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Chan, KH

Cheng, KKY

Cheng, OY

Chung, SK

Guo, VY

Ho, PWL

Kwan, JSC

Lam, KSL

Xu, A

Yeung, PKK

Hong Kong Medical Journal

HKU Scholars Hub

Title Cognitive impairment in adiponectin-knockout miceAuthor(s) Cheng, OY; Lam, KSL; Chung, SK; Xu, A; Yeung, PKK; Kwan,JSC; Ho, PWL; Cheng, KKY; Guo, VY; Chan, KHCitation19th Medical Research Conference, Department of Medicine, TheUniversity of Hong Kong, Hong Kong, 18 January 2014. In HongKong Medical Journal, 2014, v. 20 n. 1, Suppl. 1, p. 14, abstractno. 11Issued Date 2014URL http://hdl.handle.net/10722/195697Rights Hong Kong Medical Journal. Copyright © Hong Kong Academyof Medicine Press.14 XXXXHong Kong Med J  ⎥  Volume 20 Number 1 (Supplement 1)  ⎥  February 2014  ⎥  www.hkmj.org Hong Kong Med J  ⎥  Volume 20 Number 1 (Supplement 1)  ⎥  February 2014  ⎥  www.hkmj.org1211The relationship between glucose metabolism, metabolic syndrome, and bone-specific  alkaline phosphatase: a structural equation modelling approachCL Cheung, KCB Tan, KSL Lam, BMY CheungDepartment of Medicine, The University of Hong Kong, Hong KongIntroduction: Serum alkaline phosphatase plays a role in vascular calcification. It is found in various tissues, whereas bone-specific alkaline phosphatase (BAP) more specifically reflects mineral metabolism. The relationship of serum alkaline phosphatase (total and bone-specific) with diabetes and metabolic syndrome, which are two major risk factors of vascular calcification, is largely unknown. We aimed to investigate the relationships between glucose metabolism, components of metabolic syndrome (MetS), and alkaline phosphatase.Methods: Data on 3773 non-diabetic participants of the National Health and Nutrition Examination Survey 1999–2004 were examined. Serum BAP and total alkaline phosphatase were measured as outcomes. Linear regression was used to assess the association of glucose metabolism and metabolic syndrome with serum alkaline phosphatase levels.Results: In multivariable linear regression, HOMA2-IR (β = 0.068), HOMA2-B (β = 0.081), insulin (β = 0.065), mean arterial pressure (β = 0.15), and high density lipoprotein (HDL)–cholesterol (β = 0.209) were positively associated with BAP, whereas HOMA2-IS (β = –0.065) was negatively associated with BAP. On the other hand, only mean arterial pressure and HDL-cholesterol were significantly associated with total alkaline phosphatase. Moreover, structural equation model revealed that hypertension, low HDL, and insulin resistance had significant direct effects on serum BAP levels, whereas obesity and inflammation might have indirect effects on serum BAP levels. The overall model showed very good fit to the data (comparative fit index = 0.995, root mean square error of approximation = 0.037, and standardised root mean square residual = 0.006).Conclusion: Glucose metabolism and MetS are significantly related to serum BAP levels. How BAP mediates vascular calcification in diabetes and MetS warrants further studies.Cognitive impairment in adiponectin-knockout miceOY Cheng1, KSL Lam1, SK Chung2, A Xu1, PKK Yeung2, JSC Kwan1, PWL Ho1, KKY Cheng1, VY Guo1, KH Chan11 Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong2 Department of Anatomy, The University of Hong Kong, Hong KongIntroduction: Alzheimer’s disease (AD) is the most common cause of dementia in the elderly. AD is characterised by amyloid-beta (Aβ)–mediated neurotoxicity and neuronal insulin resistance. Adiponectin, an adipokine with insulin-sensitising and anti-inflammatory actions, bears potential as novel therapy for AD. We aimed to study the cognitive function of adiponectin-knockout (APN-KO) mice.Methods: APN-KO and wild type (WT) mice of 9 and 18 months old had cognitive functions assessed by Morrison water maze test and open field test. Mice were sacrificed with 1 week after cognitive functions tests and forebrain cortex was studied immunohistologically for Aβ (using 2C8 and 7A1a antibodies) and microglial activation (by Iba1 immunoreactivity). Frontal cortex homogenate was analysed for insulin receptor substrate-1 phosphorylated at serine 616 (IRS-1pS616, marker of insulin resistance) by western blot. Results: APN-KO mice of 9 months old had increased anxiety (shorter distance moved, slower velocity, less time of movement, less time in centre, more time in margin and less exploration; P < 0.05) but indifferent in spatial memory compared to WT mice of the same age. APN-KO mice of 18 months old had increased anxiety (shorter distance moved, slower velocity, less time of movement, less time in centre, more time in margin and less exploration; P < 0.05) and impaired spatial memory (longer hidden platform latency; P < 0.01) compared to WT mice of the same age. Histologically, APN-KO mice had increased immunoreactivity for Aβ (P < 0.0001) and Aβ oligomers (P < 0.0001) and increased microglial activation (P < 0.05) than WT mice. Western blot revealed that frontal cortex homogenate of APN-KO mice had higher level of IRS-1pS616 than that of WT mice of the same age (P < 0.05).Conclusion: APN-KO mice of 9 and 18 months old had impaired cognitive functions associated with increased cerebral Aβ deposition and neuronal insulin resistance compared to WT mice of the same age.

Cognitive impairment in adiponectin-knockout mice

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Cognitive impairment in adiponectin-knockout mice

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