Mixed model of dietary fat effect on postprandial glucose-insulin metabolism from carbohydrates in type 1 diabetes

2015 ◽  
Author(s):  
Claudia Cecilia Yamamoto Noguchi ◽  
Noriaki Kunikane ◽  
Shogo Hashimoto ◽  
Eiko Furutani
Keyword(s):  
Type 1 Diabetes ◽  
Dietary Fat ◽  
Mixed Model ◽  
Postprandial Glucose ◽  
Insulin Metabolism

Effects of Dietary Fat and Protein on Glucoregulatory Hormones in Adolescents and Young Adults With Type 1 Diabetes

2021 ◽  
Author(s):  
Amelia J Harray ◽  
Sabrina Binkowski ◽  
Barbara L Keating ◽  
Michael Horowitz ◽  
Scott Standfield ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Dietary Fat ◽  
Glucagon Secretion ◽  
Postprandial Glucose ◽  
High Protein ◽  
Low Protein ◽  
Insulin Clamp ◽  
Glucoregulatory Hormones ◽  
The Impact

Abstract Context Dietary fat and protein impact postprandial hyperglycemia in people with type 1 diabetes, but the underlying mechanisms are poorly understood. Glucoregulatory hormones are also known to modulate gastric emptying and may contribute to this effect. Objective Investigate the effects of fat and protein on glucagon-like peptide (GLP-1), glucagon-dependent insulinotropic polypeptide (GIP) and glucagon secretion. Methods 2 crossover euglycemic insulin clamp clinical trials at 2 Australian pediatric diabetes centers. Participants were 12-21 years (n = 21) with type 1 diabetes for ≥1 year. Participants consumed a low-protein (LP) or high-protein (HP) meal in Study 1, and low-protein/low-fat (LPLF) or high-protein/high-fat (HPHF) meal in Study 2, all containing 30 g of carbohydrate. An insulin clamp was used to maintain postprandial euglycemia and plasma glucoregulatory hormones were measured every 30 minutes for 5 hours. Data from both cohorts (n = 11, 10) were analyzed separately. The main outcome measure was area under the curve of GLP-1, GIP, and glucagon. Results Meals low in fat and protein had minimal effect on GLP-1, while there was sustained elevation after HP (80.3 ± 16.8 pmol/L) vs LP (56.9 ± 18.6), P = .016, and HPHF (103.0 ± 26.9) vs LPLF (69.5 ± 31.9) meals, P = .002. The prompt rise in GIP after all meals was greater after HP (190.2 ± 35.7 pmol/L) vs LP (152.3 ± 23.3), P = .003, and HPHF (258.6 ± 31.0) vs LPLF (151.7 ± 29.4), P < .001. A rise in glucagon was also seen in response to protein, and HP (292.5 ± 88.1 pg/mL) vs LP (182.8 ± 48.5), P = .010. Conclusion The impact of fat and protein on postprandial glucose excursions may be mediated by the differential secretion of glucoregulatory hormones. Further studies to better understand these mechanisms may lead to improved personalized postprandial glucose management.

733-P: Postprandial Glucose Variability in People with Type 1 Diabetes Is Individual and Impacted by Physiological and Clinical Parameters

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 733-P
Author(s):  
CASSY F.B. DINGENA ◽  
AILSA MARSH ◽  
RAMZI AJJAN ◽  
MATTHEW CAMPBELL
Keyword(s):  
Type 1 Diabetes ◽  
Glucose Variability ◽  
Postprandial Glucose ◽  
Clinical Parameters

Does dietary fat cause a dose dependent glycaemic response in youth with type 1 diabetes?

2021 ◽  
Author(s):  
Susan M. O'Connell ◽  
Norma M. A. O'Toole ◽  
Conor N. Cronin ◽  
Chen Saat‐Murphy ◽  
Patrick McElduff ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Dietary Fat ◽  
Glycaemic Response ◽  
Dose Dependent

scholarly journals Possible Ways to Improve Postprandial Glucose Control in Type 1 Diabetes

2018 ◽  
Vol 20 (S2) ◽  
pp. S2-24-S2-32 ◽  
Author(s):  
Halis Kaan Akturk ◽  
Amanda Rewers ◽  
Hal Joseph ◽  
Nicole Schneider ◽  
Satish K. Garg
Keyword(s):  
Type 1 Diabetes ◽  
Glucose Control ◽  
Postprandial Glucose

scholarly journals IAPP and type 1 diabetes: implications for immunity, metabolism and islet transplants

2018 ◽  
Vol 60 (2) ◽  
pp. R57-R75 ◽  
Author(s):  
Heather C Denroche ◽  
C Bruce Verchere
Keyword(s):  
Type 1 Diabetes ◽  
Glucose Metabolism ◽  
Beta Cell ◽  
Postprandial Glucose ◽  
Sterile Inflammation ◽  
Islet Amyloid ◽  
Islet Transplant ◽  
Transplant Failure ◽  
Islet Transplants

Islet amyloid polypeptide (IAPP), the main component of islet amyloid in type 2 diabetes and islet transplants, is now recognized as a contributor to beta cell dysfunction. Increasingly, evidence warrants its investigation in type 1 diabetes owing to both its immunomodulatory and metabolic actions. Autoreactive T cells to IAPP-derived epitopes have been described in humans, suggesting that IAPP is an islet autoantigen in type 1 diabetes. In addition, although aggregates of IAPP have not been implicated in type 1 diabetes, they are potent pro-inflammatory stimuli to innate immune cells, and thus, could influence autoimmunity. IAPP aggregates also occur rapidly in transplanted islets and likely contribute to islet transplant failure in type 1 diabetes through sterile inflammation. In addition, since type 1 diabetes is a disease of both insulin and IAPP deficiency, clinical trials have examined the potential benefits of IAPP replacement in type 1 diabetes with the injectable IAPP analogue, pramlintide. Pramlintide limits postprandial hyperglycemia by delaying gastric emptying and suppressing hyperglucagonemia, underlining the possible role of IAPP in postprandial glucose metabolism. Here, we review IAPP in the context of type 1 diabetes: from its potential involvement in type 1 diabetes pathogenesis, through its role in glucose metabolism and use of IAPP analogues as therapeutics, to its potential role in clinical islet transplant failure and considerations in this regard for future beta cell replacement strategies.

Postprandial Glucose Regulation via KNN Meal Classification in Type 1 Diabetes

2019 ◽  
Vol 3 (2) ◽  
pp. 230-235 ◽  
Author(s):  
Eleonora Maria Aiello ◽  
Chiara Toffanin ◽  
Mirko Messori ◽  
Claudio Cobelli ◽  
Lalo Magni
Keyword(s):  
Type 1 Diabetes ◽  
Postprandial Glucose ◽  
Glucose Regulation
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