Displaying publications 321 - 340 of 644 in total

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  1. Lau CH, Muniandy S
    PMID: 21251282 DOI: 10.1186/1475-2840-10-8
    Adiponectin and resistin are adipokines which modulate insulin action, energy, glucose and lipid homeostasis. Meta-analyses showed that hypoadiponectinemia and hyperresistinemia are strongly associated with increased risk of insulin resistance, type 2 diabetes (T2DM), metabolic syndrome (MS) and cardiovascular disease. The aim of this study was to propose a novel adiponectin-resistin (AR) index by taking into account both adiponectin and resistin levels to provide a better indicator of the metabolic homeostasis and metabolic disorders. In addition, a novel insulin resistance (IRAR) index was proposed by integration of the AR index into an existing insulin resistance index to provide an improved diagnostic biomarker of insulin sensitivity.
    Matched MeSH terms: Insulin/blood; Insulin Resistance*
  2. Marimuthu S, Menon BS
    Arch Dis Child, 2009 Jun;94(6):477.
    PMID: 19460927 DOI: 10.1136/adc.2008.155713
    Matched MeSH terms: Insulin Resistance
  3. Kanagasabapathy G, Kuppusamy UR, Abd Malek SN, Abdulla MA, Chua KH, Sabaratnam V
    PMID: 23259700 DOI: 10.1186/1472-6882-12-261
    BACKGROUND: Pleurotus sajor-caju (P. sajor-caju) has been extremely useful in the prevention of diabetes mellitus due to its low fat and high soluble fiber content for thousands of years. Insulin resistance is a key component in the development of diabetes mellitus which is caused by inflammation. In this study, we aimed to investigate the in vivo efficacy of glucan-rich polysaccharide of P. sajor-caju (GE) against diabetes mellitus and inflammation in C57BL/6J mice fed a high-fat diet.
    METHODS: Diabetes was induced in C57BL/6J mice by feeding a high-fat diet. The mice were randomly assigned to 7 groups (n=6 per group). The control groups in this study were ND (for normal diet) and HFD (for high-fat diet). The treated groups were ND240 (for normal diet) (240 mg/kg b.w) and HFD60, HFD120 and HFD240 (for high-fat), where the mice were administrated with three dosages of GE (60, 120, 240 mg GE/kg b.w respectively). Metformin (2 mg/kg b.w) served as positive control. The glucose tolerance test, glucose and insulin levels were measured at the end of 16 weeks. Expressions of genes for inflammatory markers, GLUT-4 and adiponectin in the adipose tissue of the mice were assessed. One-way ANOVA and Duncan's multiple range tests (DMRT) were used to determine the significant differences between groups.
    RESULTS: GE treated groups improved the glucose tolerance, attenuated hyperglycemia and hyperinsulinemia in the mice by up-regulating the adiponectin and GLUT-4 gene expressions. The mice in GE treated groups did not develop insulin resistance. GE also down-regulated the expression of inflammatory markers (IL-6, TNF-α, SAA2, CRP and MCP-1) via attenuation of nuclear transcription factors (NF-κB).
    CONCLUSION: Glucan-rich polysaccharide of P. sajor-caju can serve as a potential agent for prevention of glucose intolerance, insulin resistance and inflammation.
    Matched MeSH terms: Insulin/metabolism; Insulin Resistance*
  4. Ayub A, Yip WK, Seow HF
    Biomed Pharmacother, 2015 Oct;75:40-50.
    PMID: 26463630 DOI: 10.1016/j.biopha.2015.08.031
    Triple-negative breast cancers (TNBCs) are aggressive cancers that do not benefit from hormonal therapy or therapies that target HER2 receptors. Insulin-like growth factor 1 receptor (IGF-1R), which has been shown to be overexpressed in breast cancer, activates numerous downstream kinases that associate with cell proliferation and survival. This study compared the effects caused by dual treatments targeting IGF-1R, PI3K, mTORC, or MEK with those by single treatments in a TNBC cell line, MDA-MB-231. We used small-molecule kinase inhibitors, namely, NVP-AEW541, NVP-BKM120, KU0063794, and PD0325901 to target IGF-1R, PI3K, mTORC, and MEK, respectively. Combination treatments of PD0325901 with NVP-AEW541, NVP-BKM120 or KU0063794 and NVP-AEW541 with KU0063794 demonstrated a significant synergistic growth inhibition. These dual treatments increased apoptosis and/or cell cycle arrest at G0/G1 phase and enhanced the inhibition of phosphorylation of Akt or downstream molecules of mTORC1, as compared to the single treatments. Our study suggests that targeting multiple kinases in IGF-1R signaling may be a promising therapeutic approach.
    Matched MeSH terms: Insulin-Like Growth Factor I
  5. Hou Z, Imam MU, Ismail M, Ooi DJ, Ideris A, Mahmud R
    Drug Des Devel Ther, 2015;9:4115-25.
    PMID: 26316695 DOI: 10.2147/DDDT.S80743
    Estrogen deficiency alters quality of life during menopause. Hormone replacement therapy has been used to improve quality of life and prevent complications, but side effects limit its use. In this study, we evaluated the use of edible bird's nest (EBN) for prevention of cardiometabolic problems in rats with ovariectomy-induced menopause. Ovariectomized female rats were fed for 12 weeks with normal rat chow, EBN, or estrogen and compared with normal non-ovariectomized rats. Metabolic indices (insulin, estrogen, superoxide dismutase, malondialdehyde, oral glucose tolerance test, and lipid profile) were measured at the end of the experiment from serum and liver tissue homogenate, and transcriptional levels of hepatic insulin signaling genes were measured. The results showed that ovariectomy worsened metabolic indices and disrupted the normal transcriptional pattern of hepatic insulin signaling genes. EBN improved the metabolic indices and also produced transcriptional changes in hepatic insulin signaling genes that tended toward enhanced insulin sensitivity, and glucose and lipid homeostasis, even better than estrogen. The data suggest that EBN could meliorate estrogen deficiency-associated increase in risk of cardiometabolic disease in rats, and may in fact be useful as a functional food for the prevention of such a problem in humans. The clinical validity of these findings is worth studying further.
    Matched MeSH terms: Insulin/blood; Insulin/metabolism*; Insulin Resistance
  6. Ng CJ, Lai PS, Lee YK, Azmi SA, Teo CH
    Int J Clin Pract, 2015 Oct;69(10):1050-70.
    PMID: 26147376 DOI: 10.1111/ijcp.12691
    AIM: To identify the barriers and facilitators to start insulin in patients with type 2 diabetes.
    METHOD: This was a systematic review. We conducted a systematic search using PubMed, EMBASE, CINAHL and Web of Science (up to 5 June 2014) for original English articles using the terms 'type 2 diabetes', 'insulin', and free texts: 'barrier' or 'facilitate' and 'initiate'. Two pairs of reviewers independently assessed and extracted the data. Study quality was assessed with Qualsyst.
    RESULTS: A total of 9740 references were identified: 41 full-text articles were assessed for eligibility. Twenty-five articles (15 qualitative, 10 quantitative) were included in the review. Good inter-rater reliability was observed for the Qualsyst score (weighted kappa 0.7). Three main themes identified were as follows: patient-related, healthcare professional and system factors. The main patient-related barriers were fear of pain and injection (n = 18), concerns about side effects of insulin (n = 12), perception that insulin indicated end stage of diabetes (n = 11), inconvenience (n = 10), difficulty in insulin administration (n = 7), punishment (n = 7) and stigma and discrimination (n = 7). Healthcare professionals' barriers were as follows: poor knowledge and skills (n = 9), physician inertia (n = 5) and language barriers (n = 4). System barriers included lack of time (n = 5). The most common facilitators were understanding the benefits of insulin (n = 7), not being afraid of injections (n = 5), and patient education and information (n = 5).
    CONCLUSION: Major barriers to insulin initiation persist despite availability of newer and safer insulin. Healthcare professionals should explore and address these barriers. Targeted interventions should be developed to overcome these barriers.
    Matched MeSH terms: Insulin
  7. Usman A, Makmor Bakry M, Mustafa N, Rehman IU, Bukhsh A, Lee SWH, et al.
    Diabetes Metab Syndr Obes, 2019;12:1323-1338.
    PMID: 31496770 DOI: 10.2147/DMSO.S208492
    Background: During the progress and resolution of a diabetic ketoacidosis (DKA) episode, potassium levels are significantly affected by the extent of acidosis. However, none of the current guidelines take into account acidosis during resuscitation of potassium level in DKA management, which may increase the risk of cardiovascular adverse events.

    Objective: To assess literature regarding the adjustment of potassium level using pH to calculate pH-adjusted corrected potassium level, and to observe the relationship of cardiovascular outcomes with reported potassium level and pH-adjusted corrected potassium in DKA.

    Methodology: Seven databases were searched from inception to January 2018 for studies which had reported people with diabetes developing diabetic ketoacidosis, in relation to prevalence or incidence, fluid resuscitation or potassium supplementation treatment, treatment or cardiovascular outcomes, and experimentation with DKA management or insulin. Quality of studies was evaluated using Cochrane Risk of Bias and Newcastle Ottawa Scale.

    Results: Forty-seven studies were included in qualitative synthesis out of a total of 10,292 retrieved studies. Forty-one studies discussed the potassium level and blood pH at the time of admission, ten studies discussed cardiovascular outcomes, and only four studies concurrently discussed potassium level, pH, and cardiovascular outcomes. Only two studies were graded as good on the Newcastle Ottawa Scale. The reported potassium level was well within normal range (5.8 mmol/L), whereas pH rendered patients to be moderately acidotic (7.13). Surprisingly, none of the included studies mentioned pH-adjusted corrected potassium level and, hence, this was calculated later. Although mean corrected potassium was within the normal range (3.56 mmol/L), 13 studies had corrected potassium below 3.5 mmol/L and five had it below 3.0 mmol/L. Nevertheless, with the exception of one study, none discussed cardiovascular outcomes in the context of potassium or pH-adjusted potassium level.

    Conclusion: The evidence surrounding cardiovascular outcomes during DKA episodes in light of a pH-adjusted corrected potassium level is scarce. A prospective observational, or preferably, an experimental study in this regard will ensure we can modify and enhance safety of existing DKA treatment protocols.
    Matched MeSH terms: Insulin
  8. Arya A, Cheah SC, Looi CY, Taha H, Mustafa MR, Mohd MA
    Food Chem Toxicol, 2012 Nov;50(11):4209-20.
    PMID: 22939938 DOI: 10.1016/j.fct.2012.08.012
    This study aimed to ascertain the potential of Centratherum anthelminticum seeds methanolic fraction (CAMFs) for the management of type 2 diabetes and its associated complications. CAMFs was initially tested on β-TC6 cells for H(2)O(2)-induced nuclear factor-κB (NF-κB) translocation effects. The result displayed that CAMFs significantly inhibited NF-κB translocation from cytoplasm into the nucleus, dose-dependently. Furthermore, a 12-week sub-chronic CAMFs study was carried out on streptozotocin (STZ)-nicotinamide-induced type 2 diabetic rat model to evaluate glycemia, essential biochemical parameters, lipid levels, oxidative stress markers, and pro-inflammatory cytokines level. Our study result showed that CAMFs reduced hyperglycemia by increasing serum insulin, C-peptide, total protein, and albumin levels, significantly. Whereas, elevated blood glucose, glycated hemoglobin, lipids and enzyme activities were restored to near normal. CAMFs confirmed antioxidant potential by elevating glutathione (GSH) and reducing malondialdehyde (MDA) levels in diabetic rats. Interestingly, CAMFs down-regulated elevated tumor necrosis factor α (TNF-α), interleukin (IL)-1β and IL-6 in the tissues and serum of the diabetic rats. We conclude that CAMFs exerted apparent antidiabetic effects and demonstrated as a valuable candidate nutraceutical for insulin-resistant type 2 diabetes and its associated complications such as dyslipidemia, oxidative stress, and inflammation.
    Matched MeSH terms: Insulin Resistance; Insulin-Secreting Cells/drug effects; Insulin-Secreting Cells/metabolism
  9. Seok Fang Oon, Meenakshii Nallappan, Mohd Shazrul Fazry Sa’ariwijaya, Nur Kartinee Kassim, Shamarina Shohaimi, Thiam Tsui Tee, et al.
    MyJurnal
    ABSTRACTS FOR INTERNATIONAL HEALTH AND MEDICAL SCIENCES CONFERENCE 2019 (IHMSC 2019). Accelerating Innovations in Translational and Precision Medicine. Held at Taylor’s University Lakeside Campus, Subang Jaya, Selangor, Malaysia. 8-9th March, 2019
    Introduction: According to the National Health and Morbidity Survey (NHMS) 2015, 47.7% of the Malaysian population are either obese or overweight. The increased obesity prevalence has caused major health problems including cardiovascular diseases and diabetes. Although several anti-obesity drugs have been developed, they are limited due to adverse side effects. Previous studies demonstrated that xanthorrhizol (XNT) reduced the levels of serum free fatty acid and triglyceride in vivo, but the detailed anti-obesity activities and its related mechanisms are yet to be reported. Thus, this study aims to evaluate its abilities to inhibit adipocyte hyperplasia and hypertrophy employing 3T3-L1 adipocytes.
    Methods: Statistical significance was established by one-way ANOVA, where p < 0.05 was considered statistically significant.
    Results: In this study, the IC50 value of XNT (98.3% purity) from Curcuma xanthorrhiza Roxb. in 3T3-L1 adipocytes was 35 ± 0.24 μg/mL. The loss of cell viability was due to 20.01 ± 2.77% of early apoptosis and 24.13 ± 2.03% of late apoptosis. XNT elicited apoptosis via up-regulation of caspase-3 and cleaved PARP-1 protein expression for 4.09-fold and 3.12-fold, respectively. Moreover, XNT decreased adipocyte differentiation for 36.13 ± 3.64% and reduced GPDH activity to 52.26 ± 4.36%. The underlying mechanism was due to impaired expression of PPARγ to 0.36-fold and FAS to 0.38-fold, respectively. On the other hand, XNT increased glycerol release by 45.37 ± 6.08% compared to control. During lipolysis, XNT up-regulated the leptin protein for 2.08-fold but down-regulated the protein level of insulin to 0.36-fold. These results indicated that XNT reduced the volume of adipocytes through modulation of leptin and insulin.
    Conclusion: To conclude, XNT exerted its anti-obesity mechanisms by suppression of adipocyte hyperplasia through induction of apoptosis and inhibition of adipogenesis whilst reduction of adipocyte hypertrophy through stimulation of lipolysis. Thus, XNT could be developed as a potential anti-obesity agent in the future.
    Matched MeSH terms: Insulin
  10. Mohamed Shah FZ, Mohamad AF, Zainordin NA, Eddy Warman NA, Wan Muhamad Hatta SF, Abdul Ghani R
    Ann Med Surg (Lond), 2021 Apr;64:102240.
    PMID: 33868680 DOI: 10.1016/j.amsu.2021.102240
    Introduction: Insulinoma is a functioning pancreatic neuroendocrine tumor primarily leading due to hypoglycemia due to hypersecretion of insulin. This case illustrates the real challenges faced in the detection of an occult insulinoma, which resulted in a protracted course of the disease.

    Case presentation: A 33-year-old female presented with recurrent hypoglycemia. Endogenous hyperinsulinemia was confirmed by a prolonged fast, however serial imaging was negative. Incidental finding of an ovarian mass gave rise to the suspicion of an insulin-producing ovarian tumor. Subsequent multimodality pancreatic imaging remained negative, requiring more invasive investigations. The tumor was localized by specialized arteriography using calcium stimulation to support the diagnosis of an insulinoma. However, repeated negative imaging led to further delays in definitive management, with worsening hypoglycemia. The surgery was finally performed three years after the initial presentation with successful removal of the tumor using intra-operative ultrasound.

    Clinical discussion: It is important to emphasize that preoperative radiological imaging is useful to localize pancreatic lesions. However, most insulinomas could only be detected intraoperatively. The absence of suggestive radiological evidence should not deter surgeons from proceeding with definitive surgical intervention.

    Conclusion: The case highlights the importance of a multidisciplinary approach in the management of a complicated case.

    Matched MeSH terms: Hyperinsulinism; Insulin; Insulinoma
  11. Abu Bakar MH, Sarmidi MR, Tan JS, Mohamad Rosdi MN
    Eur J Pharmacol, 2017 Mar 15;799:73-83.
    PMID: 28161417 DOI: 10.1016/j.ejphar.2017.01.043
    Accumulating evidence indicates that mitochondrial dysfunction-induced inflammation is among the convergence points for the greatest hallmarks of hepatic insulin resistance. Celastrol, an anti-inflammatory compound from the root of Tripterygium Wilfordii has been reported to mitigate insulin resistance and inflammation in animal disease models. Nevertheless, the specific mechanistic actions of celastrol in modulating such improvements at the cellular level remain obscure. The present study sought to explore the mechanistic roles of celastrol upon insulin resistance induced by palmitate in C3A human hepatocytes. The hepatocytes exposed to palmitate (0.75mM) for 48h exhibited reduced both basal and insulin-stimulated glucose uptake, mitochondrial dysfunction, leading to increased mitochondrial oxidative stress with diminished fatty acid oxidation. Elevated expressions of nuclear factor-kappa B p65 (NF-κB p65), c-Jun NH(2)-terminal kinase (JNK) signaling pathways and the amplified release of pro-inflammatory cytokines including IL-8, IL-6, TNF-α and CRP were observed following palmitate treatment. Consistently, palmitate reduced and augmented phosphorylated Tyrosine-612 and Serine-307 of insulin receptor substrate-1 (IRS-1) proteins, respectively in hepatocytes. However, celastrol at the optimum concentration of 30nM was able to reverse these deleterious occasions and protected the cells from mitochondrial dysfunction and insulin resistance. Importantly, we presented evidence for the first time that celastrol efficiently prevented palmitate-induced insulin resistance in hepatocytes at least, via improved mitochondrial functions and insulin signaling pathways. In summary, the present investigation underlines a conceivable mechanism to elucidate the cytoprotective potential of celastrol in attenuating mitochondrial dysfunction and inflammation against the development of hepatic insulin resistance.
    Matched MeSH terms: Insulin/metabolism; Insulin Resistance*
  12. Bakar MH, Sarmidi MR, Kai CK, Huri HZ, Yaakob H
    Int J Mol Sci, 2014 Dec 02;15(12):22227-57.
    PMID: 25474091 DOI: 10.3390/ijms151222227
    A growing body of evidence suggests that activation of nuclear factor kappa B (NF-κB) signaling pathways is among the inflammatory mechanism involved in the development of insulin resistance and chronic low-grade inflammation in adipose tissues derived from obese animal and human subjects. Nevertheless, little is known about the roles of NF-κB pathways in regulating mitochondrial function of the adipose tissues. In the present study, we sought to investigate the direct effects of celastrol (potent NF-κB inhibitor) upon mitochondrial dysfunction-induced insulin resistance in 3T3-L1 adipocytes. Celastrol ameliorates mitochondrial dysfunction by altering mitochondrial fusion and fission in adipocytes. The levels of oxidative DNA damage, protein carbonylation and lipid peroxidation were down-regulated. Further, the morphology and quantification of intracellular lipid droplets revealed the decrease of intracellular lipid accumulation with reduced lipolysis. Moreover, massive production of the pro-inflammatory mediators tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were markedly depleted. Insulin-stimulated glucose uptake activity was restored with the enhancement of insulin signaling pathways. This study signified that the treatments modulated towards knockdown of NF-κB transcription factor may counteract these metabolic insults exacerbated in our model of synergy between mitochondrial dysfunction and inflammation. These results demonstrate for the first time that NF-κB inhibition modulates mitochondrial dysfunction induced insulin resistance in 3T3-L1 adipocytes.
    Matched MeSH terms: Insulin/pharmacology; Insulin Resistance*
  13. Abu Bakar MH, Cheng KK, Sarmidi MR, Yaakob H, Huri HZ
    Molecules, 2015 May 07;20(5):8242-69.
    PMID: 25961164 DOI: 10.3390/molecules20058242
    Mitochondrial dysfunction and inflammation are widely accepted as key hallmarks of obesity-induced skeletal muscle insulin resistance. The aim of the present study was to evaluate the functional roles of an anti-inflammatory compound, celastrol, in mitochondrial dysfunction and insulin resistance induced by antimycin A (AMA) in human skeletal muscle cells. We found that celastrol treatment improved insulin-stimulated glucose uptake activity of AMA-treated cells, apparently via PI3K/Akt pathways, with significant enhancement of mitochondrial activities. Furthermore, celastrol prevented increased levels of cellular oxidative damage where the production of several pro-inflammatory cytokines in cultures cells was greatly reduced. Celastrol significantly increased protein phosphorylation of insulin signaling cascades with amplified expression of AMPK protein and attenuated NF-κB and PKC θ activation in human skeletal muscle treated with AMA. The improvement of insulin signaling pathways by celastrol was also accompanied by augmented GLUT4 protein expression. Taken together, these results suggest that celastrol may be advocated for use as a potential therapeutic molecule to protect against mitochondrial dysfunction-induced insulin resistance in human skeletal muscle cells.
    Matched MeSH terms: Insulin/metabolism; Insulin Resistance/physiology*
  14. Arifin SA, Falasca M
    Metabolites, 2016;6(1).
    PMID: 26784247 DOI: 10.3390/metabo6010006
    Metabolism is a chemical process used by cells to transform food-derived nutrients, such as proteins, carbohydrates and fats, into chemical and thermal energy. Whenever an alteration of this process occurs, the chemical balance within the cells is impaired and this can affect their growth and response to the environment, leading to the development of a metabolic disease. Metabolic syndrome, a cluster of several metabolic risk factors such as abdominal obesity, insulin resistance, high cholesterol and high blood pressure, and atherogenic dyslipidaemia, is increasingly common in modern society. Metabolic syndrome, as well as other diseases, such as diabetes, obesity, hyperlipidaemia and hypertension, are associated with abnormal lipid metabolism. Cellular lipids are the major component of cell membranes; they represent also a valuable source of energy and therefore play a crucial role for both cellular and physiological energy homeostasis. In this review, we will focus on the physiological and pathophysiological roles of the lysophospholipid mediator lysophosphatidylinositol (LPI) and its receptor G-protein coupled receptor 55 (GPR55) in metabolic diseases. LPI is a bioactive lipid generated by phospholipase A (PLA) family of lipases which is believed to play an important role in several diseases. Indeed LPI can affect various functions such as cell growth, differentiation and motility in a number of cell-types. Recently published data suggest that LPI plays an important role in different physiological and pathological contexts, including a role in metabolism and glucose homeostasis.
    Matched MeSH terms: Insulin Resistance
  15. Yahia A, Szlávecz Á, Knopp JL, Norfiza Abdul Razak N, Abu Samah A, Shaw G, et al.
    PMID: 34078114 DOI: 10.1177/19322968211018260
    BACKGROUND: Critically ill ICU patients frequently experience acute insulin resistance and increased endogenous glucose production, manifesting as stress-induced hyperglycemia and hyperinsulinemia. STAR (Stochastic TARgeted) is a glycemic control protocol, which directly manages inter- and intra- patient variability using model-based insulin sensitivity (SI). The model behind STAR assumes a population constant for endogenous glucose production (EGP), which is not otherwise identifiable.

    OBJECTIVE: This study analyses the effect of estimating EGP for ICU patients with very low SI (severe insulin resistance) and its impact on identified, model-based insulin sensitivity identification, modeling accuracy, and model-based glycemic clinical control.

    METHODS: Using clinical data from 717 STAR patients in 3 independent cohorts (Hungary, New Zealand, and Malaysia), insulin sensitivity, time of insulin resistance, and EGP values are analyzed. A method is presented to estimate EGP in the presence of non-physiologically low SI. Performance is assessed via model accuracy.

    RESULTS: Results show 22%-62% of patients experience 1+ episodes of severe insulin resistance, representing 0.87%-9.00% of hours. Episodes primarily occur in the first 24 h, matching clinical expectations. The Malaysian cohort is most affected. In this subset of hours, constant model-based EGP values can bias identified SI and increase blood glucose (BG) fitting error. Using the EGP estimation method presented in these constrained hours significantly reduced BG fitting errors.

    CONCLUSIONS: Patients early in ICU stay may have significantly increased EGP. Increasing modeled EGP in model-based glycemic control can improve control accuracy in these hours. The results provide new insight into the frequency and level of significantly increased EGP in critical illness.

    Matched MeSH terms: Insulin Resistance
  16. Kong APS, Lew T, Lau ESH, Lim LL, Kesavadev J, Jia W, et al.
    Diabetes Obes Metab, 2020 04;22(4):669-679.
    PMID: 31903728 DOI: 10.1111/dom.13950
    AIMS: To explore the pattern of insulin use and glycaemic control in Asian people with type 2 diabetes, stratified by gender, young-onset diabetes (YOD; diagnosed before age 40 years), and diabetic kidney disease (DKD; estimated glomerular filtration rate [eGFR] insulin users (47% women, mean ± SD age 59.2 ± 11.7 years, diabetes duration 13.2 ± 8.3 years, glycated haemoglobin [HbA1c] 72 ± 21.4 mmol/mol [8.74 ± 1.95%], median total daily insulin dose [TDD] 0.27-0.82 units/kg), 25% and 29.5% had YOD and DKD, respectively. Premixed (44%) and basal-only (42%) insulin were the most common regimens. Despite being more commonly treated with these two regimens with higher insulin dosages, patients with YOD had worse HbA1c levels than their late-onset peers (73 ± 20.5 vs. 71 ± 21.2 mmol/mol [8.82 ± 1.87% vs. 8.66 ± 1.94%]; P insulin regimens with suboptimal glycaemic control, despite relatively high TDDs, which were influenced by gender, DKD, and YOD status.
    Matched MeSH terms: Insulin
  17. Ng, S.H., Wan Rosli, W.I.
    Malays J Nutr, 2014;20(2):245-253.
    MyJurnal
    Introduction: Demand for dietary fibre-enriched and low sugar bakery products is rapidly increasing due to the current high incidence of Type 2 diabetes mellitus. Cinnamon, a spice which acts as a natural sweetener and insulin mimetic is believed to have health benefits. The objective of this study was to determine the properties of butter biscuits containing cinnamon powder (CP) that partially replaced sucrose at levels of 0 (control), 2, 4 or 6%. Methods: Nutritional composition, physical properties and sensory acceptability of the biscuits were analysed using AOAC methods, texture profile analyser and 7-point hedonic scaling method, respectively. Results: Protein, ash and dietary fibre contents of the biscuits increased significantly (P < 0.05) whereas the moisture and sucrose contents were reduced significantly, proportionately to the increasing levels of CP. In texture profile analyses, increment of firmness and reduction of crispiness of the biscuits were detected with increasing levels of CP, but not significantly. The sensory scores for control and 2% CP biscuits were not significantly different for all the sensory attributes. Biscuits with 4% CP received lower scores only for aroma and appearance whereas the scores for colour, crispiness and flavour showed no significant differences compared to the control and 2% CP biscuit. Conclusion: The addition of 4% CP in biscuit could be an effective way to produce nutritious butter biscuits without any apparent change to its desirable physical properties and sensory acceptability.
    Matched MeSH terms: Insulin
  18. Yinghao L, Jing Y, Yongqi W, Jianming Z, Zeng G, Yiting T, et al.
    J Int Med Res, 2021 Sep;49(9):3000605211039564.
    PMID: 34486432 DOI: 10.1177/03000605211039564
    OBJECTIVE: To investigate the changes in serum growth hormone (GH), testosterone, and insulin-like growth factor 1 (IGF-1) during low-intensity resistance exercise under different cuff pressures.

    METHODS: We performed a single-blind, cross-over design study. Twenty-five healthy young men performed three exercise protocols as follows: 1) no blood flow restriction exercise (control group), 2) resistance exercise at 40% of arterial occlusion pressure (AOP) (low group), and 3) resistance exercise at 70% of AOP (high group). Blood lactate, GH, testosterone, and IGF-1 levels were measured at four time points.

    RESULTS: There were no differences in the indices before exercise. The blood flow restriction exercise under different pressures had different effects on each index and there was an interactive effect. GH levels were significantly higher in the high group than in the other groups after exercise. Immediately after exercise, IGF-1 and testosterone levels were significantly higher in the high group than in the other groups. At 15 minutes after exercise, testosterone levels were significantly higher in the high group than in the other groups.

    CONCLUSIONS: Low-intensity resistance exercise combined with blood flow restriction effectively increases GH, IGF-1, and testosterone levels in young men. Increasing the cuff pressure results in greater levels of hormone secretion.

    Matched MeSH terms: Insulin-Like Growth Factor I
  19. Mahmud Z, Abrahhim SA, Sulong S
    Curr Diabetes Rev, 2021;17(7):e011221190236.
    PMID: 33438543 DOI: 10.2174/1573399817999210112191330
    BACKGROUND: It is important to assess how well patients respond to their medical treatments by observing the results that appear during the clinical treatments. As such, the clinical treatments and results must obtain information on how effective recommended treatments were for patients with diabetes.

    OBJECTIVE: This study examines how patients with diabetes mellitus responded towards their clinical treatments, where the probability distribution of patients and the types of treatment received were derived from the Rasch probabilistic model.

    METHODS: This is a retrospective study wherein data were collected from patients' medical records at a local public hospital in Selangor, Malaysia. Clinical and demographic information such as fasting blood glucose, hemoglobin A1c (HbA1c), family history, type of diabetes (type 1 or type 2), types of medication (oral or insulin), compliance with treatments, gender, race and age were chosen as the agents of measurement.

    RESULTS: The use of Rasch analysis in the present study helped to compare the patients' responses towards the DM treatments and identify the types of treatment they received. Results from the Wright map show that a majority of the diabetes mellitus patients who were diagnosed with type 2 diabetes have no controlled readings of HbA1c during their first and second visits to the medical center. However, patients with a family history of diabetes mellitus who took oral medication have controlled readings of fasting blood glucose based on the probabilistic outcomes of the treatment received by the patients.

    CONCLUSION: Controlled readings were found only in the readings of fasting blood glucose during the first and second visits, followed by family history, types of medication received, and compliance with the treatment. This study has recommended that type 2 patients with diabetes without a family history of diabetes mellitus need to exercise more control over the readings of HbA1c.

    Matched MeSH terms: Insulin
  20. Nirmala Kampan, Hanis Azman, Izzat Hafiz, Hazwani Mohammad, Chuah, Su Yee, Nur Azurah Abd Ghani, et al.
    MyJurnal
    To observe the maternal and neonatal outcomes among women with diabetes mellitus in pregnancy as compared to healthy control. A case-control study involving 400 women with DM who delivered between 2005 to 2009 was done with age-matched control group. A total of 305 women (76.25%) were gestational diabetes mellitus (GDM) on diet control, 79 (19.75%) were GDM on insulin and 16 (4%) were pre-existing DM. The mean body mass index of the women with diabetes was higher compared to the age-matched healthy women (p
    Matched MeSH terms: Insulin
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