Arterial and hepatic sinusoidal plasma insulin levels in conscious dogs during the basal (−40 to 0 min) and experimental (0–240 min) periods treated with.

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Glucose homeostasis: roles of insulin and glucagon. 1A.
Distribution of the absolute percentage differences of each basal rate estimate to final basal rates. Distribution of the absolute percentage differences.
Postprandial glucose flux in nondiabetic controls.
Frequency of potential risk of hypoglycemia for each estimate method, defined as a percentage difference between the estimate and final basal rate. Frequency.
Impact of U-100 RHI administered with V-Go at OV1 (3 months after initiation) and OV2 (6 months after initiation) (n = 11) at 3 months (P = 0.32) and at.
Distribution of the percentage differences of each basal rate estimate to final basal insulin rates. Distribution of the percentage differences of each.
Patient flow chart: the final prospective study population consisted of 521 individuals, 113 on basal insulin and 408 on OADs. *Plausibility: height (130–230 cm),
Respondents’ perceptions on (A) the potential of IDegLira compared with basal-bolus therapy to improve patient motivation to reach their target blood glucose.
Improvement of insulin sensitivity by treatment of the annexin A1 receptor agonist in HFD mice. Improvement of insulin sensitivity by treatment of the.
Mean daily glucose concentration and frequency of hypoglycemia in long-term care residents with type 2 diabetes. Mean daily glucose concentration and frequency.
Hyperinsulinemic-euglycemic clamps revealed that obese TPL2KO mice have an improved insulin sensitivity compared with obese WT mice. Hyperinsulinemic-euglycemic.
Cyp8b1−/− mice have an altered circulating bile acid pool.
(A) Plasma renin activity in Wistar rats, SHRs, and DOCA-salt rats, n = 8 to 9/group; data are presented as mean ± S.E.M. Dose-response relationship on.
Overexpression of BTG2 resulted in an increase in hepatic gluconeogenesis. Overexpression of BTG2 resulted in an increase in hepatic gluconeogenesis. A:
Effects of insulin administration in streptozotocin-treated mice.
Comparison of the protective effects of R and S isomers of LA on insulin-stimulated 2-DG uptake. Comparison of the protective effects of R and S isomers.
Exogenous CRP administration causes fasting hyperglycemia and hyperinsulinemia without altering body composition. Exogenous CRP administration causes fasting.
Plasma glucose (A) and glucose specific activity (B) during euglycemic clamp experiments. Plasma glucose (A) and glucose specific activity (B) during euglycemic.
Omental FFA production, calculated from the integrated lipolysis over the last 30 min of each insulin infusion period. Omental FFA production, calculated.
Glucose infusion rate required to maintain the hyperglycemic clamp during the experimental period in sedentary and exercised dogs receiving basal or elevated.
Effect of PIs on insulin release by downstream insulin secretogogues.
Effect of the acute administration of benzylamine plus vanadate on oral glucose tolerance test in STZ-induced diabetic rats. Effect of the acute administration.
A: The change of plasma glucose in opioid μ-receptor knockout diabetic mice and wild-type controls receiving an oral intake of metformin (100 mg/kg). A:
Arterial plasma glucose level and peripheral GIR in conscious dogs during the basal (−40 to 0 min) and experimental (0–240 min) periods treated with vehicle.
Expression of VCAM-1 and inflammatory cytokines in injured carotid arteries in STZ-induced diabetic rats. Expression of VCAM-1 and inflammatory cytokines.
Modulation of insulin sensitivity by IL-6 in mice: A lack of PTP1B prevents chronic effects of IL-6. Modulation of insulin sensitivity by IL-6 in mice:
Left columns: Plasma glucose and serum insulin concentrations, circulating TF-PCA, and FVIIa activity before and during 24 h of selective hyperglycemia.
Mean ± SEM concentration of insulin in plasma and CSF and glucose in plasma 30 min after the intraperitoneal administration of DET or NPH insulin at different.
Appearance of insulin in plasma and CSF at different times after the administration of subcutaneous DET and GLAR in mice and the effect of chronic DET.
IL-6 inhibits insulin-induced formation of p85/IRS-1 complexes.
Plasma growth hormone concentrations during a 65-min infusion of acyl ghrelin at 0.3, 0.9, or 1.5 nmol/kg/h, or saline. Plasma growth hormone concentrations.
Current insulin dose (units/kg/day) during the DCCT/EDIC study by sex (black line for females) (A), DCCT intensive vs. conventional treatment group (black.
Sustained activation of AMPK α2 in muscle of subjects with type 2 diabetes after an overnight withdrawal of metformin. Sustained activation of AMPK α2.
A: The correlation between the GIR and FGU, each measured during the last 40 min of the euglycemic insulin clamp. A: The correlation between the GIR and.
The underlying physiological basis of the HOMA model.
Effects of in vivo AICAR treatment on blood glucose and lactate concentrations. Effects of in vivo AICAR treatment on blood glucose and lactate concentrations.
Glycogen synthase and glycogen phosphorylase activities after in vivo AICAR treatment. Glycogen synthase and glycogen phosphorylase activities after in.
Inhibition of glucagon-induced glycogenolysis in human primary hepatocytes. Inhibition of glucagon-induced glycogenolysis in human primary hepatocytes.
Effect of 4 weeks of an intensive exercise program on vaspin serum concentrations in normal glucose tolerant (NGT) individuals and patients with IGT or.
ATL-801 treatment increases insulin sensitivity in KKAY mice.
Arterial and portal plasma glucagon levels and the portal-arterial (P-A) glucagon gradient in the control period (−40 to 0 min) and after administration.
The portal-arterial (P-A) insulin gradient and arterial plasma c-peptide levels in the control period (−40 to 0 min) and after administration of the glycogen.
Total plasma BCAA (A) and C3 and C5 acylcarnitine (AC) (B) concentrations in the basal state and during insulin infusion in obese subjects before and after.
USP2–45 regulates hepatic gluconeogenesis.
Intracerebroventricular (ICV) insulin infusion increases TG secretion.
Effect of anandamide on blood glucose clearance and insulin sensitivity. Effect of anandamide on blood glucose clearance and insulin sensitivity. A: Intraperitoneal.
Plasma concentrations of glucose, insulin, C-peptide and glucagon observed in subjects with NFG/NGT, NFG/IGT, IFG/NGT, and IFG/IGT-D following ingestion.
Mean (±SE) plasma glucose concentrations before, during, and after infusions of octreotide (with growth hormone) with saline (•), with insulin replacement.
Food intake in response to central infusion of glucose (squares) or insulin (triangles) and in response to successive central infusion of insulin, insulin.
Effects of berberine on in vivo metabolism in two animal models of insulin resistance. Effects of berberine on in vivo metabolism in two animal models.
Loss of Phb2 in β-cells induces development of diabetes over a 3-week period in β-Phb2−/− mice. Loss of Phb2 in β-cells induces development of diabetes.
Pioglitazone administration acutely inhibits insulin secretion and increases insulin clearance in Wistar rats. Pioglitazone administration acutely inhibits.
Chronic rapamycin treatment impairs β-cell mass and insulin clearance in rats. Chronic rapamycin treatment impairs β-cell mass and insulin clearance in.
Effect of GSK-3 inhibitors on basal and insulin-stimulated glucose uptake in human muscle cells. Effect of GSK-3 inhibitors on basal and insulin-stimulated.
Effects of rhein on FBG (A) and glucose intolerance (B) in db/db mice.
Effects of vinegar (□) and placebo (⧫) on plasma glucose (A–C) and insulin (D–F) responses after a standard meal in control subjects, insulin-resistant.
Case report: male 63 years old with documented stenosis of the internal cerebral artery, diabetes duration 12 years, and treatment with 22 IU insulin glargine.
Percent binding of cross-reactive antibodies from cross-over studies in insulin-treated patients with type 1 or type 2 diabetes. Percent binding of cross-reactive.
Percent binding of cross-reactive antibodies from parallel studies in insulin-treated patients with type 1 or type 2 diabetes. Percent binding of cross-reactive.
(A) Mean glucose concentrations (standard error) over a 3-hour period in 21 placebo- and 15 pramlintide-treated patients with type 1 diabetes treated for.
Clinical responses to therapy from baseline to week 24 and end point with last observation carried forward (LOCF). Clinical responses to therapy from baseline.
Mean changes (standard error) from baseline in A1C (A and B) and body weight (C and D) for patients with type 1 (A and C) or type 2 (B and D) diabetes.
A: Pharmacokinetic (plasma insulin concentration) response to administration of an oral insulin formulation (uninterrupted line) and subcutaneous regular.
Doses of trial medication in the liraglutide groups (A) and in the placebo groups (B). Doses of trial medication in the liraglutide groups (A) and in the.
Spearman rank order correlation between suppression of hepatic glucose production with low insulin infusion and 30-min change in glucose response in women.
Outline of study protocol.
Evidence against a Physiologic Role for Acute Changes in CNS Insulin Action in the Rapid Regulation of Hepatic Glucose Production  Christopher J. Ramnanan,
(A) Twenty-four-hour plasma profiles of insulin and amylin in healthy subjects. (A) Twenty-four-hour plasma profiles of insulin and amylin in healthy subjects.
Four–time point diurnal profiles of plasma glucose concentrations (A) and AUCs (B) over quintiles of HbA1c. ○, AUC1; •, AUC2; ▴, AUC2 − AUC1 (differences.
Presentation transcript:

Arterial and hepatic sinusoidal plasma insulin levels in conscious dogs during the basal (−40 to 0 min) and experimental (0–240 min) periods treated with vehicle (○) or vildagliptin (▪) (means ± SE; n = 6 per group). Arterial and hepatic sinusoidal plasma insulin levels in conscious dogs during the basal (−40 to 0 min) and experimental (0–240 min) periods treated with vehicle (○) or vildagliptin (▪) (means ± SE; n = 6 per group). Dale S. Edgerton et al. Diabetes 2009;58:243-249 ©2009 by American Diabetes Association