ORCID Profile
0000-0002-7274-0839
Current Organisations
The University of Hong Kong
,
The Hong Kong Polytechnic University
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: Portland Press Ltd.
Date: 11-10-2016
DOI: 10.1042/CS20160465
Abstract: Both atherosclerosis and obesity, an independent atherosclerotic risk factor, are associated with enhanced systemic inflammation. Obesity is also characterized by increased adipose tissue inflammation. However, the molecular mechanism underlying the accelerated atherosclerosis in obesity remains unclear. In obesity, activation of c-Jun N-terminal kinase (JNK) contributes to adipose tissue inflammation. The present study investigated whether the suppression of fat inflammation through adipose-specific JNK inactivation could protect against atherosclerosis in mice. ApoE−/− mice were cross-bred with transgenic mice with adipose-specific expression of a dominant negative form of JNK (dnJNK) to generate apoE−/−/dnJNK (ADJ) mice. ADJ mice treated with a high-fat–high-cholesterol diet exhibited significant attenuations of visceral fat and systemic inflammation without changes in lipid or glucose metabolism, and were protected against atherosclerosis, when compared with apoE−/− mice. Lean apoE−/− mice that received transplantation of visceral fat from obese wild-type donor mice for 4 weeks showed exacerbated systemic inflammation and atherosclerotic plaque formation. Conversely, apoE−/− recipients carrying a visceral fat graft from obese dnJNK donors were protected against enhanced systemic inflammation and atherogenesis. The beneficial effects of adipose-specific JNK inactivation on atherogenesis in apoE−/− recipients were significantly compromised by continuous infusion of recombinant adipocyte–fatty acid-binding protein (A-FABP), previously shown to interact with JNK via a positive feedback loop to modulate inflammatory responses. Together these data suggested that enhanced atherosclerosis in obesity can be attributed, at least in part, to a distant cross-talk between visceral fat and the vasculature, mediated by the release of proinflammatory cytokines, such as A-FABP, from the inflamed visceral adipose tissue with JNK activation.
Publisher: JMIR Publications Inc.
Date: 29-05-2019
DOI: 10.2196/14386
Publisher: JMIR Publications Inc.
Date: 15-04-2019
Abstract: besity is a common global health problem and increases the risk of many chronic illnesses. Given the adverse effects of antiobesity agents and bariatric surgeries, the exploration of noninvasive and nonpharmacological complementary methods for weight reduction is warranted. he study aimed to determine whether self-administered auricular acupressure (AA) integrated with a smartphone app was more effective than using AA alone or the controls for weight reduction. his study is a 3-arm randomized waitlist-controlled feasibility trial. A total of 59 eligible participants were randomly ided into either group 1 (AA group, n=19), group 2 (AA plus smartphone app, n=19), or group 3 (waitlist control, n=21). A total of 6 reflective zones or acupoints for weight reduction were chosen. The smartphone app could send out daily messages to the subjects to remind them to perform self-pressing on the 6 ear acupoints. A “date picker” of the 8-week treatment course was used to enable the users to input the compliance of pressing and the number of bowel movement daily instead of using the booklet for recordings. The app also served as a reminder for the subjects regarding the dates for returning to the center for acupoint changing and assessments. Treatment was delivered 2 times a week, for 8 weeks. Generalized estimating equations were used to examine the interactions among the groups before and after intervention. ubjects in group 2 expressed that the smartphone app was useful (7.41 out of 10). The most popular features were the daily reminders for performing self-pressing (88%), the ear diagram indicating the locations and functions of the 6 ear points (71%), and ear pressing method demonstrated in the video scripts (47%). Nearly 90% of the participants completed the 8-week intervention, with a high satisfaction toward the overall arrangement (8.37 out of 10). The subjects in group 1 and 2 achieved better therapeutic effects in terms of body weight, body mass index (BMI), waist circumference, and hip circumference and perceived more fullness before meals than the waitlist controls. Although no significant differences in the pairwise comparisons between the 2 groups were detected (P .05), the decrease in body weight, BMI, body fat, visceral fat rating and leptin level, and increase in adiponectin level were notable in group 2 before and after the intervention. he high compliance rate and high satisfaction toward the trial arrangement indicate that AA can be used to achieve weight reduction and applied in future large-scale studies. AA integrated with the smartphone app has a more notable effect than using AA alone for weight reduction. Larger s le size should be considered in future trials to determine the causal relationship between treatment and effect. linicalTrials.gov NCT03442712 t2/show/NCT03442712 (Archived by WebCite at 8L2tO8Ql)
Publisher: Elsevier BV
Date: 05-2009
DOI: 10.1016/J.CMET.2009.03.013
Abstract: Hepatic insulin resistance is the major contributor to fasting hyperglycemia in type 2 diabetes. Here we report that the endosomal adaptor protein APPL1 increases hepatic insulin sensitivity by potentiating insulin-mediated suppression of the gluconeogenic program. Insulin-stimulated activation of Akt and suppression of gluconeogenesis in hepatocytes are enhanced by APPL1 overexpression, but are attenuated by APPL1 knockdown. APPL1 interacts with Akt and blocks the association of Akt with its endogenous inhibitor tribble 3 (TRB3) through direct competition, thereby promoting Akt translocation to the plasma membrane and the endosomes for further activation. In db/db diabetic mice, the blockage of the augmented interaction between Akt and TRB3 by hepatic overexpression of APPL1 is accompanied by a marked attenuation of hyperglycemia and insulin resistance. These results suggest that the potentiating effects of APPL1 on insulin-stimulated suppression of hepatic glucose production are attributed to its ability in counteracting the inhibition of Akt activation by TRB3.
No related grants have been discovered for Kenneth King Yip Cheng.