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PE-26

Physical activity and albuminuria were associated with

painful diabetic polyneuropathy in type 2 diabetes in an ethnic

Chinese population

Sheng-Shu CHIANG

1,2

, Chia-Lin LEE

1

, Hsiu-Chen LIU

1

,

Jun-Sing WANG

1

, I-Te LEE

1

, Yuh-Min SONG

1

, Chia-Po FU

1

,

Shih-Yi LIN

1

*, Wayne H.-H. SHEU

1

.

1

Divisions of Endocrinology

and MetabolismDepartment of Internal Medicine, Taichung Veterans

General Hospital,

2

Divisions of Internal Medicine, Sinying Hospital,

Taiwan

Diabetic neuropathy is a common complication in patients

with type 2 diabetes. However, prevalence of painful diabetic

polyneuropathy (PDPN) and potential influences of physical

activity and albuminuria on development of PDPN have been

rarely studied. The aim of this study was to examine the

prevalence of PDPN as well as the independent and joint

effects of physical activity and albuminuria on it.

This retrospective study enrolled 2,359 outpatients with type 2

diabetes with completed survey of Douleur Neuropathique en

4 Questions (DN4) questionnaire from January 2013 to October

2013 in one of medical center in central Taiwan. Painful

neuropathy was defined as a total score exceeding 3 points.

Independent and joint effects of physical activity and albu-

minuria on PDPN were assessed by fixed effect with logistic

regression.

Overall, 179 (7.6%) patients were diagnosed as having PDPN.

Both less physical activity and albuminuria were associated

with a higher mean DN4 score (1.07 for no exercise, 0.87 for

daily exercise duration

30 minutes, and 0.56 for daily

exercise duration >30 minutes, p for trend <0.001; 1.51 for

macroalbuminuria, 1.10 for microalbuminuria, and 0.78 for

normal UACR, p for trend <0.001). Adjusted analysis showed

that the risk of painful neuropathy increased in the groups

without physical activity (Odds ratio (OR) = 3.38, 95% CI 1.54

9.79) and daily exercise duration

30minutes (OR = 3.33, 95%CI

1.27

8.73), when compared with the group with daily exercise

duration >30 minutes (p for trend 0.006). Comparing with

normal UACR, the OR for PDPN were 0.96 (95% CI 0.61

1.50)

and 2.31 (95% CI 1.44

3.73) for microalbuminuria and macro-

albuminuria respectively (p for trend 0.002). In addition, we

observed a joint effect of macroalbuminuria and physical

inactivity on PDPN risk (OR = 6.68, 95% CI 2.23

20.04).

Less physical activity and albuminuria, respectively, increased

the risk of PDPN and had a joint effect.

PE-27

Osteocalcin improves nonalcoholic fatty liver disease in mice

through activation of Nrf2 and inhibition of JNK

Yuqian BAO

1

*, Jing DU

1

, Mingliang ZHANG

1

, Junxi LU

1

,

Xueli ZHANG

1

, Qin XIONG

1

, Yiting XU

1

, Weiping JIA

1

.

1

Department of Endocrinology and Metabolism, Shanghai Jiao Tong

University Affiliated Sixth People

s Hospital; Shanghai Clinical Center

for Diabetes; Shanghai Diabetes Institute, China

Objective:

Recent studies have demonstrated a protective

effect of osteocalcin against nonalcoholic fatty liver disease

(NAFLD), although the specific underlying mechanisms

remain unclear. Nuclear factor erythroid 2-related factor 2

(Nrf2) and c-Jun N-terminal kinase (JNK) pathways play

important roles in the pathogenesis of NAFLD. The present

study aimed to investigate whether osteocalcin protects

against NAFLD by regulating these pathways.

Methods:

Male C57/BL6J mice were fed a high-fat diet for 12

weeks to induce NAFLD and were treated with recombinant

uncarboxylated osteocalcin (30 ng/g) or vehicle by daily

intraperitoneal injection during this period. Intraperitoneal

glucosetolerance test, insulin tolerance test, measurement of

serum lipid profiles, liver enzymes and hepatic triglyceride

content were carried out. Hepatic redox state was examined.

The role of osteocalcin on Nrf2 and JNK were investigated by

Western blot and Real-time PCR.

Results:

Daily injections of osteocalcin can significantly

improve lipid metabolism, glucose tolerance and insulin

sensitivity in mice fed a high-fat diet (P < 0.05). Osteocalcin

treatment protected mice from diet-induced hepatic triglycer-

ide accumulation and liver injury. Increased levels of mal-

ondialdehyde, 8-iso-prostaglandin F2

α

and a higher ratio of

oxidized/reduced glutathione (GSSG/GSH) in the liver of mice

fed a high-fat diet were decreased by osteocalcin (P < 0.05).

Meanwhile, treatment with osteocalcin resulted in increases

in hepatic reduced GSH levels in mice fed a high-fat diet

(P < 0.05). Osteocalcin treatment not only activated Nrf2

nuclear translocation and up-regulated the expression of

antioxidant enzyme genes (catalase, superoxide dismutase,

and glutathione peroxidase) (P < 0.05), but also inhibited the

activation of JNK in the liver (P < 0.05). G protein coupled

receptor family C, group 6, subtype A (GPRC6A), the putative

receptor of osteocalcin, was found in the liver.

Conclusions:

Osteocalcin improves NAFLD by activating the

Nrf2 pathway to alleviate oxidative stress, and inhibiting JNK

pathway.

PE-28

Anterior compartment syndromewith type 1 diabetesmellitus

Min Ji KIM

1

, Sung DaeMOON

1

*, Eun Sook KIM

1

, Eun YeongMO

1

,

Je Ho HAN

1

.

1

Division of Endocrinology & Metabolism, Department

of Internal Medicine, Incheon St. Mary

s Hospital, The Catholic

University of Korea, Incheon, Korea

Compartment syndrome is defined as an elevation of the

interstitial pressure in a closed osteofascial compartment

causing microvascular compromise. The common causes

include trauma, arterial injury, limb compression and burns.

Rarely, it can also occur spontaneously in association with

type 1 diabetesmellitus. We report a case of a patient with type

1 diabetes mellitus who presented with lower limb pain

without any obvious injury and had a subsequent diagnosis

of acute compartment syndromes. Non traumatic acute

compartment syndrome secondary to diabetic muscle infarc-

tion should be considered in any diabetic patient presenting

with pain out of proportion to sustained injury.

PE-29

Prevalence of chronic kidney disease among adults with

diabetes or prediabetes in China

Qian DENG

1

, Tengfei MAN

2

, Mei ZHANG

1

, Shusen LIU

2

,

Zhenping ZHAO

1

, Tongtong WANG

3

, Zhengjing HUANG

1

,

Yichong LI

1

, Samuel S. ENGEL

3

, R. Ravi SHANKAR

3

,

Kimberly G. BRODOVICZ

3

, Yingmei TU

2

, Linhong WANG

1

,

LiminWANG

1

.

1

National Center for Chronic and Non-communicable

Disease Control and Prevention, Chinese Center for Disease Control

and Prevention,

2

Merck Sharp & Dohme (China) R&D Co., Ltd., China;

3

Merck Research Laboratories, Merck & Co., Inc., United States of

America

Background:

Chronic kidney disease (CKD) is recognized as a

global public health problem. Diabetes mellitus is the leading

cause of CKD, but little is known about the relationship

between CKD and prediabetes, especially among those who

remained long-term prediabetic state.

Objectives:

To compare the prevalence of CKD among Chinese

adults with pre-diabetes and diabetes to those with normal

glucose tolerance (NGT). To examine whether the prediabetes

progression was associated with CKD prevalence.

Methods:

1,149 Chinese adults aged over 18 years old with

prediabetes and 997 with NGT were identified from four

counties/districts in 2010, and were followed up to 2014. Blood

and urine samples were collected to assess the presence of

CKD in 2014. CKD was defined as eGFR less than 60 mL/min

per 1.73 m

2

or the presence of albuminuria (urinary albumin

to creatinine ratio >=30 mg/g), and estimated at the end of

follow-up. Pre-diabetes and diabetes were based on the criteria

Poster Presentations / Diabetes Research and Clinical Practice 120S1 (2016) S65

S211

S139