ライフサイエンスコーパス: insulin

1 ting neuroendocrine signaling (e.g., leptin, insulin).

2 tin has anti-diabetic activity comparable to insulin.

3 an "artificial pancreas" for the release of insulin.

4 , and 3) reduces metabolic clearance rate of insulin.

5 BMI (52.18 vs. 40.11, p = 0.001), insulin (19.35 vs. 8.80 mIU/L, p < 0.001) and HOMA-IR in

6 blood triglyceride (103%), glucose (68%) and insulin (59%) following identical meals.

7 roviding glycemic control without increasing insulin, ABA extract modulates the metabolic activity of

8 e training intervention increased whole-body insulin action by 26% and insulin-stimulated leg glucose

9 Insulin action in adipose tissue is crucial for whole-bo

10 with IR to serve as a feedback regulator of insulin action in control of liver metabolism.

11 that manifests with diet-induced obesity, as insulin action is preserved to protect fundamental energ

12 g reciprocity between SkM AMPK signaling and insulin action that manifests with diet-induced obesity,

13 sma insulin response to offset the defect in insulin action to maintain normal glucose tolerance.

14 egulate organismal metabolism by controlling insulin action, lipolysis, and mitochondrial respiration

15 here is compelling evidence that deregulated insulin activities or cerebral insulin resistance contri

16 MNDC, suggesting that DMNDC does not inhibit insulin aggregation.

17 evels of Gremlin 1 in key target tissues for insulin and also measured tissue and serum levels in sev

18 ed control on whole-body and skeletal muscle insulin and anabolic sensitivity.

19 p conditions (study 2), the change in plasma insulin and glucagon concentrations was comparable in su

20 provide insight into cross-talk between the insulin and Hippo pathways.

21 Insulin and PP responses may mediate the independent eff

22 ve aimed to reduce the levels of circulating insulin and to abrogate insulin signalling in cancer cel

23 waist circumference, blood lipids, glucose, insulin, and blood pressure were measured.

24 A key regulator of insulin- and exercise-stimulated glucose uptake and GLUT

25 Glucagon and its partner insulin are dually linked in both their secretion from i

26 Our results identify insulin as a previously undescribed suppressor of YAP ac

27 These findings expand the current models of insulin binding to its receptor and of its regulation.

28 (RYGB) was associated with a higher rate of insulin cessation (71.7%) than sleeve gastrectomy (SG; 6

29 total weight loss and demographic variables, insulin cessation following surgery was comparable for R

30 Insulin complexes were homogenously incorporated into PL

31 ations for T2D, fasting glucose, and fasting insulin, comprising 65, 43, and 13 single nucleotide pol

32 plasma glucagon and a decrease in the plasma insulin concentration compared with placebo.

33 togenesis (+232%) due to reductions in serum insulin concentrations (-53%) and hepatic citrate syntha

34 Low-glucose and -insulin conditions, associated with ketogenic diets, can

35 glucose-stimulated Ca(2+) flux, and reduced insulin content associated with loss of eIF4E, the mRNA

36 merging technologies, namely, self-regulated insulin delivery and cell replacement therapies, hydroge

37 A series of glucose-responsive insulin delivery mechanisms and devices have been report

38 Glucose-responsive insulin delivery systems that mimic pancreatic endocrine

39 sulin resistance, explaining why short-term, insulin-dependent glucose utilization does not promote i

40 We tested whether frequent insulin dose adjustments guided by an automated artifici

41 retion of certain anabolic hormones, such as insulin, during obesity.

42 and growth essentially depend on the hormone insulin engaging its receptor.

43 CD4 responses in NOD mice are dominated by insulin epitope B:9-23 (InsB(9-23)) specificity, and mut

44 a better glucose-lowering effect than native insulin, even with a much lower dose and less frequent i

45 eld focused on how to correct the defects in insulin exocytosis.

46 Generating insulin-expressing cells in vitro is no exception, with

47 inds to and stabilizes MafA, which activates insulin expression.

48 infections, 47 (31.1%) vs 42 (28.3%) needed insulin for glucose control, and 5 (3.3%) vs 9 (6.1%) ex

49 y insulin icodec as compared with once-daily insulin glargine U100 in patients who had not previously

50 erefore, we histologically assessed amylase, insulin, glucagon, lipase, and/or trypsinogen in 78 orga

51 it is unclear what regulates localization of insulin granules and their interactions with the PM with

52 Higher levels of circulating insulin have been associated with increased cancer risk

53 Other parameters, such as glucose, BMI, insulin, HOMA-IR and lipid profile, were also investigat

54 having an initial autoantibody only against insulin (IAA-first) or GAD (GADA-first) by unsupervised

55 igate the efficacy and safety of once-weekly insulin icodec as compared with once-daily insulin glarg

56 It is known that growth factors such as insulin, IGF-1 and HGF support beta cell growth and surv

57 le hormone (JH) and the two nutrient sensors insulin/IGF signaling (IIS) and target of rapamycin comp

58 In well-fed males, insulin-like (insulin/IGF-1 signaling [IIS]) and transforming growth f

59 The Insulin/IGF-1 signalling (IIS) pathway plays an essentia

60 e development of autoantibodies against (pro)insulin in early childhood.

61 s with type 2 diabetes (T2D) fail to secrete insulin in response to increased glucose levels that occ

62 w that Arrdc3 is differentially regulated by insulin in vivo in mice undergoing euglycemic-hyperinsul

63 creas graft survival at 52 weeks, defined by insulin independence, was 21 (100%) in the control group

64 Interestingly, insulin-induced hypoglycemia increases ARC POMC neuron a

65 but also is permissive for the normal CRR to insulin-induced hypoglycemia.

66 from human and animal studies indicate that insulin influences cerebral bioenergetics, enhances syna

67 d ages 6.5-11.5 years) with fasting glucose, insulin, insulin resistance, beta-cell function, and adi

68 Also, switchable ON/OFF release of insulin is achieved highlighting an autonomous glucose-r

69 racellular sequestration and mobilization by insulin is achieved, in part, through utilizing a region

70 hers are exposed to higher concentrations of insulin, leptin, and, to a lesser extent, CRP.

71 ort displayed a significant increase in mean insulin levels and a trend towards higher C-peptide leve

72 In well-fed males, insulin-like (insulin/IGF-1 signaling [IIS]) and transfo

73 hlighted an enrichment of the "Regulation of Insulin-like Growth Factor (IGF) transport and uptake by

74 -ERalphaKO along with higher serum levels of insulin-like growth factor (IGF)-1 as well as IGF-bindin

75 Third, we uncovered that insulin-like growth factor 1 (IGF1) is produced by tumor

76 f GH excess including significantly elevated insulin-like growth factor 1 levels, larger weight and b

77 etibial myxoedema) involves the synergism of insulin-like growth factor 1 receptor (IGF1R) with TSHR

78 physiological hypertrophy induced by IGF-1 (insulin-like growth factor 1).

79 ion and loss-of-function mutations affecting insulin-like growth factor 1, fibroblast growth factor r

80 Growth Factor (IGF) transport and uptake by Insulin-like Growth Factor Binding Proteins (IGFBPs)" ro

81 ransforming Growth Factor Beta (TGFbeta) and insulin-like growth factor-1 (IGF-1) are known to promot

82 acronutrients, milk contains calcium and the insulin-like growth factor-1 that are of major relevance

83 IGF-1 (insulin-like growth factor-1) is markedly decreased in n

84 (lipid X receptor), the growth factor IGF1 (insulin-like growth factor-1), and the splenic red pulp

85 sion, including an increase in stress marker insulin-like growth factor-binding protein 1 (IGFBP-1),

86 tissue inhibitor of metalloproteinase-2 and insulin-like growth factor-binding protein 7 was measure

87 of tissue inhibitor of metalloproteinase-2 x insulin-like growth factor-binding protein 7 was poor wi

88 We found that decima influences insulin-like peptide transcription in the GABA receptor

89 involved in homeostatic control, and express insulin-like peptides with well-established roles in reg

90 Bivalent antireceptor antibodies can elicit insulin-like signaling by mutant INSR in cultured cells,

91 Insulin measurements are not advised for cardiometabolic

92 ded miRNAs with functions in skeletal muscle insulin metabolism (miR-106b and miR-20b-5p) and miRNAs

93 iRNAs with functions in both skeletal muscle insulin metabolism and cell cycle regulation in endocrin

94 ulin sensitivity according to the prevailing insulin milieu.

95 ) play a key role in mediating the action of insulin on cell growth and the development of diabetes.

96 There was no difference in insulin or insulin resistance between the two PCOS cohor

97 he synchronization mechanism, measurement of insulin output would be more direct evidence.

98 omas are rare, benign, slowly proliferating, insulin-producing beta cell tumors that provide a molecu

99 iabetes (T1D) arises from the destruction of insulin-producing beta-cells by islet-specific autoreact

100 on-obese diabetic (NOD) mice, protecting the insulin-producing beta-cells from destruction.

101 The loss of insulin-producing beta-cells is the central pathological

102 1 diabetes (T1D) is an autoimmune disease of insulin-producing beta-cells.

103 ted in vivo with a mimic nanodrug had higher insulin-producing functionality compared to controls.

104 The primary end point was endogenous insulin production, as assessed according to the area un

105 d by insulin resistance with late failure of insulin production, severe hyperglycemia/diabetes, lipod

106 r glucose metabolism in a different way from insulin, promoting DNL and impeding TAG synthesis.

107 tomated decision support tool for optimizing insulin pump settings was non-inferior to intensive insu

108 type 1 diabetes, aged 10-21 years and using insulin pump therapy (ClinicalTrials.gov no.

109 made in the past decade in understanding the insulin receptor and its signalling pathways in cancer,

110 However, receptor-level IR (e.g., insulin receptor pathogenic variants, INSR) causes hyper

111 e also report increased concentration of the insulin receptor substrate-1 (IRS-1) in L1CAM(+) exosome

112 Moreover, extracellular SQSTM1 binds to insulin receptor, which in turn activates a nuclear fact

113 ough reduced tyrosine kinase activity of the insulin receptor; however, its impact on pancreatic beta

114 ibodies thus improve IR in an acute model of insulin receptoropathy, but these findings imply a narro

115 effect of the selective inhibitor HFI-419 on insulin-regulated aminopeptidase (EC 3.4.11.3) in the ra

116 Fine-tuning of insulin release from pancreatic beta-cells is essential

117 ensitive K(+) (K(ATP) ) channels to increase insulin release.

118 uded reductions in metabolites implicated in insulin resistance (glutamate, -29%; P=1.5x10(-55); dime

119 zed 24 adults with obesity and mild-moderate insulin resistance (homeostatic model assessment of insu

120 Body weight, insulin resistance (homeostatic model assessment of insu

121 have identified genetic loci associated with insulin resistance (IR) but pinpointing the causal genes

122 BACKGROUNDPostreceptor insulin resistance (IR) is associated with hyperglycemia

123 Insulin resistance (IR) precedes the development of type

124 With the development of insulin resistance (IR), there is a compensatory increas

125 resistance (homeostatic model assessment of insulin resistance [HOMA-IR] between 2.0 and 8.0) to wee

126 resistance (homeostatic model assessment of insulin resistance [HOMA-IR]), trunk-to-leg fat ratio, r

127 LincIRS2 loss causes elevated blood glucose, insulin resistance and aberrant glucose output in lean m

128 ocyte lipolysis and simultaneously triggered insulin resistance and hyperglycemia.

129 in both adipose tissue and ileum, leading to insulin resistance and impaired glucose and lipid metabo

130 iabetes onset, HbA(1c), BMI, and measures of insulin resistance and insulin secretion) to cluster adu

131 ial therapeutic targets for the treatment of insulin resistance and type 2 diabetes.

132 thought to be related to the development of insulin resistance and type 2 diabetes.

133 Stress hyperglycemia and insulin resistance are evolutionarily conserved metaboli

134 ial for whole-body glucose homeostasis, with insulin resistance being a major risk factor for metabol

135 There was no difference in insulin or insulin resistance between the two PCOS cohorts.

136 t deregulated insulin activities or cerebral insulin resistance contributes to neuroinflammation and

137 We found that insulin resistance correlates significantly with a shift

138 ously linked to fasting glycaemic traits and insulin resistance in genome wide association studies.

139 reduced phenylalanine flux without affecting insulin resistance in haemodialysis patients.

140 a critical role of SIRT1 in inflammation and insulin resistance in hyperinsulinemia.

141 SP8 rs2334499 risk variant with hypothalamic insulin resistance in men.

142 tribute to reduced amino acid metabolism and insulin resistance in MHD patients.

143 infection and other stresses and can promote insulin resistance in target tissues.

144 els were strongly associated with markers of insulin resistance in vivo (euglycemic clamps and HOMA o

145 injections, in non-obese diabetic mice with insulin resistance symptoms.

146 Hypomagnesemia has been linked to insulin resistance through reduced tyrosine kinase activ

147 Adipocyte-extrinsic insulin resistance was observed in liver and muscle.

148 causes the teeny phenotype, characterized by insulin resistance with late failure of insulin producti

149 tance in vivo (euglycemic clamps and HOMA of insulin resistance), and the presence of nonalcoholic fa

150 on but impairs beta-cell function, 2) causes insulin resistance, and 3) reduces metabolic clearance r

151 increased energy expenditure and ameliorated insulin resistance, associated with a smaller adipocyte

152 5-11.5 years) with fasting glucose, insulin, insulin resistance, beta-cell function, and adiponectin

153 y, this metabolic remodeling did not improve insulin resistance, but induced fibrogenic genes and inf

154 with obesity, arrhythmias, cardiac ischemia, insulin resistance, etc.

155 s must precede the insulin stimulus to cause insulin resistance, explaining why short-term, insulin-d

156 dministration of UAB126 ameliorated obesity, insulin resistance, hepatic steatosis, and hyperlipidemi

157 iber have been associated with lower risk of insulin resistance, hyperinsulinemia, and inflammation,

158 In patients with NASH and diabetes or insulin resistance, low AGER1 levels were associated wit

159 ter amplification processes that encompasses insulin resistance, lysosomal defects, decreased surviva

160 d with development of metabolic syndrome and insulin resistance, manifests when triglyceride (TG) inp

161 These mice also exhibited insulin resistance-related abnormalities of energy metab

162 tribute to a state of local inflammation and insulin resistance.

163 unction, giving rise to "lipodystrophy-like" insulin resistance.

164 reased in males indicating susceptibility to insulin resistance.

165 s not directly contribute to skeletal muscle insulin resistance.

166 lites known to contribute to skeletal muscle insulin resistance.

167 ue (AT) inflammation contributes to systemic insulin resistance.

168 nd protects mice from developing obesity and insulin resistance.

169 as an attractive target against obesity and insulin resistance.

170 (Roux-en-Y gastric bypass [RYGB]) surgery on insulin resistance.

171 enotypes without markedly causing peripheral insulin resistance.

172 pendent glucose utilization does not promote insulin resistance.

173 to reduce systemic inflammation and reverse insulin resistance.

174 liorates glucose tolerance, protects against insulin-resistance onset and remarkably reverses already

175 and remarkably reverses already established insulin-resistance.

176 Both are commonly associated with insulin resistant diabetes, usually accompanied by dysli

177 We determined that in insulin-resistant animals, portal vagal afferents failed

178 The GLP-1 system is known to be impaired in insulin-resistant conditions, and we sought to understan

179 was undertaken in a mouse model that has an insulin-resistant heart and is susceptible to AF.

180 ant, KK mice; and hyperglycemic and markedly insulin-resistant KKAy mice were used for ozone exposure

181 ry NR supplementation in middle-aged, obese, insulin-resistant men affects mitochondrial respiration,

182 ive C57BL/6J mice; hyperglycemic, but mildly insulin-resistant, KK mice; and hyperglycemic and marked

183 A declining first-phase insulin response (FPIR) is associated with positivity fo

184 ere is a compensatory increase in the plasma insulin response to offset the defect in insulin action

185 etabolism and circadian rhythm were noted in insulin-responsive tissues.

186 Dapagliflozin treatment in combination with insulin resulted in a dose-dependent increase in haemato

187 Glucose-stimulated insulin secretion (GSIS) is regulated by calcium (Ca(2+)

188 female islets, T enhanced glucose-stimulated insulin secretion (GSIS).

189 correlated with decreased glucose-stimulated insulin secretion (GSIS).

190 ugh targeting several critical regulators of insulin secretion and beta cell proliferation.

191 ometric test) enriched in pathways linked to insulin secretion and extracellular matrix-receptor inte

192 hyperglycemia for 72 h 1) increases absolute insulin secretion but impairs beta-cell function, 2) cau

193 ic pathways necessary for glucose stimulated insulin secretion for protection from viral lysis.

194 Galanin signalling suppresses insulin secretion in animal models (but not in humans),

195 n to result in truncated RIMS2 and decreased insulin secretion in mammalian cells.

196 ed the effect of diet-induced weight loss on insulin secretion in people with obesity who did not imp

197 d Ca(2+) current in mediating Ca(2+)-induced insulin secretion in response to ER stress.

198 r INS-1E, a beta-cell line, to repurpose the insulin secretion machinery, which enables the glucose-d

199 ations responding to CDC with an increase in insulin secretion under control conditions were less imp

200 Unlike GSIS, such insulin secretion was blocked with mitochondrial antioxi

201 -1, 3) additive to supra-additive effects on insulin secretion when combining SU+GIP and SU+GLP-1, re

202 es coordinated electrical activity (and thus insulin secretion) in the rest of the islet.

203 BMI, and measures of insulin resistance and insulin secretion) to cluster adult-onset diabetes patie

204 cose tolerance, increased glucose-stimulated insulin secretion, and hyperglucagonemia.

205 cell transcription factor MAFA and abolished insulin secretion, both in vitro in primary human islets

206 ) promotes NGSIS, but not glucose-stimulated insulin secretion, by increasing mitochondrial proton le

207 these channels, including but not limited to insulin secretion, cardiac protection, and blood flow re

208 icrotubule turnover, causing increased basal insulin secretion, depleting insulin vesicles from the c

209 Kisspeptin modulates glucose-stimulated insulin secretion, food intake and/or energy expenditure

210 These functions, which include insulin secretion, gastric emptying, satiety, and the he

211 We uncovered deficits in insulin secretion, partly due to reduced mitochondrial o

212 n without induction of cell death or loss of insulin secretion, suggesting that appropriate levels of

213 ithout a negative impact islet viability and insulin secretion.

214 y shown that primary cilia directly regulate insulin secretion.

215 ose tissue for storage and triggered greater insulin secretion.

216 oint of glucose-stimulated Ca(2+) influx and insulin secretion.

217 letion of insulin SG content and a defect in insulin secretion.

218 betes via potentiation of glucose-stimulated insulin secretion.

219 G protein subunit beta 5 (Gnb5) knockout on insulin secretion.

220 tion of the Delta/Notch pathway in beta-cell insulin secretion.

221 and second-phase dynamic glucose-stimulated insulin secretion.

222 TrkB.T1 show impaired glucose tolerance and insulin secretion.

223 IPF5 disruption by decreasing the demand for insulin secretion.

224 Within the pancreatic beta-cells, insulin secretory granules (SGs) exist in functionally d

225 ole in regulating Zn(2+) accumulation in the insulin secretory granules of pancreatic beta cells.

226 cebo-controlled trial in 126 overweight, non-insulin sensitive (HOMA-IR >=1.30), Chinese, Malay, and

227 y syndrome (PCOS) have been shown to be less insulin sensitive compared with control (CON) women, ind

228 Normoglycemic and insulin-sensitive C57BL/6J mice; hyperglycemic, but mild

229 ereby counteracts inflammation of peripheral insulin-sensitive tissues and, thus, obesity-associated

230 uria, renal plasma flow (RPF), fat mass, and insulin sensitivity (M/I).

231 mpared with CON:CR, eTRF improved whole-body insulin sensitivity [between-group difference (95% CI):

232 auer recovery and adult lifespan by altering insulin sensitivity according to the prevailing insulin

233 e-body glucose clearance and skeletal muscle insulin sensitivity along with enhanced autophagy (incre

234 Both groups showed similar levels of insulin sensitivity and beta-cell function.

235 improved glucose tolerance, despite impaired insulin sensitivity and enhanced pyruvate-mediated gluco

236 tformin effects result in the improvement of insulin sensitivity and glucose utilization in extrahepa

237 ed gene expressions, fasting glucose levels, insulin sensitivity and restored pancreatic islet cell m

238 ly produced acyl-ghrelin not only influences insulin sensitivity but also is permissive for the norma

239 rginal, improvements in revised Quantitative Insulin Sensitivity Check Index (QUICKI) (0.004) and pla

240 n in people with obesity who did not improve insulin sensitivity despite marked (~20%) weight loss.

241 n reducing body weight, but not on improving insulin sensitivity in both diet-induced obese and lean

242 cemic clamp studies show that BAM15 improves insulin sensitivity in multiple tissue types.

243 no statistically significant improvements in insulin sensitivity in the FMT group compared to the pla

244 ese lipids appear to be more negative toward insulin sensitivity than others.

245 This leads to increased hepatic insulin sensitivity with increased phosphorylation of FO

246 sp8 in governing hypothalamic Jnk signaling, insulin sensitivity, and systemic glucose tolerance was

247 hip between TRLP subfractions and whole-body insulin sensitivity, hepatic and visceral fat, and SCD-1

248 The primary outcome of the study was insulin sensitivity, using the Matsuda index.

249 thereby improving adipose tissue and hepatic insulin sensitivity.

250 ed metabolic indices, including promotion of insulin sensitivity.

251 porters in the small intestine and improving insulin sensitivity.

252 on in prediabetic rats without alteration in insulin sensitivity.

253 phenotypes indicating differential roles in insulin sensitization, suggesting mechanisms bridging th

254 roach to gaining insight and suggest that an insulin sensitizer may alleviate ER stress associated wi

255 limited weight-lowering efficacy and minimal insulin sensitizing action.

256 develop diabetes due to severe depletion of insulin SG content and a defect in insulin secretion.

257 s present both at the plasma membrane and on insulin SGs.

258 The resulting SC-alpha cells do not express insulin, share an ultrastructure similar to cadaveric al

259 rvival strategy that is under the control of insulin signaling and Foxo by regulating energy metaboli

260 iological role of BCKAs in regulating muscle insulin signaling and function.

261 ic benefits in vivo, wherein the dynamics of insulin signaling and receptor recycling are more comple

262 Here, we study the roles of GABA and insulin signaling in starvation-dependent modulation of

263 PQM-1 is required for the longevity of insulin signaling mutants, but surprisingly, loss of PQM

264 normal signaling and hyperstimulation of the insulin signaling pathway.

265 fespan-extending systemic down-regulation of insulin signaling results in improved late-life ejaculat

266 analyses, we examined associations of brain insulin signaling with diabetes, AD, and level of cognit

267 density, and no other associations of brain insulin signaling with neuropathology were observed.

268 findings suggest that Slug is stabilized by insulin signaling, and that it promotes lipogenesis by r

269 networks associated with growth hormone and insulin signaling, including induction of suppressor of

270 ors and a nodal cytosolic kinase involved in insulin signaling.

271 lipid metabolites to protect skeletal muscle insulin signalling following 7 days' HFHC diet.

272 evels of circulating insulin and to abrogate insulin signalling in cancer cells.

273 metabolites known to disrupt skeletal muscle insulin signalling in sedentary and obese individuals.

274 s suggest that 1 year of treatment with oral insulin slows metabolic deterioration in individuals at

275 to previous reports, PAK1 is dispensable for insulin-stimulated glucose uptake in mouse muscle.

276 over, while PAK1 KO muscles displayed normal insulin-stimulated glucose uptake in vivo and in isolate

277 Insulin-stimulated glucose uptake partly relies on PAK2

278 ucose uptake in vivo and in isolated muscle, insulin-stimulated glucose uptake was slightly reduced i

279 BC1D4-RAB10 signaling module is required for insulin-stimulated GLUT4 translocation to the PM, althou

280 lucose uptake by 53% together with increased insulin-stimulated leg blood flow and a more oxidative m

281 creased whole-body insulin action by 26% and insulin-stimulated leg glucose uptake by 53% together wi

282 sicles to the plasma membrane in response to insulin stimulation.

283 ochondrial oxidative stress must precede the insulin stimulus to cause insulin resistance, explaining

284 ly undescribed suppressor of YAP activity in insulin target cells and provide insight into cross-talk

285 Thus, Arrdc3 is an insulin target gene, and ARRDC3 protein directly interac

286 pump settings was non-inferior to intensive insulin titration provided by physicians from specialize

287 In contrast, glucose was required for insulin to increase mitochondrial oxidants.

288 Exposure to PM2.5 impaired glucose and insulin tolerance and reduced energy expenditure and 18F

289 , respiratory quotient, and fasting glucose, insulin, total and high-density lipoprotein (dHDL) chole

290 % CI 1.01-1.89, p = 0.04) versus neonates of insulin-treated mothers.

291 ts who had not previously received long-term insulin treatment and whose type 2 diabetes was inadequa

292 Insulin treatment strategies vary significantly, irrespe

293 Insulin use was lower with golimumab than with placebo.

294 Results for insulin users were in the same direction, but the overal

295 onset were unabated, despite a blocked anti-insulin vaccine response in SAP-deficient NOD mice.

296 increased basal insulin secretion, depleting insulin vesicles from the cytoplasm, and impairing GSIS.

297 l for enhancing survival while production of insulin was important for the antidiabetic effect.

298 Insulin was measured by chemiluminescence, and fasting g

299 The aggregation kinetics of insulin were not significantly affected in the presence

300 cement to the biophysical stability of human insulin while maintaining its potency.