Dietary glycemic index and glycemic load in relation to HbA1c in Japanese obese adults: a cross-sectional analysis of the Saku Control Obesity Program

Transcription

1 Goto et l. Nutrition & Metolism 2012, 9:79 RESEARCH Open Access Dietry glycemic index nd glycemic lod in reltion to HA1c in Jpnese oese dults: cross-sectionl nlysis of the Sku Control Oesity Progrm Mki Goto 1,2,3, Akemi Morit 3,4, Atsushi Goto 1,2,3, Stoshi Sski 5, Nomi Ai 6, Tkuro Shimo 7, Ysuo Teruchi 2, Motohiko Miychi 3, Mitsuhiko Nod 1,8* nd Shw Wtne 3 for the SCOP Study Group Astrct Bckground: Dietry glycemic index or lod is thought to ply n importnt role in glucose metolism. However, few studies hve investigted the reltion etween glycemic index (GI) or lod (GL) nd glycemi in Asin popultions. In this cross-sectionl nlysis of rndomized controlled tril, the Sku Control Oesity Progrm, we exmined the reltion etween the seline GI or GL nd glycemi (HA1c nd fsting plsm glucose [FPG] levels), insulin resistnce (HOMA-IR), β-cell function (HOMA-β), nd other metolic risk fctors (lipid levels, distolic nd systolic lood pressure, nd diposity mesures). Methods: The prticipnts were 227 oese Jpnese women nd men. We used multiple liner regression models nd logistic regression models to djust for potentil confounding fctors such s ge, sex, viscerl ft re, totl energy intke, nd physicl ctivity levels. Results: After djustments for potentil confounding fctors, GI ws not ssocited with HA1c, ut GL ws positively ssocited with HA1c. For incresing qurtiles of GI, the djusted men HA1c were 6.3%, 6.7%, 6.4%, nd 6.4% (P for trend = 0.991). For incresing qurtiles of GL, the djusted men HA1c were 6.2%, 6.2%, 6.6%, nd 6.5% (P for trend = 0.044). In ddition, mong prticipnts with HA1c 7.0%, 20 out of 28 (71%) hd high GL ( medin); the djusted odds rtio for HA1c 7.0% mong prticipnts with higher GL ws 3.1 (95% confidence intervl [CI] = 1.2 to 8.1) compred to the prticipnts with lower GL (<medin). Further, mong 16 prticipnts with FPG 150 mg/dl, 13 prticipnts (81.3%) hd higher GL; the djusted odds rtio for FPG 150 mg/dl mong prticipnts with higher GL ws 8.5 (95% confidence intervl = 1.7 to 43.4) compred to those with lower GL. In contrst, GI nd GL were not ssocited with metolic risk fctors other thn glycemi. Conclusions: Our findings suggest tht prticipnts with poor glycemic control tend to hve higher GL in n oese Jpnese popultion. Keywords:, Glycemic lod, HA1c, Fsting plsm glucose, Metolic risk fctors, Oesity, Jpnese * Correspondence: mnod@hosp.ncgm.go.jp 1 Deprtment of Dietes Reserch, Dietes Reserch Center, Ntionl Center for Glol Helth nd Medicine, Tokyo, Jpn 8 Deprtment of Dietes nd Metolic Medicine, Center Hospitl, Ntionl Center for Glol Helth nd Medicine, Tokyo, Jpn Full list of uthor informtion is ville t the end of the rticle 2012 Goto et l.; licensee BioMed Centrl Ltd. This is n Open Access rticle distriuted under the terms of the Cretive Commons Attriution License ( which permits unrestricted use, distriution, nd reproduction in ny medium, provided the originl work is properly cited.

2 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 2 of 19 Bckground Theprevlenceofnormlglucosetolernceisincresing, nd is growing pulic helth concern [1]. Although uncertinty exists regrding the intke of crohydrtes nd glycemi, the utility of glycemic index (GI) nd glycemic lod (GL) hs een proposed. GI mesures the ility of crohydrte-contining food to rise the lood glucose level [2], nd GL is the product of GI nd the mount of crohydrte in the food [3]. Though lower GI or GL hs een hypothesized to decrese the risk of type 2 dietes, evidence regrding the role of GI nd GL in reltion to the risk of dietes remins inconclusive. Severl studies hve reported tht higher GI nd GL vlues were ssocited with n incresed risk of dietes [4-7], ut other studies hve not confirmed these results [8-10]. Furthermore, ecuse the min sources of GL differ cross ethnicities, the ssocitions etween GI, GL, nd dietes my differ in Asin popultions, in which rice is the mjor stple food [11]. The high intke of rice, hs een reportedly ssocited with n incresed risk of type 2 dietes mellitus in Asin popultion [5,12,13], nd lso, in study of Jpnese femle frmers, GI nd GL independently correlted with glucose, HA1c, ody mss index (BMI), nd fsting triglyceride (TG) [14]. Studies mong Jpnese Brzilins hve lso ssocited higher intkes of fruit, fruit juice, white red, nd rice with glucose intolernce [15,16]. However, comprehensive investigtions of the reltions of GI nd GL with metolic risk fctors in Asin re few, nd most of the preceding studies in Asin popultions hve een limited Tle 1 Bseline chrcteristics ccording to qurtiles of glycemic index nd glycemic lod Qurtile of glycemic index Q1 Q2 Q3 Q4 P Mle / Femle (n) 24 / / / / Age (y) 55.3 ± ± ± ± BMI (kg/m 2 ) 30.8 ± ± ± ± Wist circumference (cm) 103 ± ± ± ± Viscerl ft re (cm 2 ) 143 ± ± ± ± Sucutneous ft re (cm 2 ) 308 ± ± ± ± HA1c (%) 6.2 ± ± ± ± Fsting plsm glucose (mg/dl) 111 ± ± ± ± Insulin (μiu/ml) 10.9 ± ± ± ± HOMA-IR 3.0 ± ± ± ± HOMA-β 90.2 ± ± ± ± Dily nutritionl intke Energy (kcl/dy) 2309 ± ± ± ± ± 3 65 ± 1 68 ± 1 71 ± 2 < ± ± ± ± 16 <0.001 Qurtile of glycemic lod Q1 Q2 Q3 Q4 P Mle / Femle (n) 33 / / / / Age (y) 53.4 ± ± ± ± BMI (kg/m 2 ) 30.7 ± ± ± ± Wist circumference (cm) 103 ± ± ± ± Viscerl ft re (cm 2 ) 143 ± ± ± ± Sucutneous ft re (cm 2 ) 294 ± ± ± ± 96 >0.99 HA1c (%) 6.1 ± ± ± ± Fsting plsm glucose (mg/dl) 110 ± ± ± ± Insulin (μiu/ml) 11.2 ± ± ± ± HOMA-IR 3.1 ± ± ± ± HOMA-β 92.6 ± ± ± ± Dily nutritionl intke Energy (kcl/dy) 2542 ± ± ± ± ± 5 66 ± 4 67 ± 3 69 ± 3 < ± ± 3 86 ± ± 9 <0.001 Dt re (n) or mens ± SD. Differences in seline chrcteristics etween qurtiles were tested using nlysis of vrince (ANOVA) for ctegoricl vriles nd chi-squred tests for continuous vriles.

3 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 3 of 19 Tle 2 HA1c, fsting plsm glucose, HOMA-IR, nd HOMA-β ccording to dietry glycemic index nd energydjusted dietry glycemic lod 1 Dietry vriles Qurtile of glycemic index 2 n HA1c % P for trend* Fsting plsm glucose mg/dl P for trend* HOMA-IR P for trend* HOMA-β P for trend* Q1 [60] (5.7, 6.9) (101, 131) (1.7, 4.3) (37, 116) Q2 [65] (6.0, 7.3) 120 (105, 136) 3.7 (2.4, 5.0) 90 (49, 132) Q3 [68] (5.8, 7.0) 117 (102, 132) 3.1 (1.8, 4.4) 78 (38, 118) Q4 [71] (5.8, 6.9) 117 (103, 131) 2.6 (1.4, 3.8) 66 (28, 103) Qurtile of glycemic lod 2 Q1 [58] (5.5, 6.8) (101, 131) (1.3, 4.0) (24, 105) Q2 [75] (5.5, 6.8) 111 (97, 126) 2.4 (1.1, 3.7) 68 (28, 109) Q3 [86] (6.0, 7.2) 124 (110, 139) 3.1 (1.8, 4.5) 70 (30, 110) Q4 [100] (5.9, 7.1) 117 (103, 130) 3.0 (1.8, 4.2) 76 (38, 113) Arevitions: HOMA-IR, homeosttic model ssessment for insulin resistnce; HOMA-β, homeostsis model ssessment for β-cell function. 1 Adjusted men levels nd 95% CI in prentheses. Glycemic lod ws defined s n indictor of lood glucose induced y n individul s totl ville crohydrte. 2 Medin vlue for ech qurtile in rckets. *A multiple liner regression model ws used to djust for potentil confounding fctors including ge, sex, viscerl ft re, totl energy intke, nd physicl ctivity level. to women. For these resons, in the present study, we imed to investigte whether low dietry GI nd GL vlues re ssocited with reduced glucose mesures (HA1c nd FPG levels) nd other metolic risk fctors, including diposity mesures (BMI, wist circumference, viscerl ft re, nd sucutneous ft re), lipid levels (LDL, HDL, nd TG), nd lood pressures (systolic lood pressure [SBP] nd distolic lood pressure [DBP]), in Jpnese popultion. Methods Study popultion This study is cross-sectionl nlysis of rndomized controlled tril, the Sku Control Oesity Progrm (SCOP), exmining the effect of ehviorl tretment nd exercise t the Sku Centrl Hospitl Humn Dock Center. The detils nd design of the study hve een previously descried elsewhere [17-19]. Briefly, the progrm consisted of rndomized intervention tril using cognitive-ehviorl tretment t the Sku Helth Dock Center. Among 976 memers who visited helth checkups, memers with BMI in the upper five percentile nd without history of type 1 dietes, stroke, crdiovsculr disese, dvnced cncer, or significnt renl or heptic dysfunction were invited. In totl, 237 women nd men prticipted. We used the seline dt for the nlysis. Of the 237 people prticipted in the study, 10 prticipnts did not complete the study, nd 227 prticipnts were included in the nlysis. For the multiple liner regression nlysis, we further excluded one prticipnt with missing dt. Also, for the nlysis of the FPG nd lipid levels, we excluded 3 prticipnts who did not provide fsting lood smples. The reserch pln ws reviewed nd pproved y the Ethicl Committee of the Ntionl Institute of Helth nd Nutrition nd Sku Centrl Hospitl. Prticipnts received precise explntion of the study nd provided their written informed consent. Anthropometric mesurements The height (cm) nd weight (kg) of the sujects were mesured with n utomtic scle (Tnit, BF-220, Tokyo, Jpn), in light clothing. The BMI ws clculted s the weight (kg) divided y the squred height (m 2 ). Wist circumference ws mesured twice t the umilicus level while the suject ws in stnding position using fier glss mesuring tpe; the verge mesurement ws used for the nlysis. Blood pressure ws mesured while the suject ws in sitting position using vlidted utomted lood pressure monitor (HEM-907; Omron, Kyoto, Jpn) [20]. Viscerl ft nd sucutneous ft res were ssessed using computed tomogrphy scn t the level of the umilicus in supine position (Ft scn; N2 system Corp., Jpn). The coefficients of vrition (CV) etween two oservers for the viscerl ft re nd sucutneous ft re mesurements were reported to rnge from 0.6% to 14.2% nd from 0.1% to 7.3%, respectively [21,22]. The physicl ctivity levels were otined y sking the prticipnts out their verge physicl ctivity levels for the pst month. The physicl ctivity levels were divided into four levels: light ctivity (sedentry lor most of the dy, including 1 hour wlking, or stnding for pproximtely 3 hours), light to moderte ctivity (etween sedentry nd mnul lor, including wlking for out 2 hours or stnding for 6 to 7 hours), moderte ctivity (mnul lor for pproximtely 1 hour, including wlking or stnding

4 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 4 of 19 HA1c (%) r = 0.03 P = 0.65 HA1c (%) r = 0.15 P = 0.03 c HA1c (%) r = 0.16 P = Figure 1 (See legend on next pge.) Crohydrte (g/1000 kcl)

5 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 5 of 19 (See figure on previous pge.) Figure 1 Sctter plots with regression lines of glycemic index, glycemic lod, nd crohydrte intke ginst HA1c. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 1), glycemic lod (/1000 kcl) (Figure 1), nd crohydrte intke (g/1000 kcl) (Figure 1c). Y-xis: HA1c. for pproximtely 9 hours, with hrd ctivity for 1 hour), nd vigorous ctivity (mnul lor, wlking or stnding for pproximtely 9 hours, with hrd ctivity for more thn 2 hours). Lortory procedures Following n overnight fst, lood smples were collected t the time of ech helth checkup t the Sku Helth Dock Center. Blood smples were collected in Fsting plsm glucose (mg/dl) r = 0.01 P = 0.88 Fsting plsm glucose (mg/dl) r = 0.09 P = 0.17 Figure 2 Sctter plots with regression lines of glycemic index nd glycemic lod ginst fsting plsm glucose. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 2) nd glycemic lod (/1000 kcl) (Figure 2). Y-xis: Fting plsm glucose.

6 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 6 of 19 Tle 3 Lipids nd lood pressure ccording to dietry glycemic index nd energy-djusted dietry glycemic lod 1 Dietry vriles n LDL mg/dl Qurtile of glycemic index 2 P for trend* HDL mg/dl P for trend* TG mg/dl P for trend* SBP mmhg P for trend* DBP mmhg Q1 [60] (97, 134) (39, 52) (98, 214) (115, 136) (70, 85) Q2 [65] (89, 128) 44 (38, 51) 150 (90, 211) 129 (118, 140) 79 (71, 87) Q3 [68] (89, 126) 48 (42, 54) 158 (99, 217) 128 (117, 138) 81 (73, 88) Q4 [71] (95, 130) 47 (42, 53) 154 (100, 209) 124 (113, 134) 75 (68, 83) Qurtile of glycemic lod 2 Q1 [58] (92, 130) (40, 53) (120, 238) (116, 138) (70, 86) Q2 [75] (86, 124) 48 (42, 54) 148 (90, 206) 125 (114, 136) 78 (71, 86) Q3 [86] (90, 127) 46 (39, 52) 155 (96, 214) 120 (109, 130) 75 (67, 83) Q4 [100] (98, 133) 47 (41, 53) 151 (96, 205) 126 (116, 136) 78 (70, 85) 1 Adjusted men levels nd 95% CI in prentheses. Glycemic lod ws defined s n indictor of lood glucose induced y n individul s totl ville crohydrte. 2 Medin vlue for ech qurtile in rckets. *A multiple liner regression model ws used to djust for potentil confounding fctors including ge, sex, viscerl ft re, totl energy intke, nd physicl ctivity level. P for trend* tues contining EDTA nd heprin for the mesurement of the fsting plsm glucose, insulin, nd HA1c levels, nd serum gel seprtor tues were used for the mesurement of the totl cholesterol, HDL cholesterol, nd TG levels. Routine lortory lood nlyses were performed t the Sku Centrl Hospitl. HA1c levels were mesured using high-performnce liquid chromtogrphy method (TOSOH HLC-723 G8; Tosoh Corportion, Tokyo, Jpn), with intr- nd inter-ssy coefficients of vrition (CVs) of 0.5%-1.4% nd 0.6%- 1.3%, respectively. The plsm glucose levels were nlyzed using n enzymtic method (ECO glucose uffer; A&T Corportion, Kngw, Jpn), with intr- nd inter-ssy CVs of 0.3%-0.5% nd 0.6%-0.8%, respectively. The plsm insulin levels were nlyzed using n electrochemiluminescence immunossy (Modulr E170; Roche Dignostics, Mnnheim, Germny), with intrnd inter-ssy CVs of 0.5%-2.0% nd 3.2%-3.6%, respectively. The serum totl cholesterol, HDL cholesterol, nd TG concentrtions were determined using enzymtic methods (serum totl cholesterol: Detminr L TC II, Kyow Medex, Tokyo, Jpn; HDL cholesterol: Cholestest N HDL,Sekisui Medicl Co. Ltd., Tokyo, Jpn; nd TG concentrtions: Mizuho TG-FR Type II, Mizuho Medi, Sg, Jpn) nd n utonlyzer BM-2250 (Nihon Denshi, Tokyo, Jpn), with intr- nd inter-ssy CVs of 1.7% nd 2.3%, respectively. The vlue for HA1c (%) ws estimted s n NGSP equivlent vlue (%) clculted y the formul HA1c (%) = HA1c (JDS) (%) + 0.4%, considering the reltionl expression of HA1c (JDS) (%) mesured y the previous Jpnese stndrd sustnce nd mesurement methods Tle 4 BMI, wist, nd ft re ccording to dietry glycemic index nd energy-djusted dietry glycemic lod 1 Dietry vriles n BMI kg/m 2 P for trend* Wist circumference cm P for trend* Viscerl ft P for trend* Sucutneous re cm 2 ft re cm 2 Qurtile of glycemic index 2 Q1 [60] (28.3, 31.7) (97, 106) (149, 203) (168, 270) Q2 [65] (27.9, 31.4) 100 (95, 105) 174 (146, 202) 195 (143, 248) Q3 [68] (28.0, 31.4) 101 (96, 105) 172 (145, 200) 220 (169, 272) Q4 [71] (27.8, 31.1) 99 (95, 104) 177 (151, 202) 191 (143, 239) Qurtile of glycemic lod 2 Q1 [58] (28.0, 31.5) (96, 105) (145, 200) (161, 266) Q2 [75] (27.4, 30.8) 99 (94, 103) 169 (142, 197) 197 (145, 248) Q3 [86] (27.7, 31.2) 99 (95, 104) 176 (149, 203) 204 (152, 256) Q4 [100] (28.2, 31.4) 100 (96, 105) 179 (153, 204) 203 (155, 251) 1 Adjusted men levels nd 95% CI in prentheses. Glycemic lod ws defined s n indictor of lood glucose induced y n individul s totl ville crohydrte. 2 Medin vlue for ech qurtile in rckets. *A multiple liner regression model ws used to djust for potentil confounding fctors including ge, sex, totl energy intke, nd physicl ctivity level. P for trend*

7 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 7 of 19 HOMA-IR r = 0.02 P = 0.74 HOMA-IR r = 0.03 P = 0.61 Figure 3 Sctter plots with regression lines of glycemic index nd glycemic lod ginst HOMA-IR. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 3) nd glycemic lod (/1000 kcl) (Figure 3). Y-xis: HOMA-IR. nd HA1c (NGSP) [23]. The homeostsis model ssessment for insulin resistnce (HOMA-IR) nd homeostsis model ssessment for β cell function (HOMA-β) were clculted s follows: HOMA-IR = fsting insulin (μiu/ml) fsting glucose (mmol/ml) / 22.5, nd HOMA-β =20 fsting insulin (μiu/ml) / [fsting glucose (mmol/ml) 3.5] [24,25]. Assessment of dietry intke Dietry hits were ssessed using previously vlidted, self-dministered diet history questionnire (DHQ). The methods used to clculte dietry intke nd the vlidity of the DHQ hve een pulished elsewhere [26-29]. In rief, the DHQ consists of 16-pge questionnire for ssessing dietry hits during the previous month. The Person correltion coefficient etween the DHQ nd 3- dy dietry records ws 0.48 for energy, 0.55 for ft, nd 0.48 for crohydrtes mong 48 norml-weight women [27]. The DHQ ws completed t the seline, checked y dietitins, nd missing or illogicl nswers were otined or corrected y interview. To clculte the GI, we estimted the GI ccording to strtegy used in previous study with Jpnese prticipnts [14]. Briefly, to determine the GI vlue of ech food for use in the clcultions, ech food item included in the DHQ ws directly mtched to foods in the interntionl tle of GI

8 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 8 of 19 HOMA-B r = 0.02 P = 0.73 HOMA-B r = 0.02 P = 0.73 Figure 4 Sctter plots with regression lines of glycemic index nd glycemic lod ginst HOMA-β. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 4) nd glycemic lod (/1000 kcl) (Figure 4). Y-xis: HOMA-β. or in severl pulictions on the GI of Jpnese foods [3,30,31]. The dietry GI ws clculted y multiplying the contriution of ech individul food to the dily ville crohydrte intke using the food s GI vlue nd then summing the products. The GI vlues sed on 50 grms of ville crohydrtes in common Jpnese foods nd everges, with glucose used s the reference (GI for glucose = 100), were s follows: GI of white rice = 77, white rice with rley = 67, white rice with germ = 66, rown rice = 55, so nd udon (Jpnese noodles) = 47, instnt noodles = 47, spghetti = 46, white red = 74, ornges = 39, nns = 51, pples = 37, nd soft drinks = 61. Dietry GL ws clculted y multiplying the dietry GI y the totl mount of dily ville crohydrte intke (divided y 100). For these clcultions, strtegy used in previous studies ws used nd the Person correltions etween DHQ nd dietry records for dietry GI nd GL were 0.72 nd 0.66 mong women nd 0.65 nd 0.71 mong men, respectively [32]. Dt nlysis The chrcteristics of the study popultion re presented s the men or medin for continuous vriles nd s percentge for ctegoricl vriles. We used crude vlues for dietry GI nd energy-djusted vlues for dietry GL (/1000 kcl) ecuse, y definition, dietry GI is

9 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 9 of 19 LDL (mg/dl) r = 0.09 P = 0.18 LDL (mg/dl) r = 0.07 P = 0.32 Figure 5 Sctter plots with regression lines of glycemic index nd glycemic lod ginst LDL. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 5) nd glycemic lod (/1000 kcl) (Figure 5). Y-xis: LDL. mesure of crohydrte qulity, not quntity, wheres dietry GL is mesure of the comintion of crohydrte qulity nd quntity [14]. The LDL levels were clculted using the Friedewld eqution: LDL = totl cholesterol - (HDL + [TG/5]). Differences in the seline chrcteristics mong the qurtiles were tested using n nlysis of vrince (ANOVA) for continuous vriles nd chi-squred tests for ctegoricl vriles. We treted ech mjor dietry vrile s either continuous or ctegoricl (qurtiles) vriles. To investigte the ssocitions of GI nd GL with metolic risk fctors, we used multiple liner regression model to djust for potentil confounding fctors including ge, sex, viscerl ft re, totl energy intke, nd physicl ctivity levels. We used viscerl ft re s mrker of diposity ecuse prior dt suggested tht viscerl ft plys n importnt role in the pthogenesis of metolic disese [33]. Using the BMI or wist circumference insted of the viscerl ft re did not result in mteril differences in the results. We clculted the djusted-men HA1c nd FPG; LDL, HDL, nd TG concentrtions; SBP nd DBP; nd BMI, wist circumference, viscerl ft re, nd sucutneous ft re ccording to the qurtiles of GI nd GL. Tests for trends were conducted y ssigning the medin vlue to ech qurtile nd modeling this vlue s continuous vrile.

10 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 10 of 19 HDL (mg/dl) r = 0.01 P = 0.89 HDL (mg/dl) r = 0.01 P = 0.87 Figure 6 Sctter plots with regression lines of glycemic index nd glycemic lod ginst HDL. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 6) nd glycemic lod (/1000 kcl) (Figure 6). Y-xis: HDL. We lso exmined whether the ssocitions of GI or GL with HA1c nd FPG were modified y sex. The P- vlues for the interction were clculted y further including the product terms in the regression models using t-tests. GL, ut not GI, ws positively ssocited with HA1c in the present study, suggesting tht the quntity of crohydrte my lso e ssocited with HA1c. Thus, to further exmine the ssocitions of crohydrte intke s well s GI nd GL with metolic risk fctors, we generted sctter plots nd regression lines nd computed Person correltion coefficients for ll outcome vriles. In ddition, ecuse there ws suggestive ssocition etween GL nd poor glycemic control (HA1c 7.0% or FPG 150 mg/dl), we conducted logistic regression nlysis to estimte odds rtios nd 95% confidence intervls [CIs] for poor glycemic control with djustment for potentil confounding fctors including ge, sex, viscerl ft re, totl energy intke, nd physicl ctivity levels. Two-sided P vlues <0.05 were considered to e sttisticlly significnt. Anlyses were crried out using Stt softwre (version 11; Stt Corp, College Sttion, TX). Results In totl of 227 prticipnts, the prticipnts rnged in ge from 40 to 64 yers, with men ge of 54 yers.

11 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 11 of 19 TG (mg/dl) r = 0.04 P = 0.51 TG (mg/dl) r = 0.08 P = 0.22 Figure 7 Sctter plots with regression lines of glycemic index nd glycemic lod ginst TG. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 7) nd glycemic lod (/1000 kcl) (Figure 7). Y-xis: TG. Mle prticipnts tended to hve higher GI. Their reported men totl energy intke per dy ws ± kcl. The verge dietry GI ws 66 ± 5, nd the verge dietry GL ws 79 ± 17 (/1000 kcl). The men BMI ws 30.6 ± 3.1 kg/m 2, HA1c ws 6.3 ± 1.1%, nd FPG ws 112 ± 26 mg/dl (6.2 ± 1.4 mmol/l). The seline chrcteristics of 227 prticipnts in this study ccording to the qurtiles of GI nd GL re shown in Tle 1. Prticipnts with high GI tended to hve higher GL. Also, prticipnts with high GL tended to hve higher GI nd higher HA1c. Tle 2 shows ssocitions of GI nd GL with FPG, HA1c, HOMA-IR, nd HOMA-β. GL, ut not GI, ws positively ssocited with HA1c (Tle 2 nd Figure 1). For incresing qurtiles of GI, the corresponding djusted men HA1c levels were 6.3%, 6.7%, 6.4%, nd 6.4% (P for trend = 0.991). The sctter plot of GL (/1000 kcl) ginst HA1c indicted positive liner reltion etween GL nd HA1c (r = 0.15, P = 0.026) (Figure 1). Among prticipnts with HA1c 7.0%, 20 out of 28 (71%) hd high GL ( medin) nd the djusted odds rtio for HA1c 7.0% mong prticipnts with higher GL ws 3.1 (95% confidence intervl [CI] = 1.2 to 8.1) compred to the prticipnts with lower GL (<medin). In ddition, multiple liner regression nlysis suggested positive ssocition etween GL nd

12 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 12 of 19 SBP (mmhg) r = 0.08 P = 0.26 SBP (mmhg) r = 0.02 P = 0.73 Figure 8 Sctter plots with regression lines of glycemic index nd glycemic lod ginst SBP. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 8) nd glycemic lod (/1000 kcl) (Figure 8). Y-xis: SBP. HA1c. For incresing qurtiles of GL, the corresponding djusted men HA1c were 6.2%, 6.2%, 6.6%, nd 6.5% (P for trend = 0.044) (Tle 2). Also, the ssocitions of GI or GL with HA1c nd FPG were not modified y sex (P for interction >0.10). We further exmined the ssocition of crohydrte intke with HA1c. The sctter plots of crohydrte intke (g/ 1000 kcl) ginst HA1c indicted positive liner reltion etween crohydrte intke nd HA1c (r = 0.16, P = 0.014) (Figure 1c). After djustments for potentil confounders, crohydrte intke ws lso positively ssocited with HA1c. For incresing qurtiles of crohydrte intke, the corresponding djusted men HA1c levels were 6.1%, 6.3%, 6.3%, nd 6.6% (P for trend = 0.026) (dt not shown). Although GL ws not linerly relted to FPG, individuls with high FPG ( 150 mg/dl) tended to hve high GL (Figure 2). Among 16 prticipnts with FPG 150 mg/dl, 13 prticipnts (81.3%) hd higher GL (Figure 2) nd the djusted odds rtio for FPG 150 mg/dl mong prticipnts with higher GL vlues ws 8.5 (95% confidence intervl = 1.7 to 43.4) compred to the lower GL group.

13 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 13 of 19 DBP (mmhg) r = 0.07 P = 0.31 DBP (mmhg) r = 0.04 P = 0.60 Figure 9 Sctter plots with regression lines of glycemic index nd glycemic lod ginst DBP. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 9) nd glycemic lod (/1000 kcl) (Figure 9). Y-xis: DBP. After djustments for potentil confounding fctors, the dietry GI or GL ws not ssocited with FPG, HOMA-IR, or HOMA-β (Tle 2). Also, fter djustments for potentil confounding fctors, the GI or GL ws not ssocited with the lipid levels (LDL, HDL, or TG), SBP, or DBP (Tle 3). In the nlysis of the diposity mesures (BMI, wist, viscerl ft re, or sucutneous ft re), GI or GL ws not ssocited with the diposity mesures fter djustments for potentil confounding fctors (Tle 4). The sctter plots of GI nd GL (/1000 kcl) ginst HOMA-IR, HOMA-β, lipid levels (LDL, HDL, or TG), SBP, or DBP did not indicte ny pprent ssocitions etween these mesures (Figures 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13). Discussion In this study of 227 oese Jpnese prticipnts, prticipnts with poor glycemic control tended to hve higher GL, wheres GI ws not ssocited with glycemi. No ssocition etween GI or GL nd the BMI, wist circumference, viscerl ft re, sucutneous ft re, LDL, HDL, TG, SBP, or DBP ws oserved. In preceding studies, n incresed dietes risk ws reportedly ssocited with GI nd GL [6,7,34,35], while other studies reported no ssocition [8-10]. Blood glucose levels re effectively controlled, unless there is dysregultion of glucose metolism [36], condition oserved in individuls with dietes, predietes, or

14 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 14 of 19 BMI (kg/m2) r = 0.02 P = 0.72 BMI (kg/m2) r = 0.02 P = 0.80 Figure 10 Sctter plots with regression lines of glycemic index nd glycemic lod ginst BMI. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 10) nd glycemic lod (/1000 kcl) (Figure 10). Y-xis: BMI. metolic syndrome. Therefore, the findings in preceding studies my e inconclusive in prt ecuse in some studies, there might hve een few prticipnts with norml glucose metolism t seline or during followup periods. In our study, GL showed positive reltion with HA1c. In fct, mong 28 prticipnts with HA1c 7.0%, 20 prticipnts (71%) hd higher GL. Nonetheless, longer durtion of oservtion is necessry to confirm the findings. Also, in multiple liner regression nlysis, we oserved no ssocition etween GI or GL nd FPG. Indices reflecting oth fsting nd postprndil hyperglycemi such s HA1c my hve shown stronger ssocition for GL, ecuse GL my ply mjor roles in postprndil hyperglycemi. Also, the within-suject vriility of HA1c is smller thn FPG, nd this my ccount for the stronger ssocition of GL with HA1c thn FPG [37]. Thus, we possily lcked sttisticl power to detect liner ssocition etween GL nd FPG. Indeed, when we dichotomized FPG nd GL, individuls with high FPG ( 150 mg/dl) tended to hve high GL; mong 16 prticipnts with FPG 150 mg/dl, 13 prticipnts (81.3%) hd high GL ( medin). These findings suggest tht high GL is ssocited with poor glycemic control. GI hs een reported to e positively ssocited with insulin resistnce nd metolic syndrome [38], nd in one study, it ws shown tht lthough high GI

15 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 15 of 19 Wist circumference (cm) r = 0.05 P = 0.44 Wist circumference (cm) r = 0.05 P = 0.42 Figure 11 Sctter plots with regression lines of glycemic index nd glycemic lod ginst wist circumference. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 11) nd glycemic lod (/1000 kcl) (Figure 11). Y-xis: Wist circumference. predicted the risk of type 2 dietes mong nondominlly oese individuls, no ssocition ws oserved in dominlly oese individuls [9]. Since the prticipnts of our study were oese, with men viscerl ft re of cm 2, this my hve msked the reltionship etween GI nd HA1c or FPG levels in our study. Also, the dietry GI hs een reported not to reflect the totl crohydrte intke, nd my provide miniml insight into the overll insulin demnd induced y the totl crohydrte intke [7,35]. Also, studies reported tht high dietry GL ws ssocited with other helth outcomes, such s dyslipidemi nd coronry hert disese [39]. In preceding study, GI nd GL were reported to e positively relted to the risk of metolic syndrome mong women with BMI 25 kg/ m 2 [40]. GI nd GL hve lso een reported to e inversely relted to the HDL level nd positively relted to the TG level [39]. However, in our study, no ssocitions etween GI or GL nd such metolic risk fctors were oserved. In the current study, GL ws positively relted with HA1c, while there ws no ssocition etween GI nd HA1c, suggesting tht the mount of the crohydrte intke my lso e ssocited with HA1c. Thus, we lso investigted the reltion etween crohydrte intke nd HA1c. There ws significnt reltion

16 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 16 of 19 Viscerl ft re (cm2) r = 0.08 P = 0.22 Viscerl ft re (cm2) r = 0.01 P = 0.87 Figure 12 Sctter plots with regression lines of glycemic index nd glycemic lod ginst viscerl ft re. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 12) nd glycemic lod (/1000 kcl) (Figure 12). Y-xis: Viscerl ft re. etween crohydrte intke nd HA1c (r = 0.16), nd the correltion ws similr to the reltion etween GL nd HA1c (r = 0.15). This might suggest tht the ssocition of GL with HA1c might hve een minly driven y crohydrte content. Of note, it hs een reported tht crohydrte restriction improves glycemic control [41,42], suggesting the role of crohydrte content in glycemic control. However, GL hs een found to e more powerful predictor of postprndil glycemi nd insulinemi thn ws the ville crohydrte content [43]. In ddition, severl prospective cohort studies hve ssocited GL, ut not crohydrte, with risks of coronry hert disese nd type 2 dietes [35,39]. Tken together, the superiority of crohydrte mount or GL in glycemic control still remins n open reserch question. Some limittions of the present study need to e ddressed. First, the DHQ ws not specificlly designed to mesure GI nd GL, nd the dietry records of oese people hve een reported to e inccurte [44]. More specificlly, oese people tend to underreport their cloric intke [45]. Thus, the dietry GI nd GL estimted using the DHQ might hve een more inccurte thn tht estimted y helthy individuls with norml BMI. However, the is introduced y underreporting nd the mesurement error tends to e

17 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 17 of 19 Sucutneous ft re (cm2) r = 0.10 P = 0.13 Sucutneous ft re (cm2) r = 0.03 P = 0.62 Figure 13 Sctter plots with regression lines of glycemic index nd glycemic lod ginst sucutneous ft re. Person correltion coefficients (r) nd corresponding P-vlues re shown. X-xis: glycemic index (Figure 13) nd glycemic lod (/1000 kcl) (Figure 13). Y-xis: Sucutneous ft re. non-differentil with respect to the outcomes, which tends to ttenute the ssocition. Moreover, ecuse totl energy djustments hve een reported to potentilly reduce the is cused y underreporting [46-48], we hve djusted for the totl energy intke in ll the models. Also, vlidtion study showed good greement etween the DHQ nd the dietry records for GI nd GL [32]. Second, the prticipnts in this study were oese dults who were recruited from memers who visited helth checkups. Thus, selection is nd generlizility my e prolem. Third, dietry intkes were mesured only once, nd thus my not hve reflected the long-term intke. Fourth, s is lwys the cse in oservtionl studies, there my e residul confounding y unknown or unmesured confounding fctors. However, our multiple sensitivity nlyses controlling for covrites including viscerl ft re, sucutneous ft re, BMI, nd wist circumference showed positive ssocition etween the GL nd HA1c. Finlly, it should e mentioned tht, using cross-sectionl nlysis, we re unle to estlish temporl reltionship in the ssocition etween GI or GL nd metolic risk fctors nd given the multiple testing nd the limited power of the study, the ssocition etween GL nd HA1c needs to e interpreted cutiously.

18 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 18 of 19 Conclusions Although our results do not nswer questions concerning the differentil roles of GL nd totl crohydrte intkes in the glucose metolism, our findings suggest tht prticipnts with poor glycemic control tend to hve higher GL in n oese Jpnese popultion. Competing interests The uthors declre tht they hve no competing interests. Authors contriutions MG reserched the dt, contriuted to the discussion, nd wrote the mnuscript. AM nd AG reserched the dt, contriuted to the discussion, nd reviewed / edited the mnuscript. TS nd YT contriuted to the discussion. NA, MM, SS, MN, nd SW contriuted to the discussion, nd reviewed / edited the mnuscript. All uthors red nd pproved the finl mnuscript. Acknowledgements This study ws supported y The SKYLARK Food Science Institute grnt. We would like to cknowledge ll SCOP memers for their prticiption in this reserch. We thnk Ritsuko Ymmoto-Hond, Hiroshi Kjio, nd the reviewers for helpful comments. We thnk Msnou Iked nd Tomoko Ysud for their ssistnce. Author detils 1 Deprtment of Dietes Reserch, Dietes Reserch Center, Ntionl Center for Glol Helth nd Medicine, Tokyo, Jpn. 2 Deprtment of Endocrinology nd Metolism, Yokohm City University Grdute School of Medicine, Yokohm, Jpn. 3 Ntionl Institute of Helth nd Nutrition, Tokyo, Jpn. 4 Deprtment of Nutrition, College of Nutrition, Koshien University, Hyogo, Jpn. 5 Deprtment of Socil nd Preventive Epidemiology, School of Pulic Helth, University of Tokyo, Tokyo, Jpn. 6 Deprtment of Nutrition nd Life Science, Kngw Institute of Technology, Kngw, Jpn. 7 Deprtment of Clinicl Reserch nd Informtics, Ntionl Center for Glol Helth nd Medicine, Tokyo, Jpn. 8 Deprtment of Dietes nd Metolic Medicine, Center Hospitl, Ntionl Center for Glol Helth nd Medicine, Tokyo, Jpn. Received: 26 April 2012 Accepted: 4 Septemer 2012 Pulished: 10 Septemer 2012 References 1. Wild S, Roglic G, Green A, Sicree R, King H: Glol prevlence of dietes: estimtes for the yer 2000 nd projections for Dietes Cre 2004, 27: Jenkins DJ, Wolever TM, Tylor RH, Brker H, Fielden H, Bldwin JM, Bowling AC, Newmn HC, Jenkins AL, Goff DV: of foods: physiologicl sis for crohydrte exchnge. Am J Clin Nutr 1981, 34: Foster-Powell K, Holt SH, Brnd-Miller JC: Interntionl tle of glycemic index nd glycemic lod vlues: Am J Clin Nutr 2002, 76: Skuri M, Nkmur K, Miur K, Tkmur T, Yoshit K, Morikw Y, Ishizki M, Kido T, Nruse Y, Suwzono Y, et l: Dietry glycemic index nd risk of type 2 dietes mellitus in middle-ged Jpnese men. Metolism 2012, 61: Villegs R, Liu S, Go YT, Yng G, Li H, Zheng W, Shu XO: Prospective study of dietry crohydrtes, glycemic index, glycemic lod, nd incidence of type 2 dietes mellitus in middle-ged Chinese women. Arch Intern Med 2007, 167: Schulze MB, Liu S, Rimm EB, Mnson JE, Willett WC, Hu FB:, glycemic lod, nd dietry fier intke nd incidence of type 2 dietes in younger nd middle-ged women. Am J Clin Nutr 2004, 80: Slmeron J, Ascherio A, Rimm EB, Colditz GA, Spiegelmn D, Jenkins DJ, Stmpfer MJ, Wing AL, Willett WC: Dietry fier, glycemic lod, nd risk of NIDDM in men. Dietes Cre 1997, 20: Mosdol A, Witte DR, Frost G, Mrmot MG, Brunner EJ: Dietry glycemic index nd glycemic lod re ssocited with high-density-lipoprotein cholesterol t seline ut not with incresed risk of dietes in the Whitehll II study. Am J Clin Nutr 2007, 86: Schulz M, Liese AD, Fng F, Gillird TS, Krter AJ: Is the ssocition etween dietry glycemic index nd type 2 dietes modified y wist circumference? Dietes Cre 2006, 29: Meyer KA, Kushi LH, Jcos DR Jr, Slvin J, Sellers TA, Folsom AR: Crohydrtes, dietry fier, nd incident type 2 dietes in older women. Am J Clin Nutr 2000, 71: Woo J, Ho SC, Shm A, Se MM, Lm KS, Lm TH, Jnus ED: Diet nd glucose tolernce in Chinese popultion. Eur J Clin Nutr 2003, 57: Hu EA, Pn A, Mlik V, Sun Q: White rice consumption nd risk of type 2 dietes: met-nlysis nd systemtic review. BMJ 2012, 344:e Nnri A, Mizoue T, Nod M, Tkhshi Y, Kto M, Inoue M, Tsugne S: Rice intke nd type 2 dietes in Jpnese men nd women: the Jpn Pulic Helth Center-sed Prospective Study. Am J Clin Nutr 2010, 92: Murkmi K, Sski S, Tkhshi Y, Okuo H, Hosoi Y, Horiguchi H, Ogum E, Kym F: Dietry glycemic index nd lod in reltion to metolic risk fctors in Jpnese femle frmers with trditionl dietry hits. Am J Clin Nutr 2006, 83: Srtorelli DS, Freire RD, Ferreir SR, Crdoso MA: Dietry fier nd glucose tolernce in Jpnese Brzilins. Dietes Cre 2005, 28: Srtorelli DS, Frnco LJ, Gimeno SG, Ferreir SR, Crdoso MA: Dietry fructose, fruits, fruit juices nd glucose tolernce sttus in Jpnese- Brzilins. Nutr Metol Crdiovsc Dis: NMCD 2009, 19: Wtne S, Morit A, Ai N, Miychi M, Sski S, Moriok M, Nod M, Tkeyshi T, Kimur M: Study Design of the Sku Control Oesity Progrm (SCOP). Anti Aging Med 2007, 4: Morit A, Ohmori Y, Suzuki N, Ide N, Moriok M, Ai N, Sski S, Miychi M, Nod M, Wtne S: Anthropometric nd Clinicl Findings in Oese Jpnese: The Sku Control Oesity Progrm (SCOP). Anti Aging Med 2008, 5: Tnk T, Morit A, Kto M, Hiri T, Mizoue T, Teruchi Y, Wtne S, Nod M, Group SS: Congener-specific polychlorinted iphenyls nd the prevlence of dietes in the Sku Control Oesity Progrm (SCOP). Endocr J 2011, 58: White WB, Anwr YA: Evlution of the overll efficcy of the Omron office digitl lood pressure HEM-907 monitor in dults. Blood Press Monit 2001, 6: Yoshizumi T, Nkmur T, Ymne M, Islm AH, Menju M, Ymski K, Ari T, Kotni K, Funhshi T, Ymshit S, Mtsuzw Y: Adominl ft: stndrdized techniqueformesurementtct.rdiology 1999, 211: Ok R, Miur K, Skuri M, Nkmur K, Ygi K, Miymoto S, Moriuchi T, Muchi H, Ymgishi M, Tked Y, et l: Comprison of wist circumference with ody mss index for predicting dominl dipose tissue. Dietes Res Clin Prct 2009, 83: Seino Y, Nnjo K, Tjim N, Kdowki T, Kshiwgi A, Arki E, Ito C, Ingki N, Iwmoto Y, Ksug M, et l: Report of the Committee on the clssifiction nd dignostic criteri of dietes mellitus. Dietol Int 2010, 1: Mtthews DR, Hosker JP, Rudenski AS, Nylor BA, Trecher DF, Turner RC: Homeostsis model ssessment: insulin resistnce nd et-cell function from fsting plsm glucose nd insulin concentrtions in mn. Dietologi 1985, 28: Wllce TM, Levy JC, Mtthews DR: Use nd use of HOMA modeling. Dietes Cre 2004, 27: Sski S, Ushio F, Amno K, Morihr M, Todoriki O, Uehr Y, Toyook E: Serum iomrker-sed vlidtion of self-dministered diet history questionnire for Jpnese sujects. J Nutr Sci Vitminol (Tokyo) 2000, 46: Sski S, Yngiori R, Amno K: Self-dministered diet history questionnire developed for helth eduction: reltive vlidtion of the test-version y comprison with 3-dy diet record in women. J Epidemiol 1998, 8: Sski S, Yngiori R, Amno K: Vlidity of self-dministered diet history questionnire for ssessment of sodium nd potssium: comprison with single 24-hour urinry excretion. Jpn Circ J 1998, 62: Okuo H, Sski S, Rfmntnntso HH, Ishikw-Tkt K, Okzki H, Tt I: Vlidtion of self-reported energy intke y self-dministered diet history questionnire using the douly leled wter method in 140 Jpnese dults. Eur J Clin Nutr 2008, 62:

19 Goto et l. Nutrition & Metolism 2012, 9:79 Pge 19 of Sugiym M, Tng AC, Wkki Y, Koym W: of single nd mixed mel foods mong common Jpnese foods with white rice s reference food. Eur J Clin Nutr 2003, 57: Fernndes G, Velngi A, Wolever TM: of pottoes commonly consumed in North Americ. JAmDietAssoc2005, 105: Murkmi K, Sski S, Tkhshi Y, Okuo H, Hirot N, Notsu A, Fukui M, Dte C: Reproduciility nd reltive vlidity of dietry glycemic index nd lod ssessed with self-dministered diet-history questionnire in Jpnese dults. Br J Nutr 2008, 99: Mtsushit Y, Nkgw T, Ymmoto S, Tkhshi Y, Yokoym T, Nod M, Mizoue T: Associtions of viscerl nd sucutneous ft res with the prevlence of metolic risk fctor clustering in 6,292 Jpnese individuls: the Hitchi Helth Study. Dietes Cre 2010, 33: Hodge AM, English DR, O'De K, Giles GG: nd dietry fier nd the risk of type 2 dietes. Dietes Cre 2004, 27: Slmeron J, Mnson JE, Stmpfer MJ, Colditz GA, Wing AL, Willett WC: Dietry fier, glycemic lod, nd risk of non-insulin-dependent dietes mellitus in women. JAMA 1997, 277: Aronoff SL, Berkowitz K, Shreiner B, Wnt L: Glucose Metolism nd Regultion: Beyond Insulin nd Glucgon. Dietes Spectrum 2004, 17: Rohlfing CL, Wiedmeyer HM, Little RR, Englnd JD, Tennill A, Goldstein DE: Defining the reltionship etween plsm glucose nd HA(1c): nlysis of glucose profiles nd HA(1c) in the Dietes Control nd Complictions Tril. Dietes Cre 2002, 25: McKeown NM, Meigs JB, Liu S, Sltzmn E, Wilson PW, Jcques PF: Crohydrte nutrition, insulin resistnce, nd the prevlence of the metolic syndrome in the Frminghm Offspring Cohort. Dietes Cre 2004, 27: Liu S, Mnson JE, Stmpfer MJ, Holmes MD, Hu FB, Hnkinson SE, Willett WC: Dietry glycemic lod ssessed y food-frequency questionnire in reltion to plsm high-density-lipoprotein cholesterol nd fsting plsm tricylglycerols in postmenopusl women. Am J Clin Nutr 2001, 73: Kim K, Yun SH, Choi BY, Kim MK: Cross-sectionl reltionship etween dietry crohydrte, glycemic index, glycemic lod nd risk of the metolic syndrome in Koren popultion. Br J Nutr 2008, 100: Volek JS, Feinmn RD: Crohydrte restriction improves the fetures of Metolic Syndrome. Metolic Syndrome my e defined y the response to crohydrte restriction. Nutr Met 2005, 2: Accurso A, Bernstein RK, Dhlqvist A, Drznin B, Feinmn RD, Fine EJ, Gleed A, Jcos DB, Lrson G, Lustig RH, et l: Dietry crohydrte restriction in type 2 dietes mellitus nd metolic syndrome: time for criticl pprisl. Nutr Met 2008, 5: Bo J, Atkinson F, Petocz P, Willett WC, Brnd-Miller JC: Prediction of postprndil glycemi nd insulinemi in len, young, helthy dults: glycemic lod compred with crohydrte content lone. Am J Clin Nutr 2011, 93: Lichtmn SW, Pisrsk K, Bermn ER, Pestone M, Dowling H, Offencher E, Weisel H, Heshk S, Mtthews DE, Heymsfield SB: Discrepncy etween self-reported nd ctul cloric intke nd exercise in oese sujects. N Engl J Med 1992, 327: Prentice AM, Blck AE, Cowrd WA, Dvies HL, Golderg GR, Murgtroyd PR, Ashford J, Swyer M, Whitehed RG: High levels of energy expenditure in oese women. Br Med J (Clin Res Ed) 1986, 292: Willett WC, Howe GR, Kushi LH: Adjustment for totl energy intke in epidemiologic studies. Am J Clin Nutr 1997, 65:1220S 1228S. 47. Kipnis V, Sur AF, Midthune D, Freedmn LS, Bllrd-Brsh R, Troino RP, Binghm S, Schoeller DA, Schtzkin A, Crroll RJ: Structure of dietry mesurement error: results of the OPEN iomrker study. Am J Epidemiol 2003, 158: Lu C, Toft U, Tetens I, Richelsen B, Jorgensen T, Borch-Johnsen K, Glumer C: Assocition etween dietry glycemic index, glycemic lod, nd ody mss index in the Inter99 study: is underreporting prolem? Am J Clin Nutr 2006, 84: doi: / Cite this rticle s: Goto et l.: Dietry glycemic index nd glycemic lod in reltion to HA1c in Jpnese oese dults: cross-sectionl nlysis of the Sku Control Oesity Progrm. Nutrition & Metolism :79. Sumit your next mnuscript to BioMed Centrl nd tke full dvntge of: Convenient online sumission Thorough peer review No spce constrints or color figure chrges Immedite puliction on cceptnce Inclusion in PuMed, CAS, Scopus nd Google Scholr Reserch which is freely ville for redistriution Sumit your mnuscript t