Loss of Insulin Resistance after Roux-en-Y Gastric Bypass Surgery: a Time Course Study

2005 ◽  
Vol 15 (4) ◽  
pp. 474-481 ◽  
Author(s):  
Kusal Wickremesekera ◽  
Geoff Miller ◽  
Tissa DeSilva Naotunne ◽  
Graham Knowles ◽  
Richard S. Stubbs
Keyword(s):  
Insulin Resistance ◽  
Gastric Bypass ◽  
Time Course ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery ◽  
Time Course Study

scholarly journals Improvement in insulin resistance after gastric bypass surgery is correlated with a decline in plasma 2-hydroxybutyric acid

2018 ◽  
Vol 14 (8) ◽  
pp. 1126-1132 ◽  
Author(s):  
Prapimporn Chattranukulchai Shantavasinkul ◽  
Michael J. Muehlbauer ◽  
James R. Bain ◽  
Olga R. Ilkayeva ◽  
Damian M. Craig ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gastric Bypass ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery ◽  
Hydroxybutyric Acid

Effects of Gastric Bypass Surgery on Insulin Resistance and Insulin Secretion in Nondiabetic Obese Patients

Obesity ◽  
2011 ◽  
Vol 19 (7) ◽  
pp. 1420-1426 ◽  
Author(s):  
Miriam Promintzer-Schifferl ◽  
Gerhard Prager ◽  
Christian Anderwald ◽  
Martina Mandl ◽  
Harald Esterbauer ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gastric Bypass ◽  
Insulin Secretion ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery ◽  
Obese Patients

scholarly journals Association between physical activity, insulin resistance, body fat, and leptin in patients after gastric bypass surgery, obese, and non‐obese controls

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Farah A Ramirez‐Marrero ◽  
Madhuri Somaraju ◽  
Brianna E Vaa ◽  
Shelly K Roberts ◽  
Michael J Joyner ◽  
...  
Keyword(s):  
Physical Activity ◽  
Insulin Resistance ◽  
Gastric Bypass ◽  
Body Fat ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery

Studies in Insulin Resistance following Very Low Calorie Diet and/or Gastric Bypass Surgery

2011 ◽  
Vol 21 (12) ◽  
pp. 1914-1920 ◽  
Author(s):  
Jonathan Foo ◽  
Jeremy Krebs ◽  
Mark Thomas Hayes ◽  
Damon Bell ◽  
Donia Macartney-Coxson ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gastric Bypass ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery ◽  
Very Low Calorie Diet ◽  
Low Calorie ◽  
Low Calorie Diet ◽  
Calorie Diet

GRB14, GPD1, and GDF8 as potential network collaborators in weight loss-induced improvements in insulin action in human skeletal muscle

2006 ◽  
Vol 27 (2) ◽  
pp. 114-121 ◽  
Author(s):  
Jung-Jun Park ◽  
Jason R. Berggren ◽  
Matthew W. Hulver ◽  
Joseph A Houmard ◽  
Eric P. Hoffman
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Weight Loss ◽  
Gastric Bypass ◽  
Insulin Action ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery ◽  
Morbidly Obese ◽  
Obese Women ◽  
Cross Sectional

Obesity is associated with insulin resistance in skeletal muscle; accordingly, weight loss dramatically improves insulin action. We sought to identify molecular remodeling of muscle commensurate with weight loss that could explain improvements in insulin action. Muscle from morbidly obese women was studied before and after gastric bypass surgery. Gastric bypass surgery significantly reduced body mass by ∼45% and improved insulin action. We then assessed mRNA profiles using a stringent statistical analysis (statistical concordance with three probe set algorithms), with validation in a cross-sectional study of lean ( n = 8) vs. morbidly obese ( n = 8) muscle. Growth factor receptor-bound protein 14 (GRB14), glycerol-3-phosphate dehydrogenase 1 (GPD1), and growth differentiation factor 8 (GDF8; myostatin) significantly decreased ∼2.4-, 2.2-, and 2.4-fold, respectively, after weight loss (gastric bypass). Increased expression of these transcripts was associated with increased obesity in the cross-sectional group (lean vs. morbidly obese muscle). Each transcript was validated by real-time quantitative RT-PCR assays in both study groups. Using Ingenuity Pathway Analysis, we show that all three transcripts are involved in the same regulatory network including AKT1, IGF1, TNF, PPARG, and INS. These results suggest that GRB14, GPD1, and GDF8 are weight loss-responsive genes in skeletal muscle and that the observed transcriptional modulation of these would be expected to improve insulin signaling, decrease triglyceride synthesis, and increase muscle mass, respectively, with weight loss. Thus our data provide a possible regulatory pathway involved in the development of insulin resistance in the morbidly obese state, and improvement of insulin resistance with weight loss.

scholarly journals Insulin Resistance, Inflammation, and the Metabolic Syndrome Following Roux-en-Y Gastric Bypass Surgery in Severely Obese Subjects

Diabetes Care ◽  
2007 ◽  
Vol 30 (7) ◽  
pp. 1906-1908 ◽  
Author(s):  
R. Morinigo ◽  
R. Casamitjana ◽  
S. Delgado ◽  
A. Lacy ◽  
R. Deulofeu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Gastric Bypass ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery ◽  
The Metabolic Syndrome ◽  
Severely Obese ◽  
Obese Subjects

scholarly journals The Effect of Laparoscopic Gastric Bypass Surgery on Insulin Resistance and Glycosylated Hemoglobin A1c: a 2-Year Follow-up Study

2020 ◽  
Vol 30 (9) ◽  
pp. 3489-3495
Author(s):  
Erik Stenberg ◽  
Eva Rask ◽  
Eva Szabo ◽  
Ingmar Näslund ◽  
Johan Ottosson
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Gastric Bypass ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery ◽  
Glycosylated Hemoglobin ◽  
Model Assessment ◽  
Fasting Insulin

Abstract Background Bariatric surgery improves insulin sensitivity and secretion in patients with type 2 diabetes, but the effect on patients with prediabetes or even normal glucose tolerance deserves further consideration. Methods Cohort study including patients operated with laparoscopic Roux-en-Y gastric bypass surgery (LRYGB) between November 2012 and June 2017 at the Örebro University Hospital (n = 813) with follow-up of 742 patients 2 years after surgery. Fasting insulin, glucose, glycosylated hemoglobin (HbA1c), and homeostatic model assessment of insulin resistance (HOMA-IR) were analyzed at baseline and 2 years after surgery for patients with overt type 2 diabetes, prediabetes, or non-diabetes. Results Fasting insulin levels improved for all groups (diabetics baseline 25.5 mIU/L, IQR 17.5–38.0, 2 years 7.6 mIU/L, IQR 5.4–11.1, p < 0.001; prediabetics baseline 25.0 mIU/L, IQR 17.5–35.0, 2 years 6.7mIU/L, IQR 5.3–8.8, p < 0.001; non-diabetics baseline 20.0 mIU/L, IQR 14.0–30.0, 2 years 6.4 mIU/L, IQR 5.0–8.5, p < 0.001). HbA1c improved in all groups (diabetics baseline 56 mmol/mol, IQR 49–74 [7.3%, IQP 6.6–8.9], 2 years 38 mmol/mol, IQR 36–47 [5.6%, IQR 5.4–6.4], p < 0.001; prediabetics baseline 40 mmol/mol, IQR 39–42 [5.8%, IQR5.7–6.0], 2 years 36 mmol/mol, IQR 34–38 [5.5%, IQR 5.3–5.6], p < 0.001; non-diabetics baseline 35 mmol/mol, IQR 33–37 [5.4%, IQR 5.2–5.5]; 2 years 34 mmol/mol, IQR 31–36 [5.3%, IQR 5.0–5.4], p < 0.001). HOMA-IR improved in all groups (diabetics baseline 9.3 mmol/mol, IQR 5.4–12.9, 2 years 1.9 mmol/mol, IQR 1.4–2.7, p < 0.001; prediabetics baseline 7.0 mmol/mol, IQR 4.3–9.9, 2 years 1.6 mmol/mol, IQR 1.2–2.1, p < 0.001; non-diabetics 4.9 mmol/mol, IQR 3.4–7.3, 2 years 1.4 mmol/mol, IQR 1.1–1.9, p < 0.001). Conclusion Insulin homeostasis and glucometabolic control improve in all patients after LRYGB, not only in diabetics but also in prediabetics and non-diabetic obese patients, and this improvement is sustained 2 years after surgery.

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