Acute and long-term effects of Roux-en-Y gastric bypass on glucose metabolism in subjects with Type 2 diabetes and normal glucose tolerance

2012 ◽  
Vol 303 (1) ◽  
pp. E122-E131 ◽  
Author(s):  
N. B. Jørgensen ◽  
S. H. Jacobsen ◽  
C. Dirksen ◽  
K. N. Bojsen-Møller ◽  
L. Naver ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Gastric Bypass ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Normal Glucose Tolerance ◽  
Long Term Effects ◽  
Β Cell ◽  
Liquid Meal ◽  
Normal Glucose

Our aim was to study the potential mechanisms responsible for the improvement in glucose control in Type 2 diabetes (T2D) within days after Roux-en-Y gastric bypass (RYGB). Thirteen obese subjects with T2D and twelve matched subjects with normal glucose tolerance (NGT) were examined during a liquid meal before (Pre), 1 wk, 3 mo, and 1 yr after RYGB. Glucose, insulin, C-peptide, glucagon-like peptide-1 (GLP-1), glucose-dependent-insulinotropic polypeptide (GIP), and glucagon concentrations were measured. Insulin resistance (HOMA-IR), β-cell glucose sensitivity (β-GS), and disposition index (Dβ-GS: β-GS × 1/HOMA-IR) were calculated. Within the first week after RYGB, fasting glucose [T2D Pre: 8.8 ± 2.3, 1 wk: 7.0 ± 1.2 ( P < 0.001)], and insulin concentrations decreased significantly in both groups. At 129 min, glucose concentrations decreased in T2D [Pre: 11.4 ± 3, 1 wk: 8.2 ± 2 ( P = 0.003)] but not in NGT. HOMA-IR decreased by 50% in both groups. β-GS increased in T2D [Pre: 1.03 ± 0.49, 1 wk: 1.70 ± 1.2, ( P = 0.012)] but did not change in NGT. The increase in DIβ-GS was 3-fold in T2D and 1.5-fold in NGT. After RYGB, glucagon secretion was increased in response to the meal. GIP secretion was unchanged, while GLP-1 secretion increased more than 10-fold in both groups. The changes induced by RYGB were sustained or further enhanced 3 mo and 1 yr after surgery. Improvement in glycemic control in T2D after RYGB occurs within days after surgery and is associated with increased insulin sensitivity and improved β-cell function, the latter of which may be explained by dramatic increases in GLP-1 secretion.

Liraglutide Therapy in a Prediabetic State: Rethinking the Evidence

2020 ◽  
Vol 16 (7) ◽  
pp. 699-715 ◽  
Author(s):  
Georgios S. Papaetis
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Normal Glucose Tolerance ◽  
Current Evidence ◽  
Β Cell ◽  
Prediabetic State ◽  
New Therapeutic Approaches ◽  
Normal Glucose

Background: Prediabetes is defined as a state of glucose metabolism between normal glucose tolerance and type 2 diabetes. Continuous β-cell failure and death are the reasons for the evolution from normal glucose tolerance to prediabetes and finally type 2 diabetes. Introduction: The necessity of new therapeutic approaches in order to prevent or delay the development of type 2 diabetes is obligatory. Liraglutide, a long-acting GLP-1 receptor agonist, has 97% homology for native GLP-1. Identification of the trophic and antiapoptotic properties of liraglutide in preclinical studies, together with evidence of sustained β-cell function longevity during its administration in type 2 diabetes individuals, indicated its earliest possible administration during this disease, or even before its development, so as to postpone or delay its onset. Methods: Pubmed and Google databases have been thoroughly searched and relevant studies were selected. Results: This paper explores the current evidence of liraglutide administration both in humans and animal models with prediabetes. Also, it investigates the safety profile of liraglutide treatment and its future role to postpone or delay the evolution of type 2 diabetes. Conclusion: Liralgutide remains a valuable tool in our therapeutic armamentarium for individuals who are overweight or obese and have prediabetes. Future well designed studies will give valuable information that will help clinicians to stratify individuals who will derive the most benefit from this agent, achieving targeted therapeutic strategies.

scholarly journals Dual Mechanism for Type-2 Diabetes Resolution after Roux-en-Y Gastric Bypass

2009 ◽  
Vol 75 (6) ◽  
pp. 498-503 ◽  
Author(s):  
Edward Lin ◽  
S. Scott Davis ◽  
Jahnavi Srinivasan ◽  
John F. Sweeney ◽  
Thomas R. Ziegler ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Weight Loss ◽  
Gastric Bypass ◽  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Β Cell ◽  
Peripheral Insulin Resistance

Resolution of Type-2 diabetes mellitus (DM) after weight loss surgery is well documented, but the mechanism is elusive. We evaluated the glucose-insulin metabolism of patients undergoing a Roux-en-Y gastric bypass (RYGB) using the intravenous glucose tolerance test (IVGTT) and compared it with patients who underwent laparoscopic adjustable gastric band (AB) placement. Thirty-one female patients (age range, 20 to 50 years; body mass index, 47.2 kg/m2) underwent RYGB. Nine female patients underwent AB placement and served as control subjects. All patients underwent IVGTT at baseline and 1 month and 6 months after surgery. Thirteen patients undergoing RYGB and one patient undergoing AB exhibited impaired glucose tolerance or DM defined by the American Diabetes Association. By 6 months post surgery, diabetes was resolved in all but one patient undergoing RYGB but not in the patient undergoing AB. Patients with diabetes undergoing RYGB demonstrated increased insulin secretion and β-cell responsiveness 1 month after surgery and continued this trend up to 6 months, whereas none of the patients undergoing AB had changes in β-cell function. Both patients undergoing RYGB and those undergoing AB demonstrated significant weight loss (34.6 and 35.0 kg/m2, respectively) and improved insulin sensitivity at 6 months. RYGB ameliorates DM resolution in two phases: 1) early augmentation of beta cell function at 1 month; and 2) attenuation of peripheral insulin resistance at 6 months. Patients undergoing AB only exhibited reduction in peripheral insulin resistance at 6 months but no changes in insulin secretion.

scholarly journals Exaggerated Glucagon-Like Peptide 1 Response Is Important for Improved β-Cell Function and Glucose Tolerance After Roux-en-Y Gastric Bypass in Patients With Type 2 Diabetes

Diabetes ◽  
2013 ◽  
Vol 62 (9) ◽  
pp. 3044-3052 ◽  
Author(s):  
Nils B. Jørgensen ◽  
Carsten Dirksen ◽  
Kirstine N. Bojsen-Møller ◽  
Siv H. Jacobsen ◽  
Dorte Worm ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Gastric Bypass ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Β Cell ◽  
Β Cell Function ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Evidence That Hypothalamic Gliosis Is Related to Impaired Glucose Homeostasis in Adults With Obesity

2021 ◽  
Author(s):  
Jennifer L. Rosenbaum ◽  
Susan J. Melhorn ◽  
Stefan Schoen ◽  
Mary F. Webb ◽  
Mary Rosalynn B. De Leon ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cohort Study ◽  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
Relaxation Times ◽  
Normal Glucose Tolerance ◽  
T2 Relaxation ◽  
Β Cell ◽  
Normal Glucose

Objective: Preclinical research implicates hypothalamic glial cell responses in the pathogenesis of obesity and type 2 diabetes. The current study sought to translate such findings into humans by testing if radiologic markers of gliosis in the mediobasal hypothalamus (MBH) were greater in persons with obesity and impaired glucose homeostasis or type 2 diabetes. <p>Research Design and Methods: Using cross-sectional and prospective cohort study designs, we applied a validated, quantitative magnetic resonance imaging (MRI) approach to assess gliosis in 67 adults with obesity and normal glucose tolerance, impaired glucose tolerance, or type 2 diabetes. Assessments of glucose homeostasis were conducted via oral glucose tolerance tests (OGTT) and β-cell modeling. </p> <p> Results: We found significantly greater T2 relaxation times (a marker of gliosis by MRI), that were independent of adiposity, in the impaired glucose tolerance and type 2 diabetes groups as compared to the normal glucose tolerance group. Findings were present in the MBH, but not control regions. Moreover, positive linear associations were present in the MBH but not control regions between T2 relaxation time and glucose area under the curve during an OGTT, fasting glucose concentrations, hemoglobin A1c, and visceral adipose tissue mass, whereas negative linear relationships were present in the MBH for markers of insulin sensitivity and β-cell function. In a prospective cohort study, greater MBH T2 relaxation times predicted declining insulin sensitivity over one year. </p> Conclusions: Findings support a role for hypothalamic gliosis in the progression of insulin resistance in obesity and, thus, type 2 diabetes pathogenesis in humans.

scholarly journals Evidence That Hypothalamic Gliosis Is Related to Impaired Glucose Homeostasis in Adults With Obesity

2021 ◽  
Author(s):  
Jennifer L. Rosenbaum ◽  
Susan J. Melhorn ◽  
Stefan Schoen ◽  
Mary F. Webb ◽  
Mary Rosalynn B. De Leon ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cohort Study ◽  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
Relaxation Times ◽  
Normal Glucose Tolerance ◽  
T2 Relaxation ◽  
Β Cell ◽  
Normal Glucose

Objective: Preclinical research implicates hypothalamic glial cell responses in the pathogenesis of obesity and type 2 diabetes. The current study sought to translate such findings into humans by testing if radiologic markers of gliosis in the mediobasal hypothalamus (MBH) were greater in persons with obesity and impaired glucose homeostasis or type 2 diabetes. <p>Research Design and Methods: Using cross-sectional and prospective cohort study designs, we applied a validated, quantitative magnetic resonance imaging (MRI) approach to assess gliosis in 67 adults with obesity and normal glucose tolerance, impaired glucose tolerance, or type 2 diabetes. Assessments of glucose homeostasis were conducted via oral glucose tolerance tests (OGTT) and β-cell modeling. </p> <p> Results: We found significantly greater T2 relaxation times (a marker of gliosis by MRI), that were independent of adiposity, in the impaired glucose tolerance and type 2 diabetes groups as compared to the normal glucose tolerance group. Findings were present in the MBH, but not control regions. Moreover, positive linear associations were present in the MBH but not control regions between T2 relaxation time and glucose area under the curve during an OGTT, fasting glucose concentrations, hemoglobin A1c, and visceral adipose tissue mass, whereas negative linear relationships were present in the MBH for markers of insulin sensitivity and β-cell function. In a prospective cohort study, greater MBH T2 relaxation times predicted declining insulin sensitivity over one year. </p> Conclusions: Findings support a role for hypothalamic gliosis in the progression of insulin resistance in obesity and, thus, type 2 diabetes pathogenesis in humans.

Effect of High ß-Glucan Barley on Postprandial Plasma Glucose Levels in Subjects with Normal Glucose Tolerance and Patients with Type 2 Diabetes

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 772-P
Author(s):  
MARIKO HIGA ◽  
AYANA HASHIMOTO ◽  
MOE HAYASAKA ◽  
MAI HIJIKATA ◽  
AYAMI UEDA ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Normal Glucose Tolerance ◽  
Postprandial Plasma Glucose ◽  
Glucose Levels ◽  
Normal Glucose
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