MATERIALS AND METHODS: The study included 43 obese children and 40 normal weight children. Anthropometric body measurements, bio-specimen and biochemistry assays were done. Genotyping of rs9465871 (CDKAL1) was conducted.
RESULTS: The percentages of the CC, CT, and TT genotypes of rs9465871in the lean children were 15%, 42.5%, and 42.5%, respectively. Regarding obese children, the frequencies were 18.6%, 58.1% and 23.3% respectively with no significant statistical difference. Comparison between the CDKAL1 rs 9465871 polymorphism showed that the highest value of fasting insulin was recorded in CC genotype (22.80± 15.18 [uIU/mL] Pinsulin level was higher in the CC group than in the TT+ CT group (P
METHODS: Fifty overweight/obese individuals aged 22-29 years were assigned to either no-exercise control (n=25) or HIIT (n=25) group. The HIIT group underwent a 12-week intervention, three days/week, with intensity of 65-80% of age-based maximum heart rate. Anthropometric measurements, homeostatic model of insulin resistance (HOMA-IR) and gene expression analysis were conducted at baseline and post intervention.
RESULTS: Significant time-by-group interactions (p<0.001) were found for body weight, BMI, waist circumference and body fat percentage. The HIIT group had lower body weight (2.3%, p<0.001), BMI (2.7%, p<0.001), waist circumference (2.4%, p<0.001) and body fat percentage (4.3%, p<0.001) post intervention. Compared to baseline, expressions of PGC-1∝ and AdipoR1 were increased by approximately three-fold (p=0.019) and two-fold (p=0.003) respectively, along with improved insulin sensitivity (33%, p=0.019) in the HIIT group.
CONCLUSION: Findings suggest that HIIT possibly improved insulin sensitivity through modulation of PGC-1∝ and AdipoR1. This study also showed that improved metabolic responses can occur despite modest reduction in body weight in overweight/obese individuals undergoing HIIT intervention.
MATERIALS AND METHODS: This is a cross-sectional, retrospective study design. All patients who received vildagliptin in the Pharmacy Integrated Health System (PHIS) registry database from 2016 to 2021 were included as study samples. The exclusion criteria were being less than 18 years old and having type 1 diabetes mellitus. Patients' medical records were retrieved after sampling, and data were collected. One medical record was missing, thus SPSS analysis were performed on 144 vildagliptin users.
RESULTS: In total, 84 females (58.3%) and 60 males (41.7%) with a mean age of 62.1 (±10.1) years were analysed in this study. Mean HbA1c pre-therapy was 8.5 ± 2.1%; while posttherapy 6 months demonstrated a mean HbA1c of 7.9 ± 1.8%. Use of vildagliptin alone or as an adjunct was associated with a mean reduction of 0.6% in HbA1c (p = 0.01). Factors influencing this HbA1c reduction were advancing age, specifically individuals aged 62 years and older (p = 0.02), patients who are already receiving insulin therapy (p=0.00) and those who express a willingness to commence insulin treatment during the counselling session prior to initiating the treatment plan (p = 0.00). Reasons for vildagliptin initiation documented by prescribers were non-insulin acceptance (n = 59, 40.97%), frequent hypoglycaemia (n = 6, 4.1%) and non-compliance with medications (n = 23, 15.9%). There was no association between demographic, medical background and reason for starting vildagliptin variables and HbA1c reduction (p < 0.001).
CONCLUSION: This study showed that initiating vildagliptin alone or as an adjunct therapy significantly reduced HbA1c and is beneficial for uncontrolled diabetes patients. While advancing age, concurrent administration of insulin and the patients' willingness to accept insulin treatment prior to the commencement of therapy were the factors that influenced HbA1c reduction among patients receiving vildagliptin therapy, we recommend primary care providers prioritise all of the significant variables discovered before initiating vildagliptin for their patients.
MATERIALS AND METHODS: This review utilises three databases (SCOPUS, Science Direct, and PubMed). The search phrases used are (Metabolomic* OR Metabolite*) for metabolomic study, (3T3-L1 OR Adipocyte OR "Adipose Tissue") for experimental design, and (Obesity) for obesity condition. Each of the search keywords was separated by an "AND" term in the databases. Other terms related to obesity, such as insulin resistance, heart disease, type 2 diabetes, muscular disorders, respiratory problems, and psychological problems were omitted because they did not contribute to the total number of studies discovered.
RESULTS: A total of 27 research publications were included in this scoping review. Most of the study focuses on metabolomics in obesity. Metabolites detected were found in various metabolic pathways including amino acids, carbohydrates, lipids as well as other metabolisms. Most of these metabolites discovered in obese conditions showed an alteration when compared to the level of the metabolite in normal conditions.
CONCLUSION: Unfortunately, these studies had some limitations in which the metabolites detected varied between the articles and the information concerning the relationship between the technique or instrument utilised and the metabolites detected in the samples were not well described. Therefore, using the findings obtained in this study, it can help to determine the direction of the study in the future.
MATERIALS AND METHODS: Using a cross-sectional design, cases of ovarian and breast cancer with clinical status of T2DM were selected over a 10-year period in Hospital Universiti Sains Malaysia. Immunohistochemical staining for IGFBP-rP1 was performed on paraffin-embedded tissues and the results were correlated with the patient's demographic and clinicopathological data.
RESULTS: A total of 152 breast cancer patients were recruited into the current study with 33.5% (51/152) patients were positive T2DM. Most of the breast cancer patients with T2DM were IGFBP-rP1-negative (66.7%, 34/51). The IGFBP-rP1 expression was significantly difference between breast cancer subjects with and without T2DM (p<0.001). There was no significant association of IGFBP-rP1 expression with data on the demographic and clinicopathological profiles of patients with breast cancer. Meanwhile, positive IGFBP-rP1 expression was evident in 44 out of 108 (40.74%) ovarian cancer cases. Among these cases, 36 were T2DM. In contrast to breast cancer cases, IGFBP-rP1 was mostly expressed among ovarian cancer patients with T2DM (66.7%, 24/36, p < 0.001). However, the -positive expression was not significantly associated with any sociodemographic and clinicopathological features of ovarian cancers.
CONCLUSIONS: Majority of breast cancer patients with T2DM did not express IGFBP-rP1. In contrast, majority of the ovarian cancer patients with T2DM expressed IGFBP-rP1.
Methods: For the optimisation and validation protocol, β-cells were plated onto 35 mm plastic petri dishes and maintained in RPMI-1640 media supplemented with 10 mM glucose, 10% FCS and 25 mM of N-2-hydroxyethylpiperazine-N-ethanesulfonic acid (HEPES). The treatment effects of 10 mM glucose and 30 μM fluoxetine on KATP channels NPo of β-cells were assessed via cell-attached patch-clamp recordings. For hippocampus cell experiments, hippocampi were harvested from day 17 of maternal Lister-hooded rat foetus, and then transferred to a Ca2+ and Mg2+-free HEPES-buffered Hank's salt solution (HHSS). The dissociated cells were cultured and plated onto a 25 mm round cover glasses coated with poly-d-lysine (0.1 mg/mL) in a petri dish. The KATP channels NPo of hippocampus cells when perfused with 1 mM and 10 mM of KA were determined.
Results: NPo of β-cells showed significant decreasing patterns (P < 0.001) when treated with 10 mM glucose 0.048 (0.027) as well as 30 μM fluoxetine 0.190 (0.141) as compared to basal counterpart. In hippocampus cell experiment, a significant increase (P < 0.001) in mean NPo 2.148 (0.175) of neurons when applied with 1 mM of KA as compared to basal was observed.
Conclusion: The two concentrations of KA used in the study exerted contrasting effects toward the mean of NPo. It is hypothesised that KA at lower concentration (1 mM) opens more KATP channels, leading to hyperpolarisation of the neurons, which may prevent neuronal hyper excitability. No effect was shown in 10 mM KA treatment, suggesting that only lower than 10 mM KA produced significant changes in KATP channels. This implies further validation of KA concentration to be used in the future.