ライフサイエンスコーパス: normoglycemia

1 ase in apoptosis compared with 5 mM glucose (normoglycemia).

2 with healthy periodontium (while maintaining normoglycemia).

3 aII (PKCbetaII) persisted after returning to normoglycemia.

4 imental vicious cycle despite restoration of normoglycemia.

5 at persists even after the additional 6 h of normoglycemia.

6 eta-cells play a pivotal role in maintaining normoglycemia.

7 beta-cell hyperplastic response to maintain normoglycemia.

8 ponse is not sufficient to restore sustained normoglycemia.

9 and human islets restored NRG-Akita mice to normoglycemia.

10 66, P<0.0001), predicted death compared with normoglycemia.

11 graft rejection leading to stable, long-term normoglycemia.

12 emia when compared with 3.3% in grafts under normoglycemia.

13 and beta-cell proliferation and maintaining normoglycemia.

14 ersible with insulin treatment that achieved normoglycemia.

15 pressure >12 mm Hg plus glucose to maintain normoglycemia.

16 ients required diazoxide therapy to maintain normoglycemia.

17 70% of them maintained a state of long-term normoglycemia.

18 ell reprogramming, leading to restoration of normoglycemia.

19 y remit hyperglycemia and maintain prolonged normoglycemia.

20 nalog and glucose-accessible Glut to restore normoglycemia.

21 eficiency restores functional beta-cells and normoglycemia.

22 nutrition should probably be treated to true normoglycemia.

23 lase I inhibitor provoked these responses in normoglycemia.

24 in modulating alpha cell function to restore normoglycemia.

25 transduced with a VEGF vector exhibited near normoglycemia.

26 s a more reliable and durable restoration of normoglycemia.

27 d reducing the number of islets required for normoglycemia.

28 inates autoimmunity and permanently restores normoglycemia.

29 insulin supplementation that did not restore normoglycemia.

30 animals that are already diabetic, restores normoglycemia.

31 ulating porcine C-peptide and maintenance of normoglycemia.

32 d with those who needed high AIR to maintain normoglycemia.

33 f 7 in the subcutaneous tissue site achieved normoglycemia.

34 to be enhanced during palmitate treatment at normoglycemia.

35 tential for establishing insulin-independent normoglycemia.

36 unteract the beneficial effects of sustained normoglycemia.

37 ger endogenous glucose production to restore normoglycemia.

38 h previous GD is not diminished by attaining normoglycemia.

39 e to circulating nutrient levels to maintain normoglycemia.

40 a decrease of total brain FDG uptake during normoglycemia.

41 out T2D, compared with lean individuals with normoglycemia.

42 y surgical-access but this never resulted in normoglycemia.

43 NP-depleted animals restored body weight and normoglycemia.

44 imilar between patients with prediabetes and normoglycemia.

45 f pancreatic beta-cells, thereby maintaining normoglycemia.

46 s high in obese individuals, even those with normoglycemia.

47 secretion and induce weight loss to preserve normoglycemia.

48 e of producing human insulin and maintaining normoglycemia.

49 ate insulin secretion for the maintenance of normoglycemia.

50 ion and seem to persist even after return to normoglycemia.

51 CVB infection, were transplanted to restore normoglycemia.

52 ent of type 1 diabetes is the maintenance of normoglycemia.

53 d not differ in patients with prediabetes or normoglycemia.

54 uired a small dose of octreotide to maintain normoglycemia.

55 The control group consisted of 15 rats with normoglycemia.

56 in rats with diabetes compared to those with normoglycemia.

57 e of species-specific strategies to maintain normoglycemia.

58 tibodies, with categorization into stages 1 (normoglycemia), 2 (dysglycemia), or 3 (clinical) type 1

59 d not differ in patients with prediabetes or normoglycemia (33% and 18% of the patient population, re

60 9 [10.2] years; 48 men and 54 women; 45 with normoglycemia [44.1%], 31 with prediabetes [30.4%], and

61 The patients were studied at normoglycemia (5-6 mmol/L) and hypoglycemia (2.0-2.5 mmo

62 rown in medium with glucose concentration of normoglycemia (5.5 mM).

63 mmon patterns of glycemic trajectory: stable normoglycemia; 5 patterns of impaired fasting glucose (I

64 tight glucose control (TGC) to age-adjusted normoglycemia (50-80 mg/dL at age <1 year and 70-100 mg/

65 in rats with diabetes compared to rats with normoglycemia (69% of baseline versus 93%, respectively,

66 ment/progression of DKD even after achieving normoglycemia, a phenomenon known as metabolic memory or

67 tes, we aimed to determine whether long-term normoglycemia achieved by successful simultaneous pancre

68 e risk of gestational diabetes vs those with normoglycemia (adjusted RR [aRR], 2.21; 95% CI, 1.91-2.5

69 In comparison with no GD/normoglycemia, adjusted hazard ratios (95% CIs) were 1.5

70 el data revealed that South Asian women with normoglycemia after GDM showed lower insulin secretion f

71 In mice, more diabetic recipients reached normoglycemia after intraportal islet transplantation wh

72 re treated with insulin infusion to maintain normoglycemia after surgery.

73 d not translate into a faster achievement of normoglycemia after transplantation, which suggests that

74 normoglycemia; age 3 years: beta = 3.16 mm Hg (95% confi

75 ncreasing hypoglycemia, achieved 97% in near normoglycemia and 77% in tight glycemic control, and red

76 Long-term nonfasting normoglycemia and adequate glucose clearance (tolerance

77 the regulation of glycogen synthase both in normoglycemia and diabetes.

78 ted with GDNF restored more diabetic mice to normoglycemia and for a longer period after transplantat

79 eased salvage index both among patients with normoglycemia and hyperglycemia.

80 as well as REC and Muller cells cultured in normoglycemia and hyperglycemic conditions, to investiga

81 tion in all three animals and in a return to normoglycemia and insulin independence in two of three b

82 the results of IIT with regard to attaining normoglycemia and insulin independence of type I diabeti

83 These findings demonstrate that despite normoglycemia and insulin independence, recipients of in

84 The reversal of diabetes was defined by normoglycemia and negative urine glucose maintained for

85 cose concentrations below 15 mmol/L restored normoglycemia and normalized C-peptide.

86 Restoration of normoglycemia and normoinsulinemia in ZDF rats with rosi

87 atric surgery (BS), but further WL increases normoglycemia and normotension.

88 tion of 300 microg of peptide 5 alone led to normoglycemia and permanent islet survival in three of s

89 in nondiabetic patients reliably establishes normoglycemia and phasic insulin secretion and can achie

90 To evaluate the processes that maintain normoglycemia and regulate BCM during pancreatic regener

91 SPK) transplantation is performed to restore normoglycemia and renal function in patients with type 1

92 by PD-L1 platelets can effectively maintain normoglycemia and reverse diabetes in newly hyperglycemi

93 tation with MATRIGEL can effectively achieve normoglycemia and that this is a simple and reproducible

94 were associated with durable restoration of normoglycemia and the absence of graft inflammation.

95 tic mice resulted in the restoration of near-normoglycemia and the reversal of diabetic symptoms.

96 s and MSCs resulted in significantly earlier normoglycemia and vascularization, improved glucose tole

97 lower HbA1c in patients with prediabetes or normoglycemia and was not associated with increased risk

98 deling in mouse hepatocytes in comparison to normoglycemia and younger age, respectively.

99 tegies directed at maintaining normothermia, normoglycemia, and prevention of anemia may improve outc

100 f intermediary metabolism and maintenance of normoglycemia, and there is great interest in assessing

101 ive PC subjects were restudied after 72 h of normoglycemia ( approximately 100 mg/dl; variable insuli

102 patic artery (HA protocol) to maintain liver normoglycemia as systemic glucose concentrations were sy

103 In recipients with normoglycemia at 10 y, 74% of normoalbuminuric or microa

104 h factor/fibroblast growth factor-2 achieved normoglycemia at a higher rate (78%) than control animal

105 The success rate for restoration of normoglycemia at week 4 was highest for the recipients r

106 ding a brief period of low IFG regressing to normoglycemia at younger (mean [SD] age at IFG, 35.9 [6.

107 Most (11 407 individuals [79.7%]) had normoglycemia before pregnancy, and 2895 individuals (20

108 mic excursions are uncommon in patients with normoglycemia before teprotumumab therapy.

109 When blood glucose levels return to normoglycemia beta-cell mass expansion stops, and subseq

110 MST1 deficiency completely restored normoglycemia, beta cell function and survival in vitro

111 either intensive insulin therapy (targeting normoglycemia, between 4.4 and 6.1 mmol/L) or convention

112 ith CVD or mortality among participants with normoglycemia but not participants with prediabetes.

113 and infarct size compared with patients with normoglycemia, but the salvage index and infarct size ad

114 t loss interventions increased regression to normoglycemia by 11/100 participants (95% confidence int

115 The effect of restoration of normoglycemia by a novel sodium-dependent glucose transp

116 Despite normoglycemia, CaMKIId-deficient diabetic mice developed

117 Despite normoglycemia, CaMKIIdelta-deficient diabetic mice devel

118 y individuals with normal glucose tolerance, normoglycemia can always be maintained by compensatorily

119 However, it is unclear whether attaining normoglycemia can ameliorate the excess CVD risk associa

120 Normoglycemia did not alter ACH-3P proliferation at 2.5%

121 Although control rats maintained near normoglycemia during and after exercise, the rats with i

122 ose production (HGP) is required to maintain normoglycemia during fasting.

123 l mass is a critical factor to help maintain normoglycemia during insulin resistance.

124 min(-1)) to achieve and maintain left renal normoglycemia during systemic hypoglycemia.

125 ulations in the ventrolateral medulla during normoglycemia elicits these CRRs in a site-specific mann

126 Compared with normoglycemia, exposure of HASMCs to hyperglycemia but n

127 Compared with normoglycemia, exposure of human endothelial cells to hy

128 nd glucagon-like peptide-1 despite achieving normoglycemia faster than animals with renal subcapsular

129 ogressed to diabetes, 647 (44%) regressed to normoglycemia (FG, <100 mg/dL), and 236 (16%) died.

130 ype 2 diabetes, as well as the regression to normoglycemia, follows a linear pattern.

131 and all six of the KC transplants maintained normoglycemia for > 100 days after the preimmunization r

132 dules was sufficient to restore and maintain normoglycemia for 21 days; the same number of free islet

133 ogels extended insulin activity, maintaining normoglycemia for 6 days in diabetic mice after a single

134 perglycemia, while GABA monotherapy restored normoglycemia for a short period.

135 recipients who have successfully maintained normoglycemia for an average of 10 years and up to 22 ye

136 ved Hb-C-containing microcapsules maintained normoglycemia for at least 8 weeks with normal glucose c

137 close to that of human islets and maintained normoglycemia for at least 9 months.

138 Microencapsulated API restored normoglycemia for more than 1 year in spontaneously diab

139 days, two of seven Lef-treated rats remained normoglycemia for more than 100 days.

140 al number of islets cultured in NGF attained normoglycemia for more than 120 days, whereas transplant

141 t graft from immune rejection and maintained normoglycemia for more than 80 days in mice with strepto

142 lycemia; and 2) the restoration of sustained normoglycemia for over 2 years in type I diabetic patien

143 uivalents (IEq) of islets achieved sustained normoglycemia for up to 60 days after islet transplantat

144 CTR increased significantly the time in near normoglycemia from 61 to 74%, simultaneously reducing hy

145 efficiency of engraftment, ability to reach normoglycemia, gain in body weight, response to high glu

146 .13 (1.09-4.17), and 2.02 (0.98-4.19) for GD/normoglycemia, GD/prediabetes, and GD/incident diabetes,

147 ess of transplanted islets in restoring near-normoglycemia, glycemic stability, and protection from s

148 ended to be higher for lower activity in the normoglycemia group but not for the prediabetes group (e

149 Compared with the normoglycemia group, children who experienced hypoglycem

150 0.001), and greater in hyperglycemia than in normoglycemia groups (0.503 vs 0.285, p = 0.026).

151 dL) and hyperglycemia (> or =140 mg/dL) with normoglycemia (>70 and <140 mg/dL).

152 xposure to hypoxia/hypoglycemia and normoxia/normoglycemia (H/H-N/N).

153 ive insulin therapy designed to produce near-normoglycemia (HbA(1c) 6.6%).

154 bin A1c [HbA1c] 5.7-6.4%), and 606 (16%) had normoglycemia (HbA1c <5.7%).

155 ogressed to diabetes, 148 (13%) regressed to normoglycemia (HbA1c, <5.7%), and 207 (19%) died.

156 eatment with DST and anti-CD154 mAb restored normoglycemia in 12 of 13 (92%) recipients.

157 marginal dose of 400 islets (n = 5) induced normoglycemia in 20%.

158 Anti-CD154 mAb monotherapy restored normoglycemia in 4 of 10 (40%) NPCC-engrafted, chemicall

159 s targeting IKKbeta resulted in reversion to normoglycemia in 50% of streptozotocin-induced diabetic

160 mmune encephalomyelitis, as well as maintain normoglycemia in a mouse model of type 1 diabetes.

161 rce of local immunosuppression would lead to normoglycemia in a streptozotocin-induced diabetic mouse

162 ulated glucagon release sufficient to attain normoglycemia in both diabetic and prediabetic stages.

163 vivo without immune suppression and induces normoglycemia in diabetic animals.

164 ze after coronary artery occlusion, prolongs normoglycemia in diabetic mice after pancreatic islet tr

165 pancreatic islet-like structures and support normoglycemia in diabetic mice.

166 erior to anti-CD20 monotherapy for restoring normoglycemia in diabetic NOD mice, providing important

167 transplantation aims to restore physiologic normoglycemia in diabetic patients with glomerulopathy a

168 d as a powerful clinical modality to restore normoglycemia in diabetic patients.

169 s, graft sizes of 700 or 500 islets restored normoglycemia in eight of nine or five of eight animals,

170 NPCC fully differentiated and restored normoglycemia in four of five diabetic NOD-scid recipien

171 al opinion collated, and the Web site of the Normoglycemia in Intensive Care Evaluation and Survival

172 ecently completed large international study, Normoglycemia in Intensive Care Evaluation and Survival

173 RCTs did not confirm benefit, and the large Normoglycemia in Intensive Care Evaluation-Survival Usin

174 Chronic ICV leptin infusion restored normoglycemia in leptin-infused rats while reducing bloo

175 cagon signaling is essential for maintaining normoglycemia in mammals.

176 cemia in NIDDM and may prevent attainment of normoglycemia in most patients who are using the convent

177 tigen-based therapies (ABTs) fail to restore normoglycemia in newly diabetic NOD mice, perhaps becaus

178 ta-cell replication, and effectively restore normoglycemia in newly diabetic NOD mice.

179 i-CD3 showed a strong synergism in restoring normoglycemia in newly hyperglycemic NOD mice compared w

180 reversible, impaired glucose tolerance with normoglycemia in pancreatic beta cells; wound healing an

181 ctional beta cells, which may help restoring normoglycemia in patients suffering from diabetes.

182 ortant goal for therapies aimed at restoring normoglycemia in patients with diabetes.

183 Restoration of normoglycemia in patients with long-standing T1D via kid

184 roven to be a successful strategy to restore normoglycemia in patients with type 1 diabetes (T1D).

185 n acceptable clinical modality for restoring normoglycemia in patients with type 1 diabetes mellitus

186 sive therapy with insulin, which establishes normoglycemia in rats with diabetes, prevents the delay

187 rved functional beta-cell mass, and restored normoglycemia in recent-onset NOD mice, even when hyperg

188 of specific CRRs critical for restoration of normoglycemia in response to glucose deficit.

189 ogic responses to secretagogues and restored normoglycemia in streptozotocin-induced diabetic severe

190 an encapsulation strategy to establish near-normoglycemia in subjects with T1D, assuming that glucos

191 Patient and pancreas (normoglycemia in the absence of any antidiabetic therapy

192 ion: insulin secretion increases to maintain normoglycemia in the face of insulin resistance and/or d

193 Combined treatment restored normoglycemia in the long term with apparent permanent r

194 Even though it is possible to achieve normoglycemia in the majority of recipients by this meth

195 pigs, these were not sufficient to maintain normoglycemia in the monkeys.

196 ting insulin enable the LID mice to maintain normoglycemia in the presence of apparent insulin insens

197 ve mechanism that enables the maintenance of normoglycemia in the presence of insulin resistance.

198 shown to be essential for the maintenance of normoglycemia in this obesogenic environment.

199 ppear essential for permanent restoration of normoglycemia in this T1DM model.

200 the full differentiation state and restoring normoglycemia in transgenic mice.

201 inhibitor, prolongs islet graft survival and normoglycemia in transplanted allogeneic diabetic mice,

202 n acceptable clinical modality for restoring normoglycemia in type 1 diabetic patients, there is a cr

203 pression has been shown to result in fasting normoglycemia in type 1 diabetic rats, although the trea

204 threshold group included convulsions (during normoglycemia) in one newborn and one death.

205 ses indicated that the risk of regression to normoglycemia increased, and the risk of progression to

206 ity and reduced insulin levels, yet maintain normoglycemia, indicative of enhanced insulin action.

207 Recovery with normoglycemia is accompanied by a significant improvemen

208 In many organisms, normoglycemia is achieved by a tight coupling of nutrien

209 In comparison to studies suggesting that normoglycemia is an easily achievable goal, our protocol

210 ng daily blood glucose (diabetes >300 mg/dL, normoglycemia <150 mg/dL).

211 POI by 30% with every 40-point increase from normoglycemia (<110 mg/dL).

212 ion, all recipients developed and maintained normoglycemia (<120 mg/dl) and stable renal function ind

213 and 3 achieved sustained insulin-independent normoglycemia (median rejection-free survivals 60 and 11

214 In normoglycemia, metformin-induced increases in BIGU is ac

215 to its usual inflammatory function, restores normoglycemia, most likely by localized bystander suppre

216 l dose islet transplant with nIgM to restore normoglycemia (n = 4).

217 n = 2), 11.1% in the obese participants with normoglycemia (n = 5), 29% in the obese participants wit

218 mice with nIgM (75 mug 3x per week) restored normoglycemia (n = 5), whereas severely diabetic mice re

219 erived insulin contributed to restoration of normoglycemia, near-total pancreatectomy resulted in hyp

220 (n = 5) pregnant women were stimulated under normoglycemia (NG), hyperglycemia (HG), Pg-LPS, and a du

221 ine aortic endothelial cells were exposed to normoglycemia (NG, 5.0 mM) or hyperglycemia (30 mM).

222 signed to truly optimize control within near normoglycemia of 3.9-10 mmol/L.

223 optimization yielded a device that restored normoglycemia of immunocompetent diabetic mice for over

224 Based on the stable normoglycemia of mice with type 1 diabetes during suppre

225 ever, during the study period, regression to normoglycemia or death was more frequent than progressio

226 nduced hypoglycemia was obtained by reaching normoglycemia or hyperglycemia for another 2 h and then

227 cultured retinal endothelial cells (REC) in normoglycemia or hyperglycemia to determine the interact

228 Medical record data from newborns with normoglycemia or transient hypoglycemia were matched wit

229 ulin sensitivity and lipids in patients with normoglycemia or type 2 diabetes.

230 ced fasting blood insulin levels, maintained normoglycemia over a 24-hour fast, and had no evidence o

231 rom WT to IL-18BP-Tg mice achieved prolonged normoglycemia (P = 0.031).

232 Normoglycemia persisted 10-80 days without other treatme

233 pancreatic endoderm cells (PECs) to maintain normoglycemia posttransplant and characterize the phenot

234 etransduced with Ang-1 vector exhibited near normoglycemia posttransplantation.

235 ory and subsequent glucose tolerance groups (normoglycemia, prediabetes, or incident diabetes) on ave

236 I diabetic patients and consequent long-term normoglycemia reestablishes native alpha-cell responses

237 insulin treatment, roughly 70% undergo near-normoglycemia remission and can maintain blood glucose w

238 Both tirzepatide and semaglutide showed normoglycemia restoration, remission of type 2 diabetes

239 mass, islets purified by filtration restored normoglycemia significantly faster than those isolated b

240 All three animals maintained normoglycemia thereafter.

241 that mice can survive sepsis by maintaining normoglycemia through ferritin's capacity to inactivate

242 e the number of recipients who could achieve normoglycemia through islet transplantation if the curre

243 unctional microorgan involved in maintaining normoglycemia through regulated secretion of insulin and

244 The transition of an individual from normoglycemia to diabetes has generally been thought to

245 known regarding timing and progression from normoglycemia to diabetes starting in young adulthood.

246 Islet transplantation can restore normoglycemia to patients with unstable type 1 diabetes

247 well studied is the initial transition from normoglycemia to prediabetes.

248 ate blood levels ranging from 5.9 +/- 1.8mM (normoglycemia) to 21 +/- 2.3mM.

249 rance) and -6 g/L (95% CI: -8.47, -3.53 g/L; normoglycemia)], triglycerides (-0.08 mmol/L; 95% CI: -0

250 with basal hepatic insulin production, near-normoglycemia under both fed and fasting conditions was

251 a milder phenotype that is characterized by normoglycemia, unless the animals are stressed.

252 All PEC recipients (n = 8) maintained normoglycemia until graft retrieval.

253 xperiments, all of the rats (n=4) maintained normoglycemia up to 210 days after transplantation.

254 ent hyperglycemia, VLBW infants can maintain normoglycemia via gluconeogenesis from glycerol and amin

255 day, the HR was 1.58 [95% CI, 0.85-2.93] for normoglycemia vs 1.08 [95% CI 0.67-1.74] for prediabetes

256 Of NOD-iBSTX4 mice, 73% had sustained normoglycemia vs. <20% of control NOD (NOD-Ctrl) mice by

257 he composite outcome among participants with normoglycemia (vs PAG met; hazard ratio [HR], 1.85 [95%

258 smallest graft size to consistently restore normoglycemia was 1,000 islets.

259 eic transplantation, time taken to return to normoglycemia was 15.4 +/- 3.6 days for nIgM-treated rec

260 cemia in transplanted mice within 1 week and normoglycemia was achieved after 5 weeks.

261 In allografts, after normoglycemia was achieved and stable luminescence inten

262 Normoglycemia was achieved at the same rate in both grou

263 Although normoglycemia was achieved earlier with tight glycemic c

264 Normoglycemia was achieved in all three groups 14 days a

265 Normoglycemia was achieved in only 1/7 mice receiving rA

266 Transient normoglycemia was achieved in treated mice two days afte

267 without the need for insulin injections, and normoglycemia was attained within 2 weeks.

268 Restoration of normoglycemia was attributable to an enhancement in key

269 ection may also occur in the hepatic artery, normoglycemia was established across the liver via a loc

270 However, when 40,000 IEQ/kg were infused, normoglycemia was lost within five days, but when 80,000

271 When portohepatic normoglycemia was maintained during POR(UPS), a 67% supp

272 conclude that in VLBW infants receiving TPN, normoglycemia was maintained during reduced glucose infu

273 Normoglycemia was maintained in 84% (57/68) of patients

274 reatic islet function to such an extent that normoglycemia was maintained in up to 75% of animals aft

275 after the pancreatectomy, and in both cases normoglycemia was maintained thereafter by the TIK.

276 t grafts, despite a marginal islet dose, and normoglycemia was maintained until graft explantation.

277 in-load dependent (r = 0.83, P < 0.001), and normoglycemia was maintained.

278 when 80,000 IEQ/kg were infused in one case, normoglycemia was more persistent.

279 Normoglycemia was not achieved with 1200 islets in the u

280 ion model, the median time needed to achieve normoglycemia was reduced from 17.0 days among untreated

281 The attainability of posttransplantation normoglycemia was significantly higher in the 4 degrees

282 The proportion of mice that achieved normoglycemia was significantly higher in the group impl

283 mal within 1 week after transplantation, and normoglycemia was sustained for at least 6 weeks without

284 Patients with prediabetes or diabetes vs normoglycemia were more likely to accurately self-percei

285 ltration and beta-cell division and restored normoglycemia when given to hyperglycemic mice at the pr

286 erior to wild-type donor islets in achieving normoglycemia when transplanted into KO diabetic recipie

287 ent was associated with prompt and sustained normoglycemia, whereas the untreated islet graft recipie

288 valents in GFS-VEGF+HGF were able to restore normoglycemia, whereas those transplanted in GFR failed

289 from 2 cohorts of adults with prediabetes or normoglycemia who were free of CVD at baseline visit: th

290 so appears that perioperative maintenance of normoglycemia will become a valid performance measure fo

291 nctionality in vivo: recipient mice achieved normoglycemia with a comparable tempo, whereas loss of g

292 Subjects who maintained normoglycemia with a low AIR had an increased proinsulin

293 , but they exhibited a more durable state of normoglycemia with greater insulin reserves.

294 um islet transplantation using PPCN restores normoglycemia with minimal exogenous insulin requirement

295 posures (type 2 diabetes [T2D], prediabetes, normoglycemia) with outcomes (atherosclerotic cardiovasc

296 Islet cell transplantation resulted in normoglycemia within 24 hr.

297 ransplantation into the scaffold resulted in normoglycemia within 3 days and for the duration of the

298 vels in both models, and all animals reached normoglycemia within the first days after transplantatio

299 At term equivalent age, normoglycemia without any insulin treatment was found in

300 ix portal vein experiments, animals achieved normoglycemia without exogenous insulin.