Obesity Research & Clinical Practice (2012) 6, e270—e279

REVIEW

Body adipose distribution among patients with type 2 diabetes mellitus Liang-Jun Xie, Mu-Hua Cheng ∗ Department of Nuclear Medicine, The 3rd Affiliated Hospital of Sun Yat-Sen University, No. 600, Tianhe Road, Guangzhou City, Guangdong Province, China Received 10 June 2012 ; received in revised form 17 September 2012; accepted 24 September 2012

KEYWORDS Metabolic syndrome; Obesity; Adipose tissue; Absorptiometry

Summary Both diabetes mellitus (DM) and obesity are prevalent in adults. The relationship between DM and body adipose tissue (AT) distribution is complex and although it has been investigated extensively, the subject remains controversial. Although a causal association between DM and obesity and AT distribution cannot be established on the basis of existing data, it is possible to conclude from many studies that gene, serum sex steroids level, daily physical activity and food supply can be the risk of obesity and AT redistribution factor among type 2 DM patients (T2DM). Obesity and AT redistribution of T2DM patients can increase the risk of insulin resistant (IR), cardiovascular disease and many other disorders. Even though obesity and AT redistribution screening or prophylactic treatment in all patients with T2DM is not being recommended at present, such patient populations should be given general guidelines regarding exercise, food intake control, and even medicinal treatment. The extent of diagnostic and therapeutic interventions should be based on the individual’s risk profile. © 2012 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.

Contents Introduction ............................................................................................... Body adipose distribution and type 2 diabetes mellitus .................................................... SAT and type 2 diabetes mellitus ...................................................................... VAT and type 2 diabetes mellitus ...................................................................... IMAT and type 2 diabetes mellitus..................................................................... Pathophysiology of adipose tissue redistribution in type 2 diabetes mellitus ............................... Genetic factors ....................................................................................... Sex steroids ........................................................................................... ∗

Corresponding author. Tel.: +86 020 85253137. E-mail address: [email protected] (M.-H. Cheng).

1871-403X/$ — see front matter © 2012 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.

http://dx.doi.org/10.1016/j.orcp.2012.09.003

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Relationship between diabetes mellitus and adipose tissue Decreased physical activity and increased food supply ................................................ The risk of adipose tissue redistribution with type 2 diabetes mellitus ..................................... Adipose tissue redistribution and insulin resistance ................................................... Adipose tissue redistribution and cardiovascular disease .............................................. Adipose tissue redistribution and hypertension ........................................................ Adipose tissue redistribution and some other diseases................................................. Medical care ............................................................................................... Summary and conclusion................................................................................... Conflict of interest ........................................................................................ Acknowledgements ...................................................................................... References...............................................................................................

Introduction Obesity is defined as a syndrome characterized by an increase in body adipose tissue (AT) stores. Central obesity is characterized as excess AT above the waistline and includes extra-abdominal subcutaneous AT (SAT) and visceral AT (VAT) (Fig. 1), composed of mesenteric, omental, retroperitoneal AT [1], epicardial AT (EAT) [2], and pericardial adipose tissue (PAT) [3], a particular form of VAT deposited around the heart and the subepicardial coronary arteries. AT interspersed within and surrounding skeletal muscle and yet located beneath a surrounding layer of muscle fascia commonly refer to intermuscular AT (IMAT). It is believed that body AT distribution is influenced by gender [4—6], age [7—9] and ethnicity [7,10]. Generally, men tend to accumulate more body AT around their bellies (defined as android obesity) and most obese women follow gynoid obesity, in which AT is mostly distributed on the hips and buttocks [11]. Unfortunately, excessive body AT storage, particularly preferential AT deposition in the abdominal

Figure 1 Transverse cross-sectional computerized tomography at L4—5 vertebral level showing visceral adipose tissue area (VAT), abdominal subcutaneous adipose tissue area (SAT). The fascia (arrows) separating the superficial and deep SAT is easily visualized.

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area, is demonstrated to predispose the subject to type 2 diabetes mellitus (T2DM), hyperlipemia, and cardiovascular diseases (CVD) [12]. On concern of that, there are several different methods, including the easier ‘‘gold standards’’ methodunder water weighting [13], direct method of measurement [14], and more accurate quantitative computer tomography (QCT) and magnetic resonance imaging (MRI) [15,16], are used to measure total AT and its distribution. Due to the advantage of being precise and accurate, measuring bone mineral and adipose tissue distribution simultaneously, permitting regional analysis, being safe and practical, and involving only a negligible radiation dose [17—19], dual-energy X-ray absorptiometry (DXA) for measurement of body composition in clinical and research settings is becoming more widespreadly used. In recent years, many studies devote to discussing the relation of AT and its special distribution to T2DM. To our knowledge, there is only a few article studying about AT-mass content in type 1 DM (T1DM) [20,21], with lower body mass index (BMI, the ratio of weight in kg to the square of height in meters), waist circumference (WC), total AT, VAT and SAT, and more fat-free mass (including skeletal muscle, bone and water), and similar mid-thigh IMAT and ratio of VAT/total AT compared to T2DM [22]. This review will firstly focus on AT distribution in patients with T2DM followed by a summary of the studies assessing the increased risks among patients with T2DM, and then a review of various hypotheses for the pathophysiology of this association. Finally, general suggestions are offered regarding the care that T2DM patients should receive to protect their health. The literature discussing the link between T2DM and AT distribution is reviewed below.

Body adipose distribution and type 2 diabetes mellitus Recently, it is documented that AT distribution is significant differences between T2DM and similarly

e272 obese nondiabetic subjects after adjustment for age, sex, ethnicity, height and some other factors. These differences include the distribution of SAT, VAT, and IMAT.

SAT and type 2 diabetes mellitus Many recent studies found that femoral-gluteal adiposity (predominantly SAT) was reduced in T2DM, despite of similar or an overall greater fat mass [23—28]. However, Horejsi et al. [29] reported that SAT, especially in the upper trunk, was significantly increased (up to 50.7% at the neck) in male T2DM patients compared with their healthy controls, and about 84.1% individuals were correctly classified into healthy or T2DM by their SAT by stepwise discriminant analysis. Miyazaki et al. [30] found that the SAT, due entirely to superficial SAT measured at L4—5 was significantly greater in female than in male subjects with T2DM in despite of similar BMI and total AT mass. While, there was no difference in deep SAT at L4—5 or VAT area between females and males. In addition, Gallagher et al. [23] determined that upper leg SAT was significantly greater in women than in men (9.4 ± 0.2 kg vs. 8.0 ± 0.3 kg; P < 0.001). Variation of SAT content can be found among different ethnic patients with T2DM. For example, there is significantly greater upper leg SAT in African Americans than in whites (9.0 ± 0.3 kg vs. 8.4 ± 0.2 kg; P = 0.042) [23]. Moreover, African Americans with T2DM have more lower leg SAT than the control group (2.6 ± 0.1 kg vs. 2.5 ± 0.1 kg; P = 0.5), whereas whites in theT2DM group have significantly less lower leg SAT than the control group (2.3 ± 0.1 kg vs. 2.7 ± 0.1 kg; P = 0.008).

VAT and type 2 diabetes mellitus There is more VAT in the T2DM group than in the control group for both the African Americans and whites, and the difference between groups is larger for whites [23]. T2DM subjects have significantly higher total abdominal AT and VAT than nondiabetic subjects. However, there are no significant differences in SAT, abdominal AT ratio, VAT/SAT ratio, and VAT/total AT ratio between the two groups [31]. When segregated based on sex, female T2DM subjects have significantly higher VAT (132.7 ± 37.8 cm2 vs. 110.5 ± 45.4 cm2 , P = 0.015, measured using CT) and central abdominal AT (1.6 ± 0.3 kg vs. 1.3 ± 0.5 kg, P = 0.003, measured using DXA) than female nondiabetic subjects. Nevertheless, only the difference in VAT (149.9 ± 50.2 cm2 vs. 129.3 ± 39.0 cm2 , P = 0.049) reaches statistical significance between male T2DM

L.-J. Xie, M.-H. Cheng and nondiabetic subjects. When segregated based on age, T2DM subjects less than or equal to 44 years have significantly higher VAT compared with the control group (128.1 ± 33.8 cm2 vs. 98.4 ± 40.7 cm2 , P = 0.001). Although T2DM subjects over age 44 have higher VAT, the difference do not reach statistical significance. EAT volume and hepatic adiposity are also significantly higher in patients with T2DM than in nondiabetic subjects [24,32]. Om Kumar Shrestha et al. [33] reported that VAT, measured using CT, had significantly higher correctly classified percent values for predicting T2DM in both L2 —L3 and L4 —L5 measurement sites compared to SAT. For men, VAT ≥ 77.29 cm2 or VAT ≥ 51.52% of the total AT area at L2 —L3 or VAT ≥ 130.82 cm2 or VAT ≥ 45.54% of the total AT area at L4 —L5 had the highest correctly classified value for predicting T2DM. And for women, the cutoff points were respectively set at VAT ≥ 132.27 cm2 or VAT ≥ 45.7% of the total AT area at L2 —L3 or VAT ≥ 118.56 cm2 or VAT ≥ 32.24% of the total AT area at L4 —L5 .

IMAT and type 2 diabetes mellitus T2DM is associated with more IMAT compared with nondiabetic subjects [24]. Although with similar amounts of IMAT at low levels of adiposity, the rate of increase in IMAT is more rapid in the T2DM group than the control group [23]. Moreover, the former has more IMAT at high levels of adiposity. IMAT volumes are 2.2-fold higher in the subjects with T2DM than in the control subjects with similar amounts of leg muscle and total AT volumes [34]. In addition, men have more IMAT and the amount of IMAT increased more rapidly than women [23]. In conclusion, the reviewed literature suggests that AT distribution is significantly altered in T2DM, i.e., VAT and IMAT are greater, and SAT is lower in T2DM than in healthy control subjects; SAT in women with T2DM seems to be shifted up from the legs to the upper trunk, forming a more android body shape. Now, we will discuss the pathophysiology of AT redistribution in patients with T2DM below.

Pathophysiology of adipose tissue redistribution in type 2 diabetes mellitus Genetic factors Genetic factors form the background from which obesity develops [35]. One previous study [36],

Relationship between diabetes mellitus and adipose tissue including 141 subjects with normal glucose tolerance (NGT) and 276 with T2DM of Chinese Hans residents in Anhui province, showed that the genotypes of APM1 SNP276 were 0.489 GG, 0.418 GT and 0.092 TT and the major allele was G (frequency = 0.699) in subjects with NGT. Furthermore, the distributions of genotypes and alleles of SNP276 both displayed significant difference between NGT and T2DM groups. In T2DM group, the subjects with SNP276 GG or GT genotype had higher BMI, body AT content than those with TT genotype. Whereas, in NGT group, SNP276 non-TT carrier had increased BMI, body AT content when compared with TT genotype. Stephens et al. [37] found that the IL-6 -174 C allele was associated with higher BMI in T2DM subjects, but not amongst healthy subjects. Li et al. [38] found that rs11705701 in insulin-like growth factor-2 binding protein 2 (IGF2BP2) was associated with body AT and consequently affected insulin resistant (IR) which may contribute to T2DM risk. Ruchat et al. [39] reported that IGF2BP2 rs4402960, alone or in interaction with dietary fat intake, influenced abdominal total AT and VAT. In the Shanghai Diabetes Institute study [40], uncoupling protein 3 (UCP3) gene 55 C → T variant was associated with lipid metabolism, body AT and its distribution. However, the association was dependent on sex and disease status. The study by Myles et al. [41] revealed that the Gly482Ser variant in the PPARGC1A gene was associated with BMI in Tongans but not in Maori. 1-acylglycerol-3-phosphate-O-acyltransferase 2 (AGPAT2), one of congenital generalized lipodystrophy (CGL) loci, plays a critical role in the synthesis of glycerophospholipids and triglycerides required for lipid droplet formation [42—44]. Moreover, AGPAT2 mRNA has been shown to be highly expressed in the human omental AT. Thus, it may be one of the mechanism that patients with T2DM trend to be central adiposity. There are some other genes that possibly associated with body AT distribution of patients with T2DM such as berardinelli—seip congenital lipodystrophy 2 (BSCL2), caveolin 1 (CAV1), peroxisome proliferator-activated receptor-␥ (PPARG) and vAKT murine thymoma oncogene homolog 2 (AKT2) [45].

Sex steroids Sex steroids regulate body AT distribution, and, in turn, circulating levels of sex steroids are influenced by AT distribution [46]. Low levels of testosterone (T) and sex hormone binding globulin (SHBG) predict future abdominal adiposity and T2DM [47—51]. Young IR men

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produce less T when stimulated with human choriogonadotropin (hCG) compared with non-obese men [52]. However, the association between T and waist/hip ratio (WHR) is not significant after adjustment for age and BMI, which provides further support to the notion that androgens are not strong independent correlates of AT distribution in men [53]. Tchernof et al. [54] found that the associations among adrenal and gonadal steroids and the amount of VAT might due to the variance shared between AT distribution indices and total body fatness. Indeed, when men with low or high levels of VAT were matched for the level of total body fat, no differences in androgenic steroid and SHBG levels were noted. Their results suggested that body AT, rather than AT distribution, was a major correlate of C19 steroid precursors, T, and SHBG levels in men. In contrast to men, it is generally believed that abdominal obesity in women is associated with high plasma androgen levels [55—58].

Decreased physical activity and increased food supply Physical activity of patients suffering complications of T2DM such as foot ulcer, peripheral arterial disease, peripheral neuropathy or severe foot deformity or amputation t is insufficient. More recent findings suggested that AT deposits were possibly associated with decreased physical activity. Wang and co-workers [59] documented that the association between obesity risk and 5 single nucleotide polymorphisms was only observed in children who had moderate-to-low physical activity levels or engaged in sedentary behavior, regardless of which risk alleles they carried. Tuttle et al. [60] reported that average daily step count was negatively related to IMAT. Manini et al. [61] found that decreased physical activity increased IMAT in both thigh and calf by 14.5% and 20% (P ≤ 0.005), respectively. However, there was no significant change in SAT. It is believed that increased dietary fat intake is associated with obesity, IR and metabolic disease. Davis et al. [62] found that hepatic fat fraction (HFF) was influenced by a significant interaction between genotype and diet. However, HFF was positively related to carbohydrate (r = 0.31, P = 0.04) and total sugar (r = 0.34, P = 0.02) intakes but only in children carrying the GG genotype. In addition, there was no other diet × genotype interactions significantly for hepatic fat or for any of the other adiposity measures (i.e., total AT, VAT, or SAT).

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The risk of adipose tissue redistribution with type 2 diabetes mellitus The increase in BMI is associated with an increased risk of IR, heart disease, hypertension, liver steatosis, atherothrombotic and certain cancer. When AT is centrally located in either males or females, the risk for these diseases is also increased, and it may be a more important risk factor than total weight itself [35]. The reviewed studies reported a trend towards increased risks among patients with type 2 diabetes who had AT redistribution.

Adipose tissue redistribution and insulin resistance Excessive AT distributed in the abdominal region is associated closely with IR [63,64] and predisposes the subject to T2DM [12]. VAT is closely associated with IR (both peripheral and hepatic IR) in obese nondiabetic and T2DM subjects [30,65,66] and is more strongly linked to IR and T2DM than SAT [67]. However, it conflicts with other published date [68]. People with large accumulations of lower body SAT are less likely to suffer IR or DM [69]. Although SAT is greater in obesity, it does not be correlate with insulin sensitivity [70]. Deep SAT is associated with peripheral IR as well as hepatic IR only in male T2DM [30]. Similar to VAT, IMAT depots is known to exacerbate IR [23]. Kelley [71] suggested that the accretion of IMAT appeared to be strongly correlate with IR and might not be simply a passive process. Thaete and co-workers [70] found that although IMAT accounted for only approximately 3% of thigh AT, it was a strong correlate of insulin sensitivity.

Adipose tissue redistribution and cardiovascular disease When AT is centrally located in both genders [72], or BMI increases [73], the risk for CVD is increased, and the former may be a more important risk factor [35]. Kardassis et al. [74] found that left ventricular volume, stroke volume and cardiac output were primarily associated with lean body mass, whereas blood pressure, heart rate and variables reflecting cardiac dysfunction were more related to total body AT and VAT. Some articles [75—77] suggested that PAT had inflammatory properties and the quantity of PAT was related to the presence of atherosclerosis according influenced the atherosclerotic process in the artery wall ‘from outside to inside’. Liu et al. [78] found that mesenteric AT thickness was

L.-J. Xie, M.-H. Cheng significant association with carotid intima-media thickness, which lend further support to the linking role of portal AT in obesity-related atherosclerosis, however SAT was weakly related to atherosclerosis.

Adipose tissue redistribution and hypertension AT distribution has been shown to be a strong correlate of hypertension, independent of general obesity. Ding et al. [79] showed that VAT was strongly associated with hypertension (OR per 1 SD increase in the area of VAT: 1.28, P < 0.0001) after adjustment for age, sex, ethnicity, site, height, smoking status, pack-years of smoking, alcohol consumption status, amount of alcohol consumption, and physical activity. Moreover, the association was the strongest in individuals with the least amount of total body AT. Besides VAT, SAT and thigh IMAT were also associated with hypertension in African Americans. The J-HOP Study by Ishikawa et al. [80] documented that in men, an elevated VAT/SAT ratio [OR 1.44 per 1 SD (0.52), 95% CI 1.08—1.92] and alcohol drinking habit (OR 2.16, 95% CI 1.07—4.36) were significant predictors of difficult-to-treat hypertension (but not resistant hypertension), independently of the presence of MS or the insulin level. However, the Ohtori study by Koh et al. [81] suggested that VAT rather than abdominal SAT was associated with hypertension in Japanese men. Moreover, VAT remained significantly associated with hypertension even after adjustment for abdominal SAT, total SAT, total fat area, BMI. The Jackson heart study by Liu et al. [3] showed that PAT was associated with elevated levels of systolic blood pressure and hypertension. And all associations were diminished after further adjustment for VAT.

Adipose tissue redistribution and some other diseases AT distribution is more relevant than total fat mass when assessing the possibility of liver steatosis [82]. Roullier and co-workers [82] documented that VAT and proportion of VAT were correlated to liver AT content (r = 0.307 and r = 0.249, respectively). Bajaj et al. [83] determined that mortality was greater in high WC (>102 cm in men and >88 cm in women) group than the control group in both genders (P < 0.01). Albu et al. [84] suggested that both BMI and WC are associated with increased atherothrombotic risk in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI

Relationship between diabetes mellitus and adipose tissue 2D) patients. Nakamura et al. [85] determined that the incidence of type I endometrial cancer was closely correlated with an increase in obesity-related parameters such as weight, BMI, WC, SAT and TF. In particular, the SAT was most strongly correlated with obesity-related biological parameters of type I endometrial cancer. The association of PAT with coronary artery calcification (CAC) but not with abdominal aortic artery calcification (AAC) remains significant (OR 1.34 95% CI 1.10—1.64; P < 0.004) after adjustment for VAT [3]. IMAT is negatively related to muscle performance and overall physical function in people with T2DM [60].

Medical care Patients with T2DM have problem of AT redistribution, which can increase the risk of many diseases mentioned above. Therefore, it is essential to addressing the issues of obesity, obesity-related disease risk, and treatment options with patients. Regardless of the cause, treatment for obesity should be based on an evaluation of the individual’s risk from obesity as compared with the risk of the treatment under consideration [35]. Above all, Lifestyle modification that aims to reduce food intake and increase daily physical activity is likely to be the primary treatment. Reduction in body weight can decrease cardiometabolic risk factors and the development of related diseases, for example, a 5—10% reduction in body weight improves lipid profile, insulin sensitivity, and endothelial function, and reduces thrombosis and inflammatory markers [86]. Patients with sustained weight losses, compared with their obese counterparts remaining weight stable, display superior left ventricular systolic and diastolic functions [74]. After treated with 6 week carbohydrate-restricted diet (CRD), patients’ body weight (−13%), WC (−4.5%), body AT (−10.6%), and plasma triglycerides (TG) (−38.7%) significantly decreased [87]. The level of serum low density lipoprotein (LDL), cholesterol, blood pressure (BP), glucose, insulin, and inflammatory markers also significantly decreased. This suggests that a 6-week CRD can effectively be used as a first-line diet therapy to rapidly improve features of MS and CVD risk. Besides, modifying the type of dietary fat is beneficial as well [88,89]. Tapsell et al. [90] reported that all participants lost weight and body AT after 3 month low fat (30% energy) dietary, but the low fat-low calorie (LC) groups lost more weight (p = 0.026 for diet effect). All groups had reductions in VAT, and a tendency toward a diet effect

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for changes in SAT, with the LC groups showing a larger loss. People who regularly exercise have lower AT mass in comparison with nonexercising ones [91]. This confirms that physical activity is of protective influence for obese humans. Encouraging less sedentary behavior and higher levels of physical activity can alleviate the influence of risk alleles on genetic predisposition to childhood obesity, thereby should be serving as a promising prevention strategy [59]. A randomized trial by Goodpaster et al. [92] demonstrated that participants in the initialactivity group lost significantly more weight in the first 6 months compared with those in the delayedactivity group (10.9 kg [95% CI: 9.1—12.7] vs. 8.2 kg [95% CI: 6.4—9.9], P = 0.02 for group × time interaction). Yarasheski et al. [93] revealed that exercise training could augmented the beneficial effects of pioglitazone on peripheral insulin sensitivity. And greater improvements in peripheral insulin sensitivity were associated with reductions in total body and limb AT content rather than increases in limb AT or pioglitazone-induced increases in adiponectin concentration. The HELENA Study by Ruiz and co-workers [94] showed that adolescents participating in at least 18 min/day in vigorous physical activity or at least 55 min/day in moderate to vigorous physical activity (MVPA) were significantly discriminated between normal-weight and overweight [95] + obesity categories. Those in vigorous physical activity at least 9 min/day and in MVPA at least 49 min/day were discriminated between normal-fat and overfat/obese adolescents. The risk of having overweight and obesity (OR = 1.24, 95% CI = 1.01, 1.534) and overfat and obesity (OR = 1.79, 95% CI = 1.33, 2.42) increased when adolescents did not meet the current physical activity guidelines for youth of 60 min/day in MVPA, and ORs increased when adolescents did not meet the guidelines of at least 15 min/day in vigorous physical activity. Tuttle et al. [60] reported that greater average daily step count was associated with lower calf IMAT volume (r = −0.44, P < 0.05). Marcus et al. [96] suggested that resistance exercise could decrease IMAT in older individuals with a variety of comorbid conditions. In the study by Miyatake et al. [97,98], body composition (i.e. body weight, BMI, WC, WHR, body AT percentage, SAT and VAT area) significantly reduced during 1-year daily walking. However, there were no remarkable changes in lean body mass and VAT/SAT ratio. For individuals who do not respond to above mentioned interventions or for those who also have a weight-related illness, a weight loss medication may need to be added to their treatment plan. Phentermine, a sympathomimetic amine, is an

e276 appetite-suppressing compound that received FDA approval for the short-term treatment of obesity almost 5 decades ago and remains available today [99]. Additionally, a handful of medications (topiramate, zonisamide, buproprion, and metformin) approved for the treatment of other diseases have shown promise in aiding weight loss. However, they are not approved for the treatment of obesity [99,100]. In the study by Ahn et al. [101] found that the VAT/SAT ratio and VAT/thigh muscle ratio were significantly decreased and the insulin sensitivity index was significantly increased in the growth hormone-treated group compared to the control group (1.3 ± 1.4 vs. 1.9 ± 1.0%/min, P < 0.05). Dehydroepiandrosterone (DHEA) can limit omental fat production and modulate body composition [102].

Summary and conclusion AT distribution in humans is varies between different sex, race, and changes by age. Men are usually characterized by the android type of obesity, whereas women often display the gynoid type of obesity. Patients with T2DM are at great risk of AT redistribution characterized as higher total body AT and a more android AT distribution as compared with the healthy. Regional AT distribution in obese humans is an important determinant of disease risk. Obesity is probably the most powerful predictor of the development of T2DM. The major basis for this association of obesity with T2DM is the ability of obesity, especially a central pattern of AT distribution, to induce and promote IR which is a fundamental aspect of the etiology of T2DM and is also linked to a wide array of other pathophysiologic disorders including hypertension, hyperlipidemia, atherosclerosis, hepatic steatosis, and polycystic ovarian disease. It is important to adjust AT distribution of obese humans with T2DM. There are many approaches for reaching the target including lifestyle changing, exercise, and even medicinal treatment. However, lifestyle changing and exercise seem to be the best.

Conflict of interest We declare that we have no financial and personal relationships with other people or organizations that can inappropriately influence our work, there is no professional or other personal interest of any nature or kind in any product, service and/or company that could be construed as influencing the position presented in, or the review of, the manuscript entitled.

L.-J. Xie, M.-H. Cheng

Acknowledgements All authors wrote, read and approved the final manuscript. No acknowledgements for any other individual or organizations.

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