Presentation of a New Method for Specific Measurement of in Vivo Insulin-Stimulated Glucose Disposal in Humans: Comparison of This Approach with the Insulin Clamp and Minimal Model Techniques*

Abstract Background The purpose of this study was to evaluate the changes in canal volume after root canal preparation in vivo with 3 different single-file techniques (Reciproc-Blue®, WaveOne-Gold® and XP-EndoShaper®), with a new method using CBCT and 3D reconstruction. Methods In this prospective study, thirty human lower premolars from healthy patients were used, in which extraction was indicated for orthodontic reasons. All the teeth used were caries- and restoration-free with complete root development, without signs of periodontal disease or traumatic occlusion, and with only one straight canal (up to 25º curvature). Teeth were randomly divided into three different groups: Reciproc-Blue, WaveOne-Gold and XP-EndoShaper. CBCT scans before root canal preparation were used to create a 3D reconstruction with RHINOCEROS 5.0 software to assess the initial canal volume, and then compared with 3D reconstructions after canal preparation to measure the increase in canal volume. Student’s t test for paired data were used to determine statistically significant differences between the before and after canal volumes. Anova test was used to determine statistically significant differences in the percentage of canal volume increase between the groups and Tukey's post-hoc test were used to paired comparison. Results Reciproc-Blue showed the higher increase in canal volume, followed by WaveOne-Gold and XP-EndoShaper (p = 0.003). XP-EndoShaper did not show a statistically significant increase in canal volume after root canal preparation (p = 0.06). Conclusion With this model, Reciproc-Blue showed higher increase in root canal volume, followed by WaveOne-Gold, while XP-EndoShaper did not significantly increase root canal volume during preparation.

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A New Method to Measure Type I and III Collagen Synthesis in Human Skin In Vivo: Demonstration of Decreased Collagen Synthesis After Topical Glucocorticoid Treatment

Journal of Investigative Dermatology ◽

10.1111/1523-1747.ep12555884 ◽

1992 ◽

Vol 98 (2) ◽

pp. 220-225 ◽

Cited By ~ 64

Author(s):

Aarne Oikarinen ◽

Pekka Autio ◽

Urpo Kiistala ◽

Leila Risteli ◽

Juha Risteli

Keyword(s):

Human Skin ◽

Collagen Synthesis ◽

New Method ◽

Type I ◽

Glucocorticoid Treatment

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Use of vibrational optical coherence tomography to measure viscoelastic properties of muscle and tendon: A new method to follow musculoskeletal injury and pathology In vivo

Journal of the Mechanical Behavior of Biomedical Materials ◽

10.1016/j.jmbbm.2021.104479 ◽

2021 ◽

pp. 104479

Author(s):

Frederick H. Silver ◽

Nikita Kelkar ◽

Tanmay Deshmukh

Keyword(s):

Optical Coherence Tomography ◽

Viscoelastic Properties ◽

Musculoskeletal Injury ◽

New Method ◽

Optical Coherence

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Prep1 Deficiency Induces Protection from Diabetes and Increased Insulin Sensitivity through a p160-Mediated Mechanism

Molecular and Cellular Biology ◽

10.1128/mcb.00117-08 ◽

2008 ◽

Vol 28 (18) ◽

pp. 5634-5645 ◽

Cited By ~ 35

Author(s):

Francesco Oriente ◽

Luis Cesar Fernandez Diaz ◽

Claudia Miele ◽

Salvatore Iovino ◽

Silvia Mori ◽

...

Keyword(s):

Skeletal Muscle ◽

Insulin Sensitivity ◽

Glucose Uptake ◽

Normal Glucose Tolerance ◽

Glucose Disposal ◽

Protein Levels ◽

Normal Glucose ◽

Enhanced Expression ◽

The Stability

ABSTRACT We have examined glucose homeostasis in mice hypomorphic for the homeotic transcription factor gene Prep1. Prep1-hypomorphic (Prep1 i / i ) mice exhibit an absolute reduction in circulating insulin levels but normal glucose tolerance. In addition, these mice exhibit protection from streptozotocin-induced diabetes and enhanced insulin sensitivity with improved glucose uptake and insulin-dependent glucose disposal by skeletal muscle. This muscle phenotype does not depend on reduced expression of the known Prep1 transcription partner, Pbx1. Instead, in Prep1 i / i muscle, we find normal Pbx1 but reduced levels of the recently identified novel Prep1 interactor p160. Consistent with this reduction, we find a muscle-selective increase in mRNA and protein levels of PGC-1α, accompanied by enhanced expression of the GLUT4 transporter, responsible for insulin-stimulated glucose uptake in muscle. Indeed, using L6 skeletal muscle cells, we induced the opposite effects by overexpressing Prep1 or p160, but not Pbx1. In vivo skeletal muscle delivery of p160 cDNA in Prep1 i / i mice also reverses the molecular phenotype. Finally, we show that Prep1 controls the stability of the p160 protein. We conclude that Prep1 controls insulin sensitivity through the p160-GLUT4 pathway.

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Effects of prolonged Acipimox treatment on glucose and lipid metabolism and on in vivo insulin sensitivity in patients with non-insulin dependent diabetes mellitus

Acta Endocrinologica ◽

10.1530/acta.0.1270344 ◽

1992 ◽

Vol 127 (4) ◽

pp. 344-350 ◽

Cited By ~ 32

Author(s):

Allan A Vaag ◽

Henning Beck-Nielsen

Keyword(s):

Lipid Metabolism ◽

Insulin Sensitivity ◽

Treatment Period ◽

Blood Glucose Control ◽

Glucose Disposal ◽

Prolonged Treatment ◽

Double Blind Study ◽

Glucose And Lipid Metabolism ◽

Fasting Plasma

The effect of prolonged treatment with Acipimox on in vivo peripheral insulin sensitivity, and on glucose and lipid metabolism, was investigated in patients with NIDDM in a double-blind study. Twelve NIDDM patients were randomized to treatment with either placebo or Acipimox in pharmacological doses (250 mg×3) for three months. Fasting plasma glucose, insulin, C-peptide and HbA1c concentrations were unaffected after three months of acipimox treatment. However, fasting plasma non-esterifled fatty acid (NEFA) concentrations were twofold elevated after Acipimox treatment (1.34±0.09 vs 0.66±0.09 mmol/l; p<0.05). Despite this, repeated acute Acipimox administration after the three months' treatment period enhanced total insulin-stimulated glucose disposal to the same extent as acute Acipimox administration before the treatment period (367±59 vs 392±66 mg·m−2·min−1, NS; both p<0.05 vs placebo glucose disposal) (267±44 mg·m−2·min−1). In conclusion, insulin resistance or tachyphylaxis towards the effects of Acipimox on insulin stimulated glucose disposal was not induced during prolonged Acipimox treatment. The lack of improvement of blood glucose control in the patients with NIDDM may be due to the demonstrated rebound effect of lipolysis.

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Postreceptor defect in insulin action in streptozotocin-induced diabetic rats

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1989.256.5.e624 ◽

1989 ◽

Vol 256 (5) ◽

pp. E624-E630 ◽

Cited By ~ 2

Author(s):

H. Nishimura ◽

H. Kuzuya ◽

M. Okamoto ◽

K. Yamada ◽

A. Kosaki ◽

...

Keyword(s):

Glucose Transporter ◽

Insulin Dose ◽

Insulin Binding ◽

Diabetic Rats ◽

Glucose Disposal ◽

Maximal Response ◽

Metabolic Clearance ◽

Glucose Clamp Technique

To clarify the mechanism(s) responsible for the insulin resistance in streptozotocin (STZ)-treated diabetic rats, we studied insulin-induced glucose disposal by using the glucose clamp technique and measured insulin receptor and glucose transporter of muscles. The insulin dose-response curve of the metabolic clearance rate (MCR) of glucose revealed a decrease of the maximal response without a rightward shift in STZ rats. Maximal MCR was even lower when clamped at 300 rather than 150 mg/dl of blood glucose levels. Insulin binding to the crude plasma membrane of muscles from STZ rats was increased compared with controls. The number of glucose transporter of the plasma and microsomal membranes were significantly decreased in STZ rats. These in vivo and in vitro studies using skeletal muscles suggest that in STZ-treated diabetic rats 1) a defect or defects exist in the signal transduction mechanism of insulin in postbinding steps, 2) the decreased maximal MCR is related at least partly to the decrease of glucose transporter numbers, and 3) a defect in glucose metabolism (postglucose transport defect) is also present.

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