OBJECTIVES: This study aimed to assess the distribution of missense mutations in the adrenoceptor ß2 (ADRB2) gene in an Omani cohort. METHODS: This study was carried out between May 2014 and March 2015 at the Sultan Qaboos University, Muscat, Oman. Blood samples were taken from 316 unrelated Omani subjects. Genotyping for rs1042713 (c.46A>G, p.Arg16Gly), rs1042714 (c.79C>G, p.Gln27Glu) and rs1800888 (c.491C>T, p.Thr164Ile) polymorphisms was performed by real-time polymerase chain reaction using single nucleotide polymorphism (SNP) genotyping assays. The allelic frequencies of these polymorphisms were estimated on the basis of the observed numbers of specific alleles from the genotype data for male and female subjects. The genotype frequencies for each polymorphism were tested for deviation from the Hardy-Weinberg equilibrium. RESULTS: Gly16 and Glu27 were the most frequent variants found among the cohort (63% and 75%, respectively). The Ile164 variant was not detected in the study population. There was a significant linkage disequilibrium between the rs1042713 and rs1042714 SNPs (r(2) = 0.209; P ≤0.001). The most observed haplotypes were Gly16-Gln27 and Arg16-Gln27 (0.37 and 0.38, respectively). The frequency of Gly16-Glu27 was 0.25, comprising all Glu27 carriers. CONCLUSION: The allelic distribution of variants in this Omani cohort was similar to distributions reported among Caucasian populations.

Quality of diabetes care at outpatient clinic, sultan qaboos university hospital.

OBJECTIVE: To assess the clinical care of type 2 diabetes mellitus (T2D) patients at Sultan Qaboos University Hospital (SQUH), a countrywide tertiary referral center in Muscat, Oman. . METHODS: We performed a retrospective, observational, cross-sectional study using a total of 673 Omani T2D patients from the Diabetes and Family Medicine Clinics at SQUH. We collected patient data from June 2010 to February 2012 from the Hospital Information System (HIS). Patients had to be Omani, aged more than 18 years old, and have T2D with active follow-up and at least three visits within one year to be included in the study. Ninety-three percent of the patients (n=622) were on oral hypoglycemic drugs and/or insulin, and 70% were on statins. Patients' anthropometric data, biochemical investigations, blood pressure, and duration of diabetes were recorded from the HIS. . RESULTS: Using the recommended standards and guidelines of medical care in diabetes (American Diabetes Association and the American National Cholesterol Education Program III NCDP NIII standards), we observed that 22% of the patients achieved a HbA1C goal of <7%, 47% achieved blood pressure goal of <140/80mm Hg, 48% achieved serum low density lipoprotein cholesterol goal of <2.6mmol/L, 67% achieved serum triglycerides goal of <1.7 mmol/L, 59% of males and 43% of females achieved high density lipoprotein cholesterol goals (males>1.0; females >1.3mmol/L). Almost 60% of the patients had urinary microalbumin/creatinine ratio within the normal range. . CONCLUSIONS: The clinical outcomes of the care that T2D patients get at SQUH were lower than those reported in Europe and North America. However, it is similar to those reported in other countries in the Arabian Gulf.

Association of gene variants with susceptibility to type 2 diabetes among Omanis.

AIM: To investigate the association of 10 known common gene variants with susceptibility to type 2 diabetes mellitus (T2D) among Omanis. METHODS: Using case-control design, a total of 992 diabetic patients and 294 normoglycemic Omani Arabs were genotyped, by an allelic discrimination assay-by-design TaqMan method on fast real time polymerase chain reaction system, for the following gene variants: KCNJ11 (rs5219), TCF7L2 (rs7903146), CDKAL1 (rs10946398), CDKN2A/B (rs10811661), FTO (rs9939609 and rs8050136), IGF2BP2 (rs4402960), SLC30A8 (rs13266634) CAPN10 (rs3792267) and HHEX (rs1111875). T2D patients were recruited from the Diabetes Clinic (n = 243) and inpatients (n = 749) at Sultan Qaboos Univesity Hospital (SQUH), Muscat, Oman. Adult control participants (n = 294) were volunteers from the community and from those visiting Family Medicine Clinic at SQU, for regular medical checkup. The difficulty in recruiting Omani participants with no family history of diabetes was the main reason behind the small number of control participants in this study. Almost all volunteers questioned had a relative with diabetes mellitus. Inspite of the small number of normoglycemic controls in this study, this sample was sufficient for detection of genes and loci for common alleles influencing T2D with an odds ratio of ≥ 1.3 reaching at least 80% power. Data was collected from June 2010 to February 2012. RESULTS: Using binary logistic regression analysis, four gene variants showed significant association with T2D risk: KCNJ11 (rs5219, P = 5.8 × 10(-6), OR = 1.74), TCF7L2 (rs7903146, P = 0.001, OR = 1.46), CDKAL1 (rs10946398, P = 0.002, OR = 1.44) and CDKN2A/B (rs10811661, P = 0.020, OR = 1.40). The fixation index analysis of these four gene variants indicated significant genetic differentiation between diabetics and controls {[KCNJ11 (rs5219), P < 0.001], [TCF7L2 (rs7903146), P < 0.001], [CDKAL1 (rs10946398), P < 0.05], [CDKN2A/B (rs10811661), P < 0.05]}. The highest genotype variation % between diabetics and controls was found at KCNJ11 (2.07%) and TCF7L2 (1.62%). This study was not able to detect an association of T2D risk with gene variants of IGF2BP2 (rs4402960), SLC30A8 (rs13266634), CAPN10 (rs3792267) and HHEX (rs1111875). Moreover, no association was found between FTO gene variants (rs9939609 and rs8050136) and T2D risk. However, T2D risk was found to be significantly associated with obesity (P = 0.002, OR = 2.22); and with the Waist-to-Hip ratio (n = 532, P = 1.9 ×10(-7), OR = 2.4), [among males (n = 234, P = 1.2 × 10(-4), OR = 2.0) and females (n = 298, P = 0.001, OR = 6.3)]. CONCLUSION: Results confirmed the association of KCNJ11 (rs5219), TCF7L2 (rs7903146), CDKAL1 (rs10946398) and CDKN2A/B (rs10811661) gene variants with susceptibility to T2D among Omani Arabs.

Utility of large consanguineous family-based model for investigating the genetics of type 2 diabetes mellitus.

OBJECTIVES: This study examined the utility of a family-based model for replicating the results of genome-wide association studies (GWAS) of type 2 diabetes (T2D). METHODS AND RESULTS: In a total of 232 members of a large consanguineous Omani Arab pedigree (age: 16-80years), there were 27 diabetics and 50 prediabetics (17 with impaired fasting glucose and 33 with impaired glucose tolerance). All 232 individuals underwent anthropometric and biochemical investigations and genotyped for 14 known common gene variants of modest effect on T2D risk. Power analysis at a LOD score of 3, gave 80% power to locate a single specific locus that accounts for 52% of the total phenotypic variation. Measured genotype analysis (MGA) was used to determine heritability of various quantitative traits (QTs) which ranged 25-56%. Using MGA, some common gene variants were found to have little (<5%) but significant impact on the heritability of T2D related QTs [KCNJ11 (rs5219), p=0.004]; [IGF2BP2 (rs4402960), p=0.02]; [SLC30A8 (rs13266634), p=0.05]; [CAPN10 (rs2975760), p=0.031]; [FTO (rs8050136), p=0.023]; [FTO (rs9939609), p=0.018] and [SLC30A8 (rs13266634), p=0.05]. Sib-TDT analysis showed that some gene variants were significantly associated with T2D risk but didn't reach the level of significance after Bonferroni correction [KCNJ11 (rs5219), p=0.047] and [CAPN10 (rs41266971), p=0.035]. CONCLUSION: We have demonstrated that, in principle, a family-based model with minor limitations could be used to replicate some of the results of large GWAS case-control studies. This model could successfully be applied for the future discovery, by deep sequencing, of rare gene variants.

Impaired Fasting Glucose in Omani Adults with no Family History of Type 2 Diabetes.

OBJECTIVES: The aim of this study was to estimate the prevalence of impaired fasting glucose (IFG) among Omani adults with no family history (FH) of diabetes and to investigate the factors behind the risk of developing type 2 diabetes (T2D), while excluding a FH of diabetes. METHODS: A total of 1,182 Omani adults, aged ≥40 years, visited the Family Medicine & Community Health Clinic at Sultan Qaboos University Hospital, Oman, on days other than the Diabetes Clinic days, from July 2010 to July 2011. The subjects were interviewed and asked if they had T2D or a FH of T2D. RESULTS: Only 191 (16%) reported no personal history of T2D or FH of the disease. Of these, anthropometric and biochemical data was complete in 159 subjects. Of these a total of 42 (26%) had IFG according to the American Diabetes Association criteria. Body mass index, fasting insulin, haemoglobin A1C and blood pressure (BP), were significantly higher among individuals with IFG (P <0.01, P <0.05, P <0.01 and P <0.01, respectively). In addition, fasting insulin, BP and serum lipid profile were correlated with obesity indices (P <0.05). Obesity indices were strongly associated with the risk of IFG among Omanis, with waist circumference being the strongest predictor. CONCLUSION: Despite claiming no FH of diabetes, a large number of Omani adults in this study had a high risk of developing diabetes. This is possibly due to environmental factors and endogamy. The high prevalence of obesity combined with genetically susceptible individuals is a warning that diabetes could be a future epidemic in Oman.

Familial Clustering of Type 2 Diabetes among Omanis.

OBJECTIVE: The aim of this study was to screen Omani individuals for the familial aggregation of type 2 diabetes mellitus. METHODS: A random cohort of 1182 Omani individuals visiting the Family Medicine Clinic at Sultan Qaboos University Hospital (SQUH), Muscat, Oman, for regular medical checkup, aged ≥40 years, were sampled. Patients were categorized into three groups: (1) individuals who claim not to have diabetes and had no family history of diabetes; (2) individuals who claim not to have diabetes but had family history of diabetes; (3) individuals with diabetes. Only 16% of these Omani individuals had no diabetes and no family history of diabetes. Another separate random cohort of 234 Omani type 2 diabetes mellitus patients, from the Diabetes Clinic at SQUH, were interviewed and questioned about their family history of type 2 diabetes mellitus. RESULTS: Ninety five percent of the patients had a family history of diabetes. Eighty percent had first degree relatives with diabetes and 46% had second degree relatives with diabetes. At least one parent with diabetes was reported among 55% of these diabetics, while maternal diabetes (55%) was found to be higher than paternal diabetes (47%). However, only 15% had both parents with diabetes. Furthermore, almost half of the 234 diabetics were having at least one of the following relatives with diabetes: brother, sister, aunt or an uncle. CONCLUSION: The findings of this study confirm familial aggregation of diabetes among the Omani population. Compared to other populations, familial aggregation of type 2 diabetes mellitus among Omanis is relatively very high, and is perhaps due to the very high degree of consanguinity among Omanis. Since almost everyone seems to have a genetic predisposition to diabetes, the dramatic lifestyle changes over the past 25 years, could tip the population into an epidemic of type 2 diabetes mellitus.

Serum myoglobin in patients with thyroid dysfunction.

OBJECTIVES: To assess the pattern of change in serum myoglobin concentration in subjects with thyroid dysfunction. METHODS: Serum samples were selected from 150 subjects with suspected thyroid disorder who were referred to the Royal Hospital, Muscat, Oman. The subjects were 35 males and 115 females, aged 14-56 years with mean ± SD of 34.3 ± 12.7 years. They were classified on the basis of thyroid stimulating hormone (TSH) and free thyroxine (FT4) into 3 groups, each consisting of 50 subjects: hypothyroid, hyperthyroid, and euthyroid subjects. RESULTS: The mean serum myoglobin concentration was higher in hypothyroid patients compared to hyperthyroid and euthyroid subjects (mean ± SD was 38.5 ± 23.1 µg/L in hypothyroid; 18.1 ± 7.0µg/L in hyperthyroid; 17.4 ± 5.7µg/L in euthyroid). There was a significant difference in myoglobin concentration between hypothyroid and euthyroid groups (F = 36.1, p <0.001), however, there was no significant difference between the hyperthyroid and euthyroid groups. When the mean ± 2SD for myoglobin in euthyroid subjects was calculated, the reference range was 6-29 µg/L. Of the hypothyroid subjects, 29 (58%) had high myoglobin and 21 (42%) had normal myoglobin level. No significant correlation was noticed between TSH or FT4 and myoglobin in all studied subjects. CONCLUSION: Raised serum myoglobin may be observed in patients with hypothyroidism. Hence hypothyroidism should be considered in the differential diagnosis of patients with raised serum myoglobin concentration.