ライフサイエンスコーパス: NIDDM

1 NIDDM and obesity are characterized by decreased insulin

2 NIDDM is a polygenic disease characterized by insulin re

3 NIDDM is associated with excessive rates of endogenous g

4 NIDDM is characterized by islet amyloid deposits and dec

5 NIDDM is characterized by progressive insulin resistance

6 NIDDM is usually characterized by beta-cell failure and

7 NIDDM prevalence was increased among those subjects pres

8 NIDDM was positively associated with the probability of

9 +/- 1 vs. 15 +/- 1 micromol x kg-1 x min-1, NIDDM patients vs. control subjects, P < 0.002) and nono

10 For the 100 NIDDM patients with normoalbuminuria at baseline, the in

11 ease patients with (n=13) and without (n=13) NIDDM.

12 A total of 154 NIDDM patients were randomized to receive troglitazone 8

13 A total of 498 individuals, including 159 NIDDM patients with an average age at diagnosis of 47 ye

14 e-stimulated conditions in 17 healthy and 16 NIDDM subjects; high-performance liquid chromatography (

15 in the two NBF regions of the SUR gene in 35 NIDDM patients.

16 determined insulin sensitivity (S(I)) in 479 NIDDM subjects by minimal model analyses of frequently s

17 crease in hepatic sensitivity to glucagon, 9 NIDDM and 10 nondiabetic subjects were studied on three

18 utes the beta cell dysfunction of adipogenic NIDDM to an excessive accumulation of fat in the pancrea

19 in man, is also effective in the adipogenic NIDDM of Zucker diabetic fatty (ZDF) rats.

20 We concluded that although NIDDM is not associated with an intrinsic alteration in

21 d that a high proportion of African-American NIDDM subjects are insulin sensitive.

22 mic activity was measured in vitro and in an NIDDM mouse model to generate the first structure-bioact

23 previous studies), these results suggest an NIDDM-associated increased rate of alveolar bone loss pr

24 s. basal, obese 1.30 +/- 0.16, P < 0.05, and NIDDM 1.25 +/- 0.14, P < 0.05).

25 ed the association between breastfeeding and NIDDM in a population with a high prevalence of this dis

26 The obese controls and NIDDM patients were insulin resistant with glucose dispo

27 Both dwarfism and NIDDM are most likely due to the loss of expression of i

28 between the three infant-feeding groups and NIDDM was analysed by multiple logistic regression.

29 t proinsulin are similar in both healthy and NIDDM subjects, the orderly cleavage of proinsulin at it

30 The authors conclude that hypertension and NIDDM were independently associated with the risk of kid

31 IGT and NIDDM were defined in all studies by World Health Organi

32 ression of Rad mRNA levels among IS, IR, and NIDDM groups using a ribonuclease protection assay (0.22

33 In the lean and NIDDM patients, muscle PPARgamma1 levels correlated with

34 sulinemia in both diabetic animal models and NIDDM subjects.

35 sulinemia in both diabetic animal models and NIDDM subjects.

36 vation of IRTK was apparent in the obese and NIDDM groups.

37 The obese and NIDDM subjects had marked delays in activation of GDR (T

38 In conclusion, 1) in obese and NIDDM subjects, insulin-mediated GDR and LGU are delayed

39 HK I and II were similar in lean, obese and NIDDM subjects.

40 However, molecular links between obesity and NIDDM are only beginning to emerge.

41 forms, to examine the effects of obesity and NIDDM, and the effects of insulin, on skeletal muscle le

42 ole in the insulin resistance of obesity and NIDDM.

43 ity to induce HKII expression in obesity and NIDDM.

44 ute to the insulin resistance of obesity and NIDDM.

45 n resistance in individuals with obesity and NIDDM.

46 idate contributing to insulin resistance and NIDDM in other populations.

47 trait loci (QTLs), Tanidd1-3 (TH-associated NIDDM) linked to hyperglycemia.

48 obtained evidence suggesting linkage between NIDDM and markers D20S119, D20S178, and D20S197 (allele

49 tomography, is increased in those with both NIDDM and CHD.

50 are late-onset and frequently accompanied by NIDDM.

51 Age, calculus, NIDDM status, time to follow-up examination, and baselin

52 eptibility in African-American and Caucasian NIDDM-affected sibling pairs with a history of adult-ons

53 In conclusion, NIDDM patients treated with troglitazone do not show any

54 ne loss at baseline, and who did not develop NIDDM nor lose any teeth during the 2-year study period.

55 levels in subjects who subsequently develop NIDDM.

56 Their F1 male progeny consistently developed NIDDM.

57 rome: namely, noninsulin-dependent diabetes (NIDDM) and increased body mass index (BMI).

58 disease, and non-insulin-dependent diabetes (NIDDM).

59 pancreas of patients with type II diabetes (NIDDM).

60 m diabetes and other major chronic diseases, NIDDM incidence was followed from 1986 to 1994.

61 The cause of amyloid formation during NIDDM is not known, nor is the mechanism by which membra

62 During fasting, NIDDM hearts demonstrated lower fractional extraction of

63 ) and first-pass SGU (r = 0.87, P < 0.05 for NIDDM patients; r = 0.84, P < 0.05 for nondiabetic patie

64 gnificantly with SGU (r = 0.87, P < 0.05 for NIDDM patients; r = 0.94, P < 0.01 for nondiabetic patie

65 One possible therapeutic agent for NIDDM is the insulinotropic hormone glucagon-like peptid

66 factor 4) is an unlikely candidate gene for NIDDM in our families, since it is located about 8 cM ce

67 l. found significant evidence of linkage for NIDDM on chromosome 2q37 and named the putative disease

68 e identified several susceptibility loci for NIDDM within the human genome.

69 The cumulative odds ratio for NIDDM at each threshold of the ordered response was 4.23

70 The odds ratio for NIDDM in exclusively breastfed people, compared with tho

71 by which celiac disease affects the risk for NIDDM and metabolic syndrome.

72 the utility of these traits in searching for NIDDM susceptibility genes in those populations can be f

73 ay provide a new and effective treatment for NIDDM.

74 rgoing clinical evaluation as treatments for NIDDM.

75 -six patients with celiac disease (3.1%) had NIDDM compared with 81 controls (9.6%) (P < .0001).

76 The other 24 subjects had NIDDM at baseline, but met the other selection criteria.

77 ut not in the three studies with the highest NIDDM incidence rates.

78 In NIDDM subjects, levels of both basal (44.6 +/- 9.6 vs. 9

79 ry blood flow, but this effect was absent in NIDDM.

80 by many observers to also be accelerated in NIDDM, we sought to determine whether the same salutary

81 ion of IAPP has a role in beta-cell death in NIDDM, the mechanism remains unknown.

82 imulated expression of HK-II is decreased in NIDDM and obese subjects.

83 oral glucose administration is decreased in NIDDM as measured by both methods, and (b) SGU during th

84 sulin infusion; and 3) The kinetic defect in NIDDM and obesity most likely involves intracellular loc

85 n of progression of macrovascular disease in NIDDM is discussed.

86 its conversion intermediates are elevated in NIDDM patients.

87 oc analysis in the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAA

88 ith the use of the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAA

89 abolism could induce IAPP fiber formation in NIDDM.

90 Although IRI was higher in NIDDM than in control subjects under basal conditions (1

91 ated to SGU and first-pass SGU during HVC in NIDDM.

92 levels, CET remained abnormally increased in NIDDM patients treated rigorously with conventional subc

93 PI/IRI ratios were increased in NIDDM subjects under both basal (43.3 +/- 5.0 vs. 14.0 +

94 (PI)-like molecules (PI/IRI) is increased in NIDDM.

95 didate for a susceptibility gene involved in NIDDM.

96 The increase in PI/IRI in NIDDM under basal and especially under stimulated condit

97 ee; 2) mass action normalizes GDR and LGU in NIDDM, but only after several hours of insulin infusion;

98 he overproduction of glucose by the liver in NIDDM patients markedly contributes to their fasting hyp

99 ese control subjects; but HK-II was lower in NIDDM patients than in lean subjects (1.42 +/- 0.16 [SE]

100 1 +/- 8.1 pmol/l; P = 0.05), it was lower in NIDDM than in control subjects following stimulation (in

101 se to the development of microalbuminuria in NIDDM.

102 o 3.7+/-0.4% and 18.3+/-3.5 micromol. min in NIDDM and to 5.4+/-0.7% and 17.7+/-4.3 micromol. min in

103 0.1 +/- 6.7% of proinsulin-like molecules in NIDDM individuals (n = 9) and 30.1 +/- 5.6% in healthy s

104 otentially lower cardiovascular morbidity in NIDDM patients.

105 ) and HbAlc (both P < 0.05) were observed in NIDDM subjects during treatment; plasma glucose was unch

106 in skeletal muscle that is overexpressed in NIDDM.

107 -II may contribute to insulin resistance in NIDDM and obesity.

108 on is unlikely to be playing a major role in NIDDM susceptibility in the Finnish Caucasian population

109 The decrease in SGU in NIDDM might contribute to postprandial hyperglycemia in

110 h methods and was increased significantly in NIDDM patients (73.1+/-5.1 g for HVC, 76.5+/-5.5 for OG-

111 In most survival studies in NIDDM, microalbuminuria (urinary albumin excretion rate

112 the recently developed OG-CLAMP technique in NIDDM by comparing SGU and first-pass SGU during HVC wit

113 f atherosclerosis and vascular thrombosis in NIDDM is reviewed.

114 Thus, in NIDDM patients, SGU (7.4+/-2.1 vs. 37.8+/-5.9% in nondia

115 mouse model of streptozotocin (STZ)-induced NIDDM.

116 llitus (NIDDM) risk, but the fasting insulin-NIDDM association may be confounded by insulin secretion

117 Thus, in this large NIDDM study, weight loss, smoking cessation, and aggress

118 ing non-insulin dependent diabetes mellitus (NIDDM) and coronary heart disease (CHD).

119 ith non-insulin dependent diabetes mellitus (NIDDM) and insulin resistance in childhood and adulthood

120 for non-insulin-dependent diabetes mellitus (NIDDM) and metabolic syndrome are affected by celiac dis

121 s of noninsulin-dependent diabetes mellitus (NIDDM) and obesity, RXR agonists function as insulin sen

122 ith non-insulin-dependent diabetes mellitus (NIDDM) exhibit poor clinical outcomes from myocardial is

123 in non-insulin-dependent diabetes mellitus (NIDDM) has not been established conclusively.

124 ith non-insulin dependent diabetes mellitus (NIDDM) have greater risk of more severe alveolar bone lo

125 eat non-insulin-dependent diabetes mellitus (NIDDM) in man, is also effective in the adipogenic NIDDM

126 Non-insulin-dependent diabetes mellitus (NIDDM) is a multifactoral disease with both environmenta

127 sulin-dependent (type II) diabetes mellitus (NIDDM) is characterized by dysfunction and depletion of

128 to non-insulin-dependent diabetes mellitus (NIDDM) is largely genetically determined.

129 or non-insulin-dependent diabetes mellitus (NIDDM) is the most common form of diabetes worldwide, af

130 Non-insulin-dependent diabetes mellitus (NIDDM) may cause vulnerability to moderate zinc deficien

131 in non-insulin-dependent diabetes mellitus (NIDDM) nephropathy.

132 of non-insulin-dependent diabetes mellitus (NIDDM) risk, but the fasting insulin-NIDDM association m

133 ith non-insulin-dependent diabetes mellitus (NIDDM) underwent echocardiography, hemodynamic assessmen

134 of non-insulin-dependent diabetes mellitus (NIDDM) using MIF(-/-) mice and a mouse model of streptoz

135 and non-insulin dependent diabetes mellitus (NIDDM) were randomized into 5 treatment groups.

136 ith non-insulin-dependent diabetes mellitus (NIDDM) who were not taking insulin and 9.4 micrograms/mi

137 ith non-insulin-dependent diabetes mellitus (NIDDM), by activating PPARgamma, and possibly by inducin

138 for non-insulin-dependent diabetes mellitus (NIDDM), Hanis et al. found significant evidence of linka

139 er, non-insulin-dependent diabetes mellitus (NIDDM), inflammatory bowel disease, asthma and multiple

140 ith non-insulin-dependent diabetes mellitus (NIDDM), obesity, atherosclerosis, and hypertension.

141 to non-insulin-dependent diabetes mellitus (NIDDM).

142 ent non-insulin-dependent diabetes mellitus (NIDDM).

143 for non-insulin-dependent diabetes mellitus (NIDDM).

144 of non-insulin-dependent diabetes mellitus (NIDDM).

145 ith non-insulin-dependent diabetes mellitus (NIDDM).

146 ing non-insulin-dependent diabetes mellitus (NIDDM).

147 ith non-insulin dependent diabetes mellitus (NIDDM).

148 of non-insulin-dependent diabetes mellitus (NIDDM).

149 of non-insulin-dependent diabetes mellitus (NIDDM).

150 of non-insulin-dependent diabetes mellitus (NIDDM).

151 sulin-dependent (type II) diabetes mellitus (NIDDM).

152 for non-insulin-dependent diabetes mellitus (NIDDM).

153 for noninsulin-dependent diabetes mellitus (NIDDM).

154 and non-insulin-dependent diabetes mellitus (NIDDM).

155 of non-insulin-dependent diabetes mellitus (NIDDM).

156 and non-insulin dependent diabetes mellitus (NIDDM).

157 ns; non-insulin-dependent diabetes mellitus (NIDDM); and hypertension (HTN).

158 insulin dependent form of diabetes mellitus (NIDDM)], is associated with an increased relative risk f

159 es (non-insulin-dependent diabetes mellitus, NIDDM).

160 on chromosome 20q that contains one or more NIDDM genes distinct from the recently identified MODY1

161 17 obese nondiabetic subjects, and 14 obese NIDDM patients were studied.

162 om insulin-resistant animal models and obese NIDDM humans.

163 ays a role in the development of the obesity/NIDDM syndrome, troglitazone may prove useful in its tre

164 single-gene disorder responsible for 2-5% of NIDDM, is characterized by autosomal dominant inheritanc

165 losely mimics the metabolic abnormalities of NIDDM.

166 sults indicate that skeletal muscle cells of NIDDM subjects grown and fused in normal culture conditi

167 impaired insulin secretion characteristic of NIDDM in Caucasian patients.

168 tion plays a role in the secretory defect of NIDDM, but the mechanisms underlying this refractoriness

169 a good model for studying the development of NIDDM without the complications associated with obesity.

170 causative factor in the early development of NIDDM, possibly through loss of ss cell mass.

171 omosome 20 contributes to the development of NIDDM, we conducted linkage studies in 29 extended Cauca

172 iopsy-proven celiac disease for diagnoses of NIDDM, hypertension, or hyperlipidemia; body mass index

173 4 families whose average age at diagnosis of NIDDM was above the median (47 years) for all families.

174 e inheritance of obesity-associated forms of NIDDM in humans.

175 , to outbred ICR mice following induction of NIDDM significantly lowered blood glucose levels in the

176 d the Finland-United States Investigation of NIDDM Genetics (FUSION) studies.

177 The Finland-United States Investigation Of NIDDM Genetics (FUSION) study aims to identify genetic v

178 f the Finland-United States Investigation of NIDDM Genetics (FUSION) study is to identify genes that

179 f the Finland-United States Investigation of NIDDM Genetics (FUSION) study, we observe a near one-to-

180 amples of 526 (Finland-U.S. Investigation of NIDDM Genetics [FUSION] 1) and 255 (FUSION 2) index case

181 n the Finland-United States Investigation of NIDDM Genetics study.

182 tosis, the secretory granule in the islet of NIDDM subjects contains an increased proportion of incom

183 analysis also showed evidence for linkage of NIDDM with the same three markers.

184 y be critical to the pathogenic mechanism of NIDDM, as other amyloid pores may be to Alzheimer's dise

185 of Goto-Kakizaki (GK) rats, a novel model of NIDDM, and normal rats.

186 clusion, lean insulin-resistant offspring of NIDDM parents showed 1) trimodal distribution of insulin

187 04 +/- 3% of ideal body weight) offspring of NIDDM patients.

188 The onset of NIDDM in obese Zucker diabetic fatty (fa/fa) rats is pre

189 that MIF is involved in the pathogenesis of NIDDM and is a therapeutic target to treat this disease.

190 ucose disposal underlies the pathogenesis of NIDDM and is associated with hypertension, obesity, and

191 beta cell dysfunction in the pathogenesis of NIDDM by significantly increasing the basal rate of insu

192 olism may play a role in the pathogenesis of NIDDM.

193 ations contributed to the pathophysiology of NIDDM by decreasing both insulin-mediated glucose dispos

194 rence are powerful independent predictors of NIDDM in US women.

195 overall and central obesity as predictors of NIDDM risk have not been as well studied, especially in

196 African Americans have a high prevalence of NIDDM and hypertension, and are relatively resistant to

197 We examined the prevalence of NIDDM and metabolic syndrome among adults with celiac di

198 The prevalence of NIDDM and metabolic syndrome are lower among patients wi

199 The prevalence of NIDDM and metabolic syndrome in the celiac disease cohor

200 ssociated with a significantly lower rate of NIDDM in Pima indians.

201 cross the six studies, the incidence rate of NIDDM was 57.2/1,000 person-years and ranged from 35.8/1

202 y breastfed had significantly lower rates of NIDDM than those who were exclusively bottlefed in all a

203 First-degree relatives of NIDDM patients have an approximately 40% lifetime risk o

204 everal dietary factors, the relative risk of NIDDM for the 90th percentile of body mass index (BMI) (

205 actors responsible for the increased risk of NIDDM seen among MA adults are demonstrable in childhood

206 ability to identify persons at high risk of NIDDM should facilitate clinical trials in diabetes prev

207 se was still associated with a lower risk of NIDDM, after controlling for BMI.

208 tribute to the impaired insulin secretion of NIDDM.

209 -sensitizing agents used in the treatment of NIDDM and are potent agonists for the nuclear hormone re

210 dione under development for the treatment of NIDDM and potentially other insulin-resistant disease st

211 diabetes of the young 3 (MODY3) is a type of NIDDM caused by mutations in the transcription factor he

212 history of early onset, more severe type of NIDDM, linking the amylin gene to this disease.

213 The effect of baseline age on NIDDM incidence rates differed among the studies; the ra

214 diabetes in German subjects with early-onset NIDDM and a family history of diabetes.

215 ay be indicated in subjects with early-onset NIDDM.

216 n the HNF-4 alpha gene may cause early-onset NIDDM/MODY in Japanese but they are less common than mut

217 unrelated Japanese subjects with early-onset NIDDM/MODY of unknown cause.

218 ignificantly in the obese (1.12 +/- 0.24) or NIDDM (1.14 +/- 0.18) groups.

219 ml leg vol) than in obese (1.46 +/- 0.50) or NIDDM (0.53 +/- 0.25, P < 0.05) patients.

220 tered as a function of insulin resistance or NIDDM in humans.

221 clinicians in counseling patients regarding NIDDM risk and risk reduction.

222 ffect could be achieved in insulin-requiring NIDDM men before and 7 months after randomization to an

223 and the development of a syndrome resembling NIDDM.

224 is well recognized that insulin resistance, NIDDM, and other metabolic disorders are associated more

225 onclude that the number of insulin-sensitive NIDDM subjects is low and similar among non-Hispanic whi

226 In summary, NIDDM patients have lower muscle HK-II activity basally

227 ing both type 1 (T1DM/IDDM) and type 2 (T2DM/NIDDM) diabetes.

228 age disequilibria did not differ between the NIDDM and control groups.

229 missense variants were compared between the NIDDM group (n = 306) and nondiabetic control subjects (

230 f both assays, which was evident in both the NIDDM and IDDM subgroups.

231 ee measurements reached normal levels in the NIDDM group after 4-5 h of insulin infusion.

232 glucose uptake and glucose oxidation in the NIDDM heart.

233 subjects (r = 0.58, P < 0.05) but not in the NIDDM patients.

234 perinsulinemia; no increase was found in the NIDDM patients.

235 mass and isotopic assays was greater in the NIDDM subjects than in nondiabetic control subjects (P <

236 This NIDDM mouse model in which diabetes arises in an age-dep

237 e results suggest that genes contributing to NIDDM in the general Caucasian population are located in

238 -onset diabetes of the young (MODY) genes to NIDDM susceptibility in African-American and Caucasian N

239 ion from impaired glucose tolerance (IGT) to NIDDM are reached.

240 ion from impaired glucose tolerance (IGT) to NIDDM were examined in data from six prospective studies

241 ed the role of dietary conditions leading to NIDDM-like insulin resistance on amyloidosis in Tg2576 m

242 Evidence for linkage to NIDDM was found with polymorphic loci that map to the lo

243 ker D20S197 provides evidence for linkage to NIDDM with a P value of 0.005 in Caucasian sib pairs usi

244 and D12S86 provides evidence for linkage to NIDDM with P values of 0.04 and 0.006, respectively, in

245 hromosome 3 that contains a region linked to NIDDM in the GK rat.

246 ce for linkage of MODY1 and MODY3 markers to NIDDM in African-American sib pairs was observed.

247 was transmitted from heterozygous parents to NIDDM offspring more frequently than expected (P < 0.01)

248 lipogenic capacity that might predispose to NIDDM, the metabolism of long-chain fatty acids was comp

249 The predisposition to NIDDM and vascular disease is likely to be the result of

250 , insulin resistance, and the progression to NIDDM.

251 may precede obesity in populations prone to NIDDM, such as Pima Indians or Pacific Islanders.

252 ry of diabetes were generally not related to NIDDM progression.

253 ul traits to study genetic susceptibility to NIDDM.

254 cal increase in CET in these insulin-treated NIDDM men, normalization was only achieved in those trea

255 stinguish false-positive linkage from a true NIDDM susceptibility locus.

256 th normal glucose tolerance and in untreated NIDDM patients.

257 week study was conducted to evaluate whether NIDDM patients treated with troglitazone develop any car

258 a hospital-based cohort comprising 146 white NIDDM patients without clinical albuminuria.

259 ies in which many members were affected with NIDDM.

260 reases proteinuria in African Americans with NIDDM and nephropathy.

261 ts of captopril in 31 African Americans with NIDDM and proteinuria (> or = 500 mg/day).

262 trol, particularly in African-Americans with NIDDM, would appear to be important in improving exercis

263 BMI was associated with NIDDM incidence independently of fasting and 2-h post ch

264 levels were both positively associated with NIDDM incidence, incidence rates were sharply higher for

265 rcumference) were positively associated with NIDDM incidence.

266 3.1, one of the genomic loci associated with NIDDM.

267 a predicts incident clinical CHD in men with NIDDM.

268 secretion, which correlates negatively with NIDDM risk and positively with fasting insulin level.

269 Ten adult children of parents with NIDDM and eight normal subjects were studied before star

270 pring (48 men, 59 women) of two parents with NIDDM.

271 We studied seven patients with NIDDM (body mass index, 32+/-1 kg/m2), seven lean (24+/-

272 atory secretion is impaired in patients with NIDDM and in their near relatives suggests that such der

273 Patients with NIDDM and microalbuminuria are more insulin resistant th

274 re, we investigated SGU in six patients with NIDDM and six weight-matched control subjects by means o

275 bese normal subjects and eight patients with NIDDM before and at 3 and 5 h of a hyperinsulinemic (80

276 stance and microalbuminuria in patients with NIDDM could be due to hyperglycemia, which can cause bot

277 From 1988 to 1994, 1056 patients with NIDDM defined by stimulated C-peptide criteria) were stu

278 The estimated fraction of patients with NIDDM due to mtDNA-mutation involvement is 22% (95% conf

279 vasculature, the myocardium of patients with NIDDM expresses a competent insulin-response system with

280 en the TRF length from WBCs of patients with NIDDM versus nondiabetic subjects.

281 sing 54 patients with IDDM, 74 patients with NIDDM, and 106 control subjects.

282 35 Northern-European Caucasian patients with NIDDM, six sequence variants were detected: Glu10gag-->L

283 People with NIDDM are resistant to insulin.

284 oaches to glycemic regulation in people with NIDDM are reviewed.

285 in concentrations is abnormal in people with NIDDM.

286 improve the quality of life for people with NIDDM.

287 n and 9.4 micrograms/minute for persons with NIDDM who were taking insulin (p < 0.0001).

288 ite subjects from Germany who presented with NIDDM before 35 years of age and had a first-degree rela

289 of age and had a first-degree relative with NIDDM.

290 )) isoglycemic clamps in seven subjects with NIDDM (194 +/- 29 mg/dl) and in seven lean and seven obe

291 imes and propagation rates for subjects with NIDDM and for moderately zinc-deficient rats, were uncha

292 uces glucose concentrations in subjects with NIDDM and IGT but is not known to affect insulin secreti

293 nd nonglucose secretogogues in subjects with NIDDM are not known.

294 to that previously reported in subjects with NIDDM or increased BMI, suggests the possibility that ac

295 eficiency occurs frequently in subjects with NIDDM.

296 noted association of the SUR1 variants with NIDDM and 2) did not contribute to the impaired insulin

297 Placebo, given to 20 other women with NIDDM, had no effects on these indexes nor on any others

298 dant enzyme, in 20 postmenopausal women with NIDDM.

299 supplementation in persons with and without NIDDM may be related to greater insulin sensitivity (SI)

300 sion over a 2-year period than those without NIDDM.