ライフサイエンスコーパス: insulin

1 betes receiving multiple daily injections of insulin.

2 een successfully demonstrated on the protein insulin.

3 Similar results were obtained for insulin.

4 ay, they were administered either intranasal insulin (60 IU) or placebo, following which they partici

5 w that hepatic ILK deletion has no effect on insulin action in lean mice but sensitizes the liver to

6 To determine the role of ILK in hepatic insulin action in vivo, male C57BL/6J ILK(lox/lox) mice

7 d CRY1 degradation as an important target of insulin action on glucose homeostasis.

8 during a clamp, reaffirming that the site of insulin action to control EGP is extrahepatic.

9 ; activation of glucokinase was restored and insulin action was improved, stimulating muscle glucose

10 of resistance to the antilipolytic effect of insulin (adipose tissue IR [Adipo-IR]) in a large group

11 found to have chaperone-like activity in an insulin aggregation assay, which we propose facilitates

12 Intranasal insulin also increased circulating cortisol levels (F=12

13 added saccharide units to insulin to create insulin analogs with affinity for both the insulin recep

14 osylated proteins, a principle used to endow insulin analogs with glucose responsivity.

15 ormones and previous studies of glycosylated insulin analogues, this natural glycosylation may provid

16 modified the association of uMg with fasting insulin and fat mass in a general population.

17 In conclusion, insulin and glucose exposure acutely alter the DNA methy

18 ocus are associated with plasma adiponectin, insulin and HDL cholesterol concentrations, obesity, and

19 1K genetic variant in relation to changes in insulin and HOMA-B (P-interaction = 0.006 and 0.002, res

20 aternal protein intake and offspring fasting insulin and homeostasis model assessment of insulin resi

21 n sensitivity, and low circulating levels of insulin and insulin-like growth factor 1 (IGF-1).

22 Given the importance of insulin and its related peptide hormones and previous st

23 ombined action of paracrine factors, such as insulin and somatostatin, and juxtacrine signals between

24 s mellitus for >10 years, 58% were receiving insulin, and 84% were taking angiotensin-converting enzy

25 nduced a greater increase in plasma glucose, insulin, and GIP concentrations after surgery, which was

26 and lactoferrin decreased plasma leptin and insulin, and lactalbumin increased peptide YY.

27 spillover into circulation after intranasal insulin application was mimicked by an intravenous insul

28 ages of disease indicated by markers such as insulin autoantibodies.

29 These cells respond to an insulin B-chain (InsB) epitope presented by the HLA-DQ8

30 the influence of a fourth disulfide bond on insulin bioactivity.

31 n application was mimicked by an intravenous insulin bolus on placebo day.

32 It enhances the secretion of insulin, but attenuates insulin's metabolic actions in t

33 groups showed similar reductions in insulin, insulin C-peptide, glycated hemoglobin, and homeostasis

34 After being conjugated with the glucosamine, insulin can efficiently bind to RBC membranes.

35 leads to an impaired hippocampal response to insulin, caused by altered IRS-1 and PTEN (phosphatase a

36 ectronic medical record, recommendations for insulin changes were entered in a vGMS note, which could

37 ys post-injection, total insulin content and insulin:chromogranin A immunoreactivity were reduced by

38 Insulin clamp studies have shown that the suppressive ac

39 ssibility that septic patients have impaired insulin clearance, which could increase their susceptibi

40 [U-(13)C]palmitate infusion to determine the insulin concentration needed to suppress palmitate flux

41 amines in IUGR fetuses persistently inhibits insulin concentrations and secretion.

42 eficient in GATA6 activity display decreased insulin content and impaired insulin secretion.

43 s was preserved 8 days post-injection, total insulin content and insulin:chromogranin A immunoreactiv

44 Islet size and insulin content in pancreata of A2AAR-deficient mice wer

45 n, improved glucose tolerance, and increased insulin content.

46 We propose that under normal conditions, insulin decreases dynein binding to APC to stimulate min

47 To determine whether insulin degludec is noninferior or superior to insulin g

48 ate whether day-and-night hybrid closed-loop insulin delivery can improve glucose control while allev

49 beta-cells are unable to adapt to peripheral insulin demands.

50 This recruitment is activated by an insulin-dependent pathway and therefore responds to fed/

51 The risk associated with insulin detemir was not significantly elevated (HR, 1.17

52 the sole presence of diabetes not requiring insulin did not imply an increased thromboembolic risk.

53 heroids, while the latter, in the absence of insulin, did not consume glucose as efficiently.

54 as challenged in a report demonstrating oral insulin does not prevent T1D in NOD mice, possibly due t

55 cantly suppressed, both temporally and in an insulin dose response.

56 ion in lean mice but sensitizes the liver to insulin during the challenge of HF feeding.

57 y, we demonstrate that ectopic expression of insulin epitope B:9-23 (InsB9-23) by thymic APCs is insu

58 The increase in insulin exocytosis was attributed mainly to an enhanced

59 alpha and beta cells producing glucagon and insulin for glucose homeostasis.

60 Recently, insulin/FOXO signaling has been implicated in the regula

61 lity, metabolic outcome, graft survival, and insulin-free survival after salvage IAT were not differe

62 sulin degludec is noninferior or superior to insulin glargine U100 in reducing the rate of symptomati

63 ucose and plasma gut-hormone concentrations [insulin, glucagon, ghrelin, cholecystokinin, gastric inh

64 Based on review of the insulin/glucose chart in the electronic medical record,

65 e by effective prevention and control of the insulin homeostasis.

66 GF-1) and insulin resistance (i.e. decreased insulin/IGF-1) have been reported in other neurodegenera

67 ve to chronic AbetaO exposure, which reduced insulin/IGF1 expression.

68 hyperglycemic conditions nor the absence of insulin in culture medium were sufficient to promote cel

69 in vivo oligomeric state and conformation of insulin in its storage granules in the pancreas are not

70 cells are functionally programmed to release insulin in response to changes in plasma glucose concent

71 f (two weeks) HFD on glucose uptake (GU) +/- insulin in single fibers that were also characterized fo

72 on in explanted wing discs in the absence of insulin, incidentally providing novel insight into the h

73 Insulin increased DNA methylation in the gene body of DA

74 stigated the mechanism by which glucagon and insulin increased FGF21 gene transcription in primary he

75 gerated spike in triglycerides, glucose, and insulin-increases cardiovascular disease risk by inducin

76 r exclusion, leading to Baf60c induction and insulin-independent AKT activation.

77 echanistically, we find that mutp53 augments insulin-induced AKT1 activation by binding and inhibitin

78 monitoring (CGM) and continuous subcutaneous insulin infusion can be used to improve the treatment of

79 nsulin pump therapy (continuous subcutaneous insulin infusion; CSII) in patients with type 1 diabetes

80 Insulin inhibits hepatic glucose production and promotes

81 n pump therapy or with multiple (>/=4) daily insulin injections.

82 Insulin insensitivity and adipokine abnormalities (the h

83 The groups showed similar reductions in insulin, insulin C-peptide, glycated hemoglobin, and hom

84 Metabolic variables, including glucose, insulin, insulin-like growth factor I, triglycerides, ch

85 Impaired insulin/insulin-like growth factor-1 signalling (IGF-1)

86 explain why GLP-1 secretion, but not that of insulin, is activated by these secretagogues in vivo.

87 ssociated with an increase in fasting plasma insulin level and risk of type 2 diabetes.

88 Of note, Ad36E4ORF1 significantly reduced insulin levels in db/db and DIO mice.

89 tolerance and circulating leptin, GLP-1, and insulin levels were reduced.

90 d insulin release in islets but also lowered insulin levels while increasing blood glucose in vivo.

91 in adult males via interaction with relaxin/insulin-like family peptide receptor 2 (RXFP2).

92 A focus on reversible mechanisms identified Insulin-like growth factor (IGF1) deficiency with inadeq

93 y, and low circulating levels of insulin and insulin-like growth factor 1 (IGF-1).

94 Insulin-like growth factor 2 (IGF2) is the major fetal g

95 Inhibition of the insulin-like growth factor I receptor (IGF-IR) is a new

96 bolic variables, including glucose, insulin, insulin-like growth factor I, triglycerides, cholesterol

97 st the effects of systemic administration of insulin-like growth factor II (IGF-II), a polypeptide th

98 inases, including the highly cancer relevant insulin-like growth factor type 1 receptor (IGF-1R).

99 Insulin-like growth factor type 2 (IGF2) receptor (IGF2R

100 , SP and its metabolites in combination with insulin-like growth factor-1 are shown to promote the co

101 mmunohistochemical positivity for p4E-BP1 or insulin-like growth factor-1 receptor was statistically

102 ng roles for cancer progression, such as the insulin-like growth factors.

103 In silico target prediction identified that insulin-like peptides 7 and 8 (ilp7 and ilp8) are putati

104 response to photoreceptor-EGF, glia produce insulin-like peptides, which induce lamina neuronal diff

105 ng those that secrete some of the Drosophila insulin-like peptides.

106 In contrast, the MHC stable insulin mimetope (InsB9-23 R22E) efficiently deletes ins

107 olerogenic vaccination with a strong agonist insulin mimetope in type 1 diabetes.

108 Glucose-responsive delivery of insulin mimicking the function of pancreatic beta-cells

109 Our results indicate that insulin misregulation underlies the circadian and cognit

110 ineage tracing confirmed that LDB1-depleted, insulin-negative beta cells express NEUROG3 but do not a

111 s have shown that the suppressive actions of insulin on endogenous glucose production (EGP) are marke

112 Importantly, insulin prevented the AbetaO-induced inhibition of AMPK.

113 e of the loss of only a single cell type-the insulin-producing beta-cell.

114 ss of the mutation or diabetes status, these insulin-producing cells are immature, a common downfall

115 Type 1 diabetes (T1D) manifests when the insulin-producing pancreatic beta cells are destroyed as

116 e 1 diabetes is characterized by the loss of insulin production caused by beta-cell dysfunction and/o

117 Pancreatic beta-cell insulin production is orchestrated by a complex circuitr

118 vity and induce Sox2 and Ngn3 expression and insulin production.

119 eration of ovalbumin-specific T cells in rat insulin promoter-membrane-bound ovalbumin transgenic mic

120 Daily injections of insulin provide lifesaving benefits to millions of diabe

121 The benefit of initiation of insulin pump therapy (continuous subcutaneous insulin in

122 Type 1 diabetes treated with insulin pump therapy or with multiple (>/=4) daily insul

123 o regulate the transcriptional activation of insulin receptor (InR) and adipose lipase brummer (bmm).

124 e insulin analogs with affinity for both the insulin receptor (IR) and mannose receptor C-type 1 (MR)

125 In primary neurons, apoE4 interacts with insulin receptor and impairs its trafficking by trapping

126 d expression of the key downstream messenger insulin receptor substrate-1 phosphorylated at serine re

127 es signals from multiple receptors including insulin receptors, pathogen-associated molecular pattern

128 ut4 and that this mechanism is essential for insulin-regulated glucose homeostasis.

129 These splicing regulators play key roles in insulin release and beta cell survival, and their dysfun

130 Rs) and have opposing physiological roles in insulin release and glucose homeostasis.

131 in beta-cells of adult mice greatly impairs insulin release and glucose tolerance in mice fed with a

132 ist 5d not only blocked exendin-4-stimulated insulin release in islets but also lowered insulin level

133 e main study group (n = 389) had first-phase insulin release on an intravenous glucose tolerance test

134 possible mechanism underlying KCC2-dependent insulin release.

135 VMH Trx-1 overexpression also lowered the insulin requirement to prevent severe hyperglycemia in S

136 insulin and homeostasis model assessment of insulin resistance (HOMA-IR).

137 -like growth factor-1 signalling (IGF-1) and insulin resistance (i.e. decreased insulin/IGF-1) have b

138 rotein catabolism, obesity, and/or increased insulin resistance (IR) or impaired tissue metabolism is

139 ogressive relation among metabolic syndrome, insulin resistance (IR), and dementia has recently been

140 showed a metabolic phenotype (p < 0.05) and insulin resistance (p < 0.001).

141 ink between obesity-induced inflammation and insulin resistance and as potential target for treatment

142 onents develop and progress in parallel with insulin resistance and could be a clinically relevant pr

143 (AAAs) have been shown to be associated with insulin resistance and diabetes risk.

144 otein kinase II, which promoted both hepatic insulin resistance and gluconeogenesis.

145 ction are key pathophysiological features of insulin resistance and obesity.

146 iple system atrophy is associated with brain insulin resistance and showed increased expression of th

147 Type 2 diabetes and insulin resistance are associated with reduced glucose u

148 Diets promoting obesity and insulin resistance can lead to severe metabolic diseases

149 ulin-stimulated glucose disposal, and muscle insulin resistance confers many negative health outcomes

150 onsistent evidence of glucose intolerance or insulin resistance during pregnancy.

151 FGF21 might be involved in protein-mediated insulin resistance in humans.

152 t from metabolically healthy subjects caused insulin resistance in IgG-deficient mice via FcgammaRIIB

153 ochondrial dysfunction, hepatosteatosis, and insulin resistance in mice.

154 Therefore, brain insulin resistance in obesity may have unfavorable conse

155 arly steps in the insulin signaling cascade, insulin resistance in obesity seems to be largely elicit

156 dy identifies Vps34 as a new drug target for insulin resistance in Type-2 diabetes, in which the unme

157 Insulin resistance is a key mediator of obesity-related

158 d and carbohydrate metabolism resulting from insulin resistance leads to hyperglycemia, the hallmark

159 New findings also connect insulin resistance to extensive metabolic cross-talk bet

160 resistant to hepatic steatosis, obesity and insulin resistance under a lipogenic diet.

161 gulate myocyte metabolism, and contribute to insulin resistance via paracrine effects.

162 own adipose tissues, glucose intolerance and insulin resistance while exhibiting suppressed aromatase

163 ce were better protected against obesity and insulin resistance with increased circulating fibroblast

164 Obesity causes insulin resistance, and PPARgamma ligands such as rosigl

165 of fat resulted in a measurable increase in insulin resistance, hepatic triglycerides, and gluconeog

166 glycemia, homeostasis model of assessment of insulin resistance, serum ferritin, lipid profile, and l

167 Hepatic insulin resistance, synergistically with lowered insulin

168 emic stroke or transient ischemic attack and insulin resistance, those at higher risk for future stro

169 ctions between hyperinsulinemia, obesity and insulin resistance.

170 r endothelial FcgammaRIIB in obesity-induced insulin resistance.

171 d as expected in the setting of diet-induced insulin resistance.

172 steatosis and severe whole-body and hepatic insulin resistance.

173 for therapeutic development in the field of insulin resistance.

174 epatic lipid storage, energy metabolism, and insulin resistance.

175 ated fasting blood glucose, fatty liver, and insulin resistance.

176 and is associated with ectopic lipid-induced insulin resistance.

177 sure and metabolism with type 2 diabetes and insulin resistance.

178 g obesity to adipose tissue inflammation and insulin resistance.

179 oxidation in the development of obesity and insulin resistance.

180 induced liver steatosis and improves hepatic insulin resistance.

181 of a high fat diet on glucose tolerance and insulin resistance.

182 able option for the treatment of obesity and insulin resistance.

183 oglobin, and homeostasis model assessment of insulin resistance.

184 The downstream mediators of insulin-resistant pathophysiology remain unclear.

185 In obese, insulin-resistant patients with nonalcoholic fatty liver

186 95% CI, -4.36, -1.77) decline in HOMA-IR and insulin respectively, and a 2.55% (95% CI, 0.93, 4.21) i

187 As a result, Glut4 cannot reach the insulin-responsive compartment, and insulin-stimulated g

188 ces the secretion of insulin, but attenuates insulin's metabolic actions in the liver, skeletal muscl

189 Thus, insulin secreted into the circulation stimulated glucose

190 Meg3 overexpression in a mouse insulin-secreting PNET cell line, MIN6, downregulates c-

191 n(-1), respectively; P = 0.9) or first-phase insulin secretion (-21 +/- 212 compared with 24 +/- 184

192 own that ghrelin inhibits glucose-stimulated insulin secretion (GSIS), the effect of obestatin on GSI

193 asis, partly by enhancing glucose-stimulated insulin secretion (GSIS).

194 ociated with small differences in markers of insulin secretion and beta-cell function.

195 cells increases basal and glucose-stimulated insulin secretion and Ca(2+) uptake in the presence of g

196 lation of LDB1 in mature beta cells impaired insulin secretion and glucose homeostasis.

197 will potentially create an imbalance between insulin secretion and insulin-stimulated glucose utiliza

198 aired glucose-stimulated Ca(2+) dynamics and insulin secretion and recapitulated the pattern of impro

199 Although glucose is known to stimulate insulin secretion by beta cells, whether it directly eng

200 dult islets, since Ex-4 treatment stimulated insulin secretion by both juvenile and adult human beta

201 We aim to increase insulin secretion by developing strategies that work thr

202 We found that glucose-induced insulin secretion declined by 50% in rats housed at 5 de

203 s physical activity, 24-h glycemia, and 24-h insulin secretion did not differ between intervention da

204 ensing are likely to contribute to defective insulin secretion in human carriers of PAX6 mutations.

205 These findings suggest that insulin secretion in pancreatic cells is regulated by Ca

206 oss of this organization underlies disturbed insulin secretion kinetics in T2D.

207 intake alone did increase beta cell mass and insulin secretion moderately.

208 e (cGMP) analog on KATP channel activity and insulin secretion point to participation of the cGMP/PKG

209 e and 4-hydrpxnonenal both assayed by ELISA, insulin secretion quantified using ELISA or radioimmunoa

210 nergetics reveals that Drp1 does not control insulin secretion via its effect on proton leak but inst

211 by approximately 60%, and glucose-stimulated insulin secretion was eliminated.

212 ses energy expenditure, insulin sensitivity, insulin secretion, and glucose tolerance.

213 mass, impaired glucose tolerance, defective insulin secretion, and increased apoptosis when a combin

214 lin resistance, synergistically with lowered insulin secretion, increases serum glucose levels, which

215 or glucose homeostasis, insulin sensitivity, insulin secretion, steatosis, metabolic inflammation, pa

216 splay decreased insulin content and impaired insulin secretion.

217 s, barr2 knockdown abolished glucose-induced insulin secretion.

218 ucose homeostasis resulting from an enhanced insulin secretion.

219 S: (1/GlyRa x fasting insulin) x first-phase insulin secretion.

220 tivator of muscarinic M3 receptor-stimulated insulin secretion.

221 ayed marked glucose intolerance with reduced insulin secretion.

222 from defects in both insulin sensitivity and insulin secretion.

223 ial bioenergetics control glucose-stimulated insulin secretion.

224 are e, f, g, diabetes-associated protein in insulin-sensitive tissues (DAPIT), and the 6.8-kDa prote

225 d placebo groups did not differ in change in insulin sensitivity (0.02 +/- 2.0 compared with -0.03 +/

226 ificant heritability for measures of fasting insulin sensitivity and beta-cell function, for time spe

227 nsin II, aldosterone, and neprilysin) impair insulin sensitivity and contribute to microvascular dise

228 s and act locally or systemically to promote insulin sensitivity and glucose tolerance; as a class, t

229 Type 2 diabetes results from defects in both insulin sensitivity and insulin secretion.

230 l nutrients should also cause a reduction of insulin sensitivity and/or secretion (anti-incretin effe

231 to-fat ratio, and show dramatically improved insulin sensitivity despite prolonged high-fat diet feed

232 HFHS feeding perturbed maternal insulin sensitivity in late pregnancy; hepatic insulin s

233 aired glucose effectiveness in the liver and insulin sensitivity in muscle by eliminating glucotoxici

234 n levels, larger adipocyte size, and reduced insulin sensitivity in WTs.

235 one signature, they classified mice based on insulin sensitivity more accurately than each metabolite

236 lude that chronic vagal stimulation improves insulin sensitivity substantially in diet-induced obesit

237 sulin sensitivity in late pregnancy; hepatic insulin sensitivity was higher, whereas sensitivity of t

238 from lean mice improve glucose tolerance and insulin sensitivity when administered to obese recipient

239 , any observations of altered adipose tissue insulin sensitivity with extended morning fasting do not

240 gest that dietary soy ameliorates adiposity, insulin sensitivity, adipose tissue inflammation, and ar

241 cy (GHRD) results in short stature, enhanced insulin sensitivity, and low circulating levels of insul

242 dy weight, reduced total adiposity, improved insulin sensitivity, enhanced energy expenditure, and fa

243 d hormone that increases energy expenditure, insulin sensitivity, insulin secretion, and glucose tole

244 ice were phenotyped for glucose homeostasis, insulin sensitivity, insulin secretion, steatosis, metab

245 machine learning to segregate mice based on insulin sensitivity, we identified C22:1-CoA, C2-carniti

246 e accumulation in association with increased insulin sensitivity.

247 e intolerance and diabetes without affecting insulin sensitivity.

248 rance did not change, owing to a doubling of insulin sensitivity.

249 lamps were performed to determine whole-body insulin sensitivity.

250 of CTRP6 in modulating both inflammation and insulin sensitivity.

251 The insulin sensitizing glitazone drugs, rosiglitazone (ROS)

252 PPARgamma ligands such as rosiglitazone are insulin sensitizing, yet the mechanisms remain unclear.

253 infarction (MI) derive more benefit from the insulin-sensitizing drug pioglitazone hydrochloride comp

254 Insulin-sensitizing thiazolidinediones have shown effica

255 ing it in the endosomes, leading to impaired insulin signaling and insulin-stimulated mitochondrial r

256 h attention has addressed early steps in the insulin signaling cascade, insulin resistance in obesity

257 el function of tau protein as a regulator of insulin signaling in the brain.

258 iated homology-directed repair revealed that insulin signaling is up-regulated in response to miR-277

259 in Alzheimer's disease, impairment of brain insulin signaling might occur via tau loss of function.

260 s extend earlier work linking the immune and insulin signaling pathways and identify new targets of i

261 Hyperglycemia or blockade of insulin signaling reduces the expression of ORAI1-3.

262 gnaling pathways and identify new targets of insulin signaling that could serve as potential drug tar

263 DAG, which is known not to activate PKC, and insulin signaling was intact.

264 ly mediated by changes in host vitellogenin, insulin signaling, and gustatory response.

265 e and body weight by modulating hypothalamic insulin signaling.MANF is a neurotrophic factor that is

266 implicating p41ARC as a new component of the insulin-signaling cascade and connecting PAK1 signaling

267 genes involved in lipid turnover (ACADM) and insulin signalling (IRS2) in subcutaneous abdominal adip

268 gevity by other factors including diet, sex, insulin signalling and population density.

269 asting do not necessarily require changes in insulin signalling proximal to Akt.

270 mimetope (InsB9-23 R22E) efficiently deletes insulin-specific T cells and prevents escape of high-aff

271 Insulin spillover into circulation after intranasal insu

272 In contrast, loss of CTRP6 enhanced insulin-stimulated Akt activation in adipose tissue.

273 Skeletal muscle is the major site for insulin-stimulated glucose disposal, and muscle insulin

274 each the insulin-responsive compartment, and insulin-stimulated glucose uptake in adipocytes is suppr

275 Loss of Rab20 impairs insulin-stimulated glucose uptake in human and mouse ske

276 These results expand the model of insulin-stimulated glucose uptake in skeletal muscle cel

277 e an imbalance between insulin secretion and insulin-stimulated glucose utilization in the neonate wh

278 s, leading to impaired insulin signaling and insulin-stimulated mitochondrial respiration and glycoly

279 lowers glycemia and insulinemia by enhancing insulin-stimulated suppression of endogenous glucose pro

280 Moreover, insulin stimulation of their phosphorylation was signifi

281 t production platform for expressing relaxin/insulin superfamily peptides.

282 t not in rats with type 1 diabetes receiving insulin supplementation that did not restore normoglycem

283 ter intravitreal bevacizumab was prepared in insulin syringes by a compounding pharmacy.

284 Participants receiving insulin therapy had greater hazard of infection (hazard

285 (26 of 312) to 0% (0 of 35) but the need for insulin therapy remained constant (9%, three of 35).

286 iabetes without insulin therapy, diabetes on insulin therapy).

287 abetes status (no diabetes, diabetes without insulin therapy, diabetes on insulin therapy).

288 tau deletion impairs hippocampal response to insulin through IRS-1 and PTEN dysregulation and suggest

289 The approach added saccharide units to insulin to create insulin analogs with affinity for both

290 tement of drug use, we formulated intranasal insulin to evaluate its efficacy during acute abstinence

291 Overall, 6600 of the diabetic patients were insulin treated (IT).

292 d pressure (SBP) (ORper 10mmHg+ = 1.19), and insulin treatment (ORinsulin+ = 2.44).

293 eight, food intake, adiposity index, fasting insulin, triglycerides and cholesterol levels were all s

294 Insulin use appears to be associated with a 38% excess f

295 duration of 10 years or longer at baseline, insulin use, and glycemic control.

296 Body fat, leptin, and insulin were increased in male, but not in female, F1 WD

297 Plasma metabolites and insulin were measured at baseline, 15, 30, 60, 90 and 12

298 Here, we show that codelivery of insulin with otherwise sublethal doses of LPS induced hy

299 materials that form photoactivated depots of insulin without the need for polymers, by linking photol

300 I was calculated as ATIS: (1/GlyRa x fasting insulin) x first-phase insulin secretion.