Faculty Opinions recommendation of Gastric bypass and banding equally improve insulin sensitivity and β cell function.

Author(s):  
Naveed Sattar
2012 ◽  
Vol 122 (12) ◽  
pp. 4667-4674 ◽  
Author(s):  
David Bradley ◽  
Caterina Conte ◽  
Bettina Mittendorfer ◽  
J. Christopher Eagon ◽  
J. Esteban Varela ◽  
...  

2021 ◽  
Author(s):  
Malini Prasad ◽  
Victoria Mark ◽  
Chanel Ligon ◽  
Roxanne Dutia ◽  
Nandini Nair ◽  
...  

<i>Objective</i>: The role of the gut in diabetes remission after gastric bypass (RYGB) is incompletely understood. We therefore assessed the temporal change in insulin secretory capacity after RYGB, using oral and intravenous (IV) glucose, in individuals with type 2 diabetes. <p><i>Research Design and Methods:</i> Longitudinal, prospective measures of β-cell function after oral glucose and IV graded glucose infusion in individuals with severe obesity and diabetes studied at 0, 3 (n=29), 12 (n=24) and 24 (n=20) months after RYGB. Data were collected between 2015 and 2019 in an academic clinical research center.</p> <p><i>Results</i>: The decreases in body weight, fat mass, waist circumference and insulin resistance after surgery (all p<0.001 at 12 and 24 months), did not differ according to diabetes remission status. In contrast, both the magnitude and temporal changes in β-cell glucose sensitivity after oral glucose differed by remission status (p=0.04): greater (6.5 fold, p<0.01) and sustained in full remitters, moderate and not sustained past 12 months in partial remitters (3.3 fold, p<0.001), minimal in non-remitters (2.7 fold, p=ns). The improvement in β-cell function after IV glucose was not apparent until 12 months, significant only in full remitters, and only ~1/3 of that observed after oral glucose.</p> <p>Pre-intervention β-cell function and its change after surgery predicted remission; weight loss and insulin sensitivity did not. </p> <p><i>Conclusion</i>: Our data show the time course of changes in β-cell function after RYGB. The improvement in β-cell function after RYGB, but not changes in weight loss or insulin sensitivity, drives diabetes remission.</p>


2015 ◽  
Vol 167 (5) ◽  
pp. 1042-1048.e1 ◽  
Author(s):  
Thomas H. Inge ◽  
Ronald L. Prigeon ◽  
Deborah A. Elder ◽  
Todd M. Jenkins ◽  
Robert M. Cohen ◽  
...  

2021 ◽  
Author(s):  
Malini Prasad ◽  
Victoria Mark ◽  
Chanel Ligon ◽  
Roxanne Dutia ◽  
Nandini Nair ◽  
...  

<i>Objective</i>: The role of the gut in diabetes remission after gastric bypass (RYGB) is incompletely understood. We therefore assessed the temporal change in insulin secretory capacity after RYGB, using oral and intravenous (IV) glucose, in individuals with type 2 diabetes. <p><i>Research Design and Methods:</i> Longitudinal, prospective measures of β-cell function after oral glucose and IV graded glucose infusion in individuals with severe obesity and diabetes studied at 0, 3 (n=29), 12 (n=24) and 24 (n=20) months after RYGB. Data were collected between 2015 and 2019 in an academic clinical research center.</p> <p><i>Results</i>: The decreases in body weight, fat mass, waist circumference and insulin resistance after surgery (all p<0.001 at 12 and 24 months), did not differ according to diabetes remission status. In contrast, both the magnitude and temporal changes in β-cell glucose sensitivity after oral glucose differed by remission status (p=0.04): greater (6.5 fold, p<0.01) and sustained in full remitters, moderate and not sustained past 12 months in partial remitters (3.3 fold, p<0.001), minimal in non-remitters (2.7 fold, p=ns). The improvement in β-cell function after IV glucose was not apparent until 12 months, significant only in full remitters, and only ~1/3 of that observed after oral glucose.</p> <p>Pre-intervention β-cell function and its change after surgery predicted remission; weight loss and insulin sensitivity did not. </p> <p><i>Conclusion</i>: Our data show the time course of changes in β-cell function after RYGB. The improvement in β-cell function after RYGB, but not changes in weight loss or insulin sensitivity, drives diabetes remission.</p>


Obesity ◽  
2021 ◽  
Author(s):  
Anny H. Xiang ◽  
Mayra P. Martinez ◽  
Enrique Trigo ◽  
Kristina M. Utzschneider ◽  
Melanie Cree‐Green ◽  
...  

2019 ◽  
Vol 21 (1) ◽  
pp. 18-27
Author(s):  
Joon Young Kim ◽  
Hala Tfayli ◽  
Fida Bacha ◽  
SoJung Lee ◽  
Sara F. Michaliszyn ◽  
...  

Diabetes Care ◽  
2016 ◽  
Vol 40 (1) ◽  
pp. 85-93 ◽  
Author(s):  
Silva Arslanian ◽  
Laure El ghormli ◽  
Fida Bacha ◽  
Sonia Caprio ◽  
Robin Goland ◽  
...  

1998 ◽  
Vol 83 (2) ◽  
pp. 503-508
Author(s):  
Victor C. Pardini ◽  
Ivana M. N. Victória ◽  
Selma M. V. Rocha ◽  
Danielle G. Andrade ◽  
Aline M. Rocha ◽  
...  

Lipoatropic diabetes (LD) designates a group of syndromes characterized by diabetes mellitus with marked insulin resistance and either a localized or generalized absence of adipose tissue. In this study, we evaluated plasma leptin levels in subjects with congenital generalized lipoatropic diabetes (CGLD, n = 11) or acquired generalized lipoatropic diabetes (AGLD, n = 11), and assessed correlations between leptin levels and estimations of insulin secretion and insulin sensitivity using homeostasis model assessment (HOMA). Leptin levels were 0.86 ± 0.32, 1.76 ± 0.78, and 6.9 ± 4.4 ng/mL in subjects with CGLD, AGLD, and controls (n = 19), respectively (ANOVA P &lt; 0.0001). Specific insulin levels were 154 ± 172, 177 ± 137 and 43 ± 22 pmol/L, respectively (P &lt; 0.0001). Insulin sensitivity was significantly decreased in both groups with LD (P&lt; 0.0001), whereas HOMA β-cell function was not significantly different when compared with controls. Leptin levels were significantly correlated with body mass index, insulin levels, and HOMA β-cell function, and inversely correlated with insulin sensitivity in control subjects but not in subjects with generalized LD. In conclusion, decreased leptin levels were observed in subjects with generalized LD, with a trend towards lower levels in the acquired than in the congenital form (P = 0.06). The temporal relationship between the decrease in leptin levels and the development of lipoatrophy should be investigated in at-risk young relatives of subjects with the acquired forms to assess the usefulness of leptin levels as a marker of lipoatrophy.


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