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.

Slides:



Advertisements
Similar presentations
Ali Ardestani, David Rhoads, Ali Tavakkoli
Advertisements

Necdin–E2F4 interaction provides insulin-sensitizing effect after weight loss induced by gastric bypass surgery  Zehra N. Pamuklar, M.D., Ph.D., Jiegen.
Volume 5, Issue 10, Pages (October 2016)
Fig. 1. Effect of bariatric surgery on BMI and plasma leptin concentration. BMI (A) and plasma leptin concentrations (B) were determined in 27 morbidly.
Plasma insulin concentrations (A) and insulin secretion rates (B) in response to molar increments of plasma glucose concentration during the graded glucose.
Key clinical efficacy outcomes for (A) hemoglobin A1c (HbA1c), (B) weight change. Key clinical efficacy outcomes for (A) hemoglobin A1c (HbA1c), (B) weight.
David Bradley, Faidon Magkos, Samuel Klein  Gastroenterology 
Figure 1. Plasma urea concentrations in apolipoprotein E–deficient (apo-E −/−) mice with chronic renal failure (CRF). Figure 1. Plasma urea concentrations.
Distribution of the absolute percentage differences of each basal rate estimate to final basal rates. Distribution of the absolute percentage differences.
Insulin and glucagon secretion: nondiabetic and diabetic subjects.
Necdin–E2F4 interaction provides insulin-sensitizing effect after weight loss induced by gastric bypass surgery  Zehra N. Pamuklar, M.D., Ph.D., Jiegen.
Volume 139, Issue 2, Pages (August 2010)
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.
Body weight and oral glucose tolerance in diet-induced obese rats at 5 weeks post-surgery. Body weight and oral glucose tolerance in diet-induced obese.
Dandan Wang et al. BTS 2018;3: Down-Regulation of miR-24 in Response to Insulin Infusion in Human Plasma Human plasma insulin (A), glucose (B),
Correlation of E/e’ with age (A), gender (B), fasting insulin (C), and sulfonylurea use (SU) (D) among patients with type 2 diabetes mellitus. Correlation.
Mean daily glucose concentration and frequency of hypoglycemia in long-term care residents with type 2 diabetes. Mean daily glucose concentration and frequency.
(A) Correlation between change in HbA1c and change in weight from baseline to week 24 in the liraglutide group. (A) Correlation between change in HbA1c.
Volume 142, Issue 7, Pages e2 (June 2012)
Change in %A1C over 5 years in response to 12-week intensive lifestyle intervention used in a real-world clinical practice. Change in %A1C over 5 years.
Exosomes transfected with obesity-associated miRNAs induce glucose intolerance dissociated from obesity. Exosomes transfected with obesity-associated miRNAs.
Hyperinsulinemic-euglycemic clamps revealed that obese TPL2KO mice have an improved insulin sensitivity compared with obese WT mice. Hyperinsulinemic-euglycemic.
Lypolytic activity (glycerol release, mg/ml) measured in adipocytes culture medium after 2 h incubation with isoproterenol or 8-Cl-cAMP. Lypolytic activity.
A–L: Xenin-25 amplifies the effects of GIP on plasma insulin, C-peptide, and glucose levels and ISRs in humans with NGT and IGT but not T2DM. A–L: Xenin-25.
Deletion of neuronal insulin receptor signaling reduces TG secretion, while the targeted knockout of insulin receptors restricted to the periphery increases.
Effect of insulin on hepcidin expression in HepG2 cells.
A and B: Plasma levels of IR-GIP and xenin-25 during GGIs
Glucose, insulin, and AGE levels during an OGC before and after RT
Homeostasis model assessment of insulin resistance (HOMA-IR) scores in obese women and obese women with gestational diabetes mellitus (GDM) at approximately.
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.
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.
Insulin secretion/insulin resistance (disposition) index (ΔINS/ΔGLU ÷ IR) in subjects with normal glucose tolerance (NGT), impaired glucose tolerance (IGT),
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.
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.
Loss of protection by linagliptin against obesity-related inflammation and insulin resistance in MIP-1α−/− mice. Loss of protection by linagliptin against.
Unlabeled and tracer glucocorticoids in plasma from arterialized samples and veins draining skeletal muscle and subcutaneous adipose tissue. Unlabeled.
The underlying physiological basis of the HOMA model.
Clustering of fat mass loss profiles in obese subjects and relation with scWAT fibrosis. Clustering of fat mass loss profiles in obese subjects and relation.
BAFF-deficient (BAFFnull) and anti-BAFF antibody (Ab)–treated obese mice exhibit superior glucose metabolic control compared with WT and Bnull mice. BAFF-deficient.
Insulin sensitivity in athletes and sedentary normal-weight and obese, young, and old individuals. Insulin sensitivity in athletes and sedentary normal-weight.
DPP4 release of explants obtained from adipose tissue of lean controls and obese patients before and after bariatric surgery, and linear correlation with.
The effect of VSG on body weight and body fat in GLP-1r KO mice.
Mean plasma concentrations of ampicillin/sulbactam in plasma of critically ill patients with AKI undergoing extended dialysis (duration depicted by box.
ATL-801 treatment increases insulin sensitivity in KKAY mice.
USP2–45 regulates hepatic gluconeogenesis.
Intracerebroventricular (ICV) insulin infusion increases TG secretion.
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.
Insulin resistance and hepatic steatosis in ASKO mice.
Metabolic effects of VSG in GLP-1r KO mice.
Plasma glucose, GIR, rates of EGP and glucose utilization, and plasma concentrations of free fatty acids (FFAs) and β-hydroxy-butyrate after a subcutaneous.
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.
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.
Bubble graph representing the relationship between the difference in estimated fat mass and the difference in plasma NEFA concentration in 43 independent.
ORs of receiving metformin for outcome measures, including age, number of comorbidities, provider age, A1C level, history of CHF, and use of medications,
Effects of vinegar (□) and placebo (⧫) on plasma glucose (A–C) and insulin (D–F) responses after a standard meal in control subjects, insulin-resistant.
(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.
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.
(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.
The ADA research program supports research across the broad spectrum of diabetes types and research topic areas (proportions of 2011 allocations in dollars).
Cumulative distributions of A1C and fasting plasma glucose values for the U.S. population aged ≥12 years without diabetes for each survey cycle: 1999–2000,
Presentation transcript:

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 20% weight loss induced by LAGB or RYGB. Values are means ± SEM (n = 10 for each surgery group). *Value after weight loss is significantly different from value before weight loss, P < 0.05. 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 20% weight loss induced by LAGB or RYGB. Values are means ± SEM (n = 10 for each surgery group). *Value after weight loss is significantly different from value before weight loss, P < 0.05. Faidon Magkos et al. Diabetes 2013;62:2757-2761 ©2013 by American Diabetes Association