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排序方式: 共有102条查询结果,搜索用时 109 毫秒
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Manijheh Sabokdast Mehran Habibi-Rezaei Ali Akbar Moosavi-Movahedi Maryam Ferdousi Effat Azimzadeh-Irani Najmeh Poursasan 《Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences》2015,23(1)
Background
Diabetes mellitus is characterized jointly by hyperglycemia and hyperinsulinemia that make insulin more prone to be glycated and evolve insulin advanced glycation end products (Insulin- AGE). Here, we report the effect of beta-hydroxy butyrate (BHB) (the predominant ketone body) on the formation of insulin-AGE, insulin glycation derived liposomal lipid peroxidation and insulin-AGE toxicity in microglial cells.Methods
The inhibitory effect of BHB was monitored as a result of insulin incubation in the presence of glucose or fructose using AGE-dependent fluorescence, Tyr fluorescence as well as anilinonaphthalenesulfonate (ANS) andthioflavin T (ThT) binding, and circular dichroism (CD) investigations. To study lipid peroxidation induced by insulin glycation, thiobarbituric acid (TBA) assay and thiobarbituric acid reactive substance (TBARS) monitoring were used. The effect of insulin–AGE on microglial viability was investigated by 3-(4, 5 dimethylthiazol-2-yl)—2, 5-diphenyltetrazoliumbromide (MTT) cell assay and Annexin V/propidium iodide (PI) staining.Results
Here we are reporting the inhibitory effect of BHB on insulin glycation and generation of insulin-AGE as a possible explanation for insulin resistance. Moreover, the protective effect of BHB on consequential glycation derived liposomal lipid peroxidation as a causative event in microglial apoptosis is reported.Conclusion
The reduced insulin fibril formation, structural inertia to glycation involved conformational changes, anti-lipid peroxidation effect, and increasing microglia viability indicated the protective effect of BHB that disclose insight on the possible preventive effect of BHB on Alzheimer’s disease. 相似文献3.
Fara Wahida Rezali Yit Siew Chin Zalilah Mohd Shariff Barakatun Nisak Mohd Yusof Kaartina Sanker Fui Chee Woon 《Nutrition Research And Practice》2015,9(5):511-516
BACKGROUND/OBJECTIVES
This study aims to determine contribution of meal frequency, self-efficacy for healthy eating, and availability of healthy foods towards diet quality of adolescents in Kuala Lumpur, Malaysia.SUBJECTS/METHODS
This study was conducted among 373 adolescents aged from 13 to 16 years old. Diet quality of the respondents was assessed using the Healthy Eating Index for Malaysians. Meal frequency, self-efficacy for healthy eating, and availability of healthy foods were assessed through the Eating Behaviours Questionnaire (EBQ), self-efficacy for healthy eating scale, and availability of healthy foods scale, respectively.RESULTS
The majority of the respondents (80.7%) were at risk of poor diet quality. Males (mean = 34.2 ± 8.2%) had poorer diet quality than females (mean = 39.9 ± 9.0%) (t = -5.941, P < 0.05). Malay respondents (mean = 36.9 ± 8.7%) had poorer diet quality than Indian respondents (mean = 41.3 ± 10.0%) (F = 2.762, P < 0.05). Age (r = 0.123, P < 0.05), self-efficacy for healthy eating (r = 0.129, P < 0.05), and availability of healthy foods (r = 0.159, P < 0.05) were positively correlated with the diet quality of the respondents. However, meal frequency was not correlated with the diet quality of the respondents. Multiple linear regression analysis showed that being a male, being a Malay, low self-efficacy for healthy eating, and low availability of healthy foods contributed significantly towards poor diet quality among respondents.CONCLUSIONS
In short, sex, ethnicity, self-efficacy for healthy eating, and availability of healthy foods were associated with diet quality among adolescents. Health practitioners should take into consideration of differences in sex and ethnicity during implementation of nutrition-related intervention programs. Self-efficacy for healthy eating and availability of healthy foods should be included as important components in improving diet quality of adolescents. 相似文献4.
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John S. Millar Gissette Reyes-Soffer Patricia Jumes Richard L. Dunbar Emil M. deGoma Amanda L. Baer Wahida Karmally Daniel S. Donovan Hashmi Rafeek Laura Pollan Junichiro Tohyama Amy O. Johnson-Levonas John A. Wagner Stephen Holleran Joseph Obunike Yang Liu Rajasekhar Ramakrishnan Michael E. Lassman David E. Gutstein Henry N. Ginsberg Daniel J. Rader 《The Journal of clinical investigation》2015,125(6):2510-2522
BACKGROUND. Individuals treated with the cholesteryl ester transfer protein (CETP) inhibitor anacetrapib exhibit a reduction in both LDL cholesterol and apolipoprotein B (ApoB) in response to monotherapy or combination therapy with a statin. It is not clear how anacetrapib exerts these effects; therefore, the goal of this study was to determine the kinetic mechanism responsible for the reduction in LDL and ApoB in response to anacetrapib.METHODS. We performed a trial of the effects of anacetrapib on ApoB kinetics. Mildly hypercholesterolemic subjects were randomized to background treatment of either placebo (n = 10) or 20 mg atorvastatin (ATV) (n = 29) for 4 weeks. All subjects then added 100 mg anacetrapib to background treatment for 8 weeks. Following each study period, subjects underwent a metabolic study to determine the LDL-ApoB-100 and proprotein convertase subtilisin/kexin type 9 (PCSK9) production rate (PR) and fractional catabolic rate (FCR).RESULTS. Anacetrapib markedly reduced the LDL-ApoB-100 pool size (PS) in both the placebo and ATV groups. These changes in PS resulted from substantial increases in LDL-ApoB-100 FCRs in both groups. Anacetrapib had no effect on LDL-ApoB-100 PRs in either treatment group. Moreover, there were no changes in the PCSK9 PS, FCR, or PR in either group. Anacetrapib treatment was associated with considerable increases in the LDL triglyceride/cholesterol ratio and LDL size by NMR.CONCLUSION. These data indicate that anacetrapib, given alone or in combination with a statin, reduces LDL-ApoB-100 levels by increasing the rate of ApoB-100 fractional clearance.TRIAL REGISTRATION. ClinicalTrials.gov .FUNDING. Merck & Co. Inc., Kenilworth, New Jersey, USA. Additional support for instrumentation was obtained from the National Center for Advancing Translational Sciences (UL1TR000003 and UL1TR000040). NCT00990808相似文献
6.
Shazli Azmi Maryam Ferdousi Ioannis N. Petropoulos Georgios Ponirakis Uazman Alam Hassan Fadavi Omar Asghar Andrew Marshall Andrew J. Atkinson Wendy Jones Andrew J.M. Boulton Mitra Tavakoli Maria Jeziorska Rayaz A. Malik 《Diabetes care》2015,38(8):1502-1508
OBJECTIVEImpaired glucose tolerance (IGT) through to type 2 diabetes is thought to confer a continuum of risk for neuropathy. Identification of subjects at high risk of developing type 2 diabetes and, hence, worsening neuropathy would allow identification and risk stratification for more aggressive management.RESULTSTen subjects who developed type 2 diabetes had a significantly lower CNFD (P = 0.003), CNBD (P = 0.04), and CNFL (P = 0.04) compared with control subjects at baseline and a further reduction in CNFL (P = 0.006), intraepidermal nerve fiber density (IENFD) (P = 0.02), and mean dendritic length (MDL) (P = 0.02) over 3 years. Fifteen subjects who remained IGT and 5 subjects who returned to normal glucose tolerance had no significant baseline abnormality on CCM or IENFD but had a lower MDL (P < 0.0001) compared with control subjects. The IGT subjects showed a significant decrease in IENFD (P = 0.02) but no change in MDL or CCM over 3 years. Those who returned to NGT showed an increase in CNFD (P = 0.05), CNBD (P = 0.04), and CNFL (P = 0.05), but a decrease in IENFD (P = 0.02), over 3 years.CONCLUSIONSCCM and skin biopsy detect a small-fiber neuropathy in subjects with IGT who develop type 2 diabetes and also show a dynamic worsening or improvement in corneal and intraepidermal nerve morphology in relation to change in glucose tolerance status. 相似文献
7.
Xin Chen Jim Graham Mohammad A. Dabbah Ioannis N. Petropoulos Georgios Ponirakis Omar Asghar Uazman Alam Andrew Marshall Hassan Fadavi Maryam Ferdousi Shazli Azmi Mitra Tavakoli Nathan Efron Maria Jeziorska Rayaz A. Malik 《Diabetes care》2015,38(6):1138-1144
OBJECTIVE
Quantitative assessment of small fiber damage is key to the early diagnosis and assessment of progression or regression of diabetic sensorimotor polyneuropathy (DSPN). Intraepidermal nerve fiber density (IENFD) is the current gold standard, but corneal confocal microscopy (CCM), an in vivo ophthalmic imaging modality, has the potential to be a noninvasive and objective image biomarker for identifying small fiber damage. The purpose of this study was to determine the diagnostic performance of CCM and IENFD by using the current guidelines as the reference standard.RESEARCH DESIGN AND METHODS
Eighty-nine subjects (26 control subjects and 63 patients with type 1 diabetes), with and without DSPN, underwent a detailed assessment of neuropathy, including CCM and skin biopsy.RESULTS
Manual and automated corneal nerve fiber density (CNFD) (P < 0.0001), branch density (CNBD) (P < 0.0001) and length (CNFL) (P < 0.0001), and IENFD (P < 0.001) were significantly reduced in patients with diabetes with DSPN compared with control subjects. The area under the receiver operating characteristic curve for identifying DSPN was 0.82 for manual CNFD, 0.80 for automated CNFD, and 0.66 for IENFD, which did not differ significantly (P = 0.14).CONCLUSIONS
This study shows comparable diagnostic efficiency between CCM and IENFD, providing further support for the clinical utility of CCM as a surrogate end point for DSPN. 相似文献8.
9.
Luca D'Onofrio Alise Kalteniece Maryam Ferdousi Shazli Azmi Ioannis N. Petropoulos Georgios Ponirakis Uazman Alam Omar Asghar Andrew Marshall Andrew J M. Boulton Nathan Efron Raffaella Buzzetti Handrean Soran Rayaz A. Malik 《Investigative ophthalmology & visual science》2021,62(6)
PurposeIncreased corneal and epidermal Langerhans cells (LCs) have been reported in patients with diabetic neuropathy. The aim of this study was to quantify the density of LCs in relation to corneal nerve morphology and the presence of diabetic neuropathy and to determine if this differed in patients with type 1 diabetes mellitus (T1DM), type 2 diabetes mellitus (T2DM), and latent autoimmune diabetes of adults (LADA).MethodsPatients with T1DM (n = 25), T2DM (n = 36), or LADA (n = 23) and control subjects (n = 23) underwent detailed assessment of peripheral neuropathy and corneal confocal microscopy. Corneal nerve fiber density (CNFD), branch density (CNBD), length (CNFL) and total, immature and mature LC densities were quantified.ResultsLower CNFD (P < 0.001), CNBD (P < 0.0001), and CNFL (P < 0.0001) and higher LC density (P = 0.03) were detected in patients with T1DM, T2DM, and LADA compared to controls. CNBD was inversely correlated with mature (r = –0.5; P = 0.008), immature (r = –0.4; P = 0.02) and total (r = –0.5; P = 0.01) LC density, and CNFL was inversely correlated with immature LC density (r = –0.4; P = 0.03) in patients with T1DM but not in patients with T2DM and LADA.ConclusionsThis study shows significant corneal nerve loss and an increase in LC density in patients with T1DM, T2DM, and LADA. Furthermore, increased LC density correlated with corneal nerve loss in patients with T1DM. 相似文献
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