Mechanisms for abnormal postprandial glucose metabolism in type 2 diabetes

2006 ◽  
Vol 290 (1) ◽  
pp. E67-E77 ◽  
Author(s):  
Hans J. Woerle ◽  
Ervin Szoke ◽  
Christian Meyer ◽  
Jean M. Dostou ◽  
Steven D. Wittlin ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Postprandial Glucose ◽  
Postprandial Hyperglycemia ◽  
Glucose Disposal ◽  
Glucose Release ◽  
Isotope Technique ◽  
Glucose Storage ◽  
And Storage

To assess mechanisms for postprandial hyperglycemia, we used a triple-isotope technique ([\3-3H]glucose and [14C]bicarbonate and oral [6,6-dideutero]glucose iv) and indirect calorimetry to compare components of glucose release and pathways for glucose disposal in 26 subjects with type 2 diabetes and 15 age-, weight-, and sex-matched normal volunteers after a standard meal. The results were as follows: 1) diabetic subjects had greater postprandial glucose release ( P < 0.001) because of both increased endogenous and meal-glucose release; 2) the greater endogenous glucose release ( P < 0.001) was due to increased gluconeogenesis ( P < 0.001) and glycogenolysis ( P = 0.01); 3) overall tissue glucose uptake, glycolysis, and storage were comparable in both groups ( P > 0.3); 4) glucose clearance ( P < 0.001) and oxidation ( P = 0.004) were reduced, whereas nonoxidative glycolysis was increased ( P = 0.04); and 5) net splanchnic glucose storage was reduced by ∼45% ( P = 0.008) because of increased glycogen cycling ( P = 0.03). Thus in type 2 diabetes, postprandial hyperglycemia is primarily due to increased glucose release; hyperglycemia overcomes the effects of impaired insulin secretion and sensitivity on glucose transport, but intracellular defects persist so that pathways of glucose metabolism are abnormal and glucose is shunted away from normal sites of storage (e.g., liver and muscle) into other tissues.

Abnormal renal, hepatic, and muscle glucose metabolism following glucose ingestion in type 2 diabetes

2004 ◽  
Vol 287 (6) ◽  
pp. E1049-E1056 ◽  
Author(s):  
Christian Meyer ◽  
Hans J. Woerle ◽  
Jean M. Dostou ◽  
Stephen L. Welle ◽  
John E. Gerich
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Postprandial Glucose ◽  
Glucose Disposal ◽  
Glucose Release ◽  
Glucose Ingestion ◽  
Endogenous Glucose

Recent studies indicate an important role of the kidney in postprandial glucose homeostasis in normal humans. To determine its role in the abnormal postprandial glucose metabolism in type 2 diabetes mellitus (T2DM), we used a combination of the dual-isotope technique and net balance measurements across kidney and skeletal muscle in 10 subjects with T2DM and 10 age-, weight-, and sex-matched nondiabetic volunteers after ingestion of 75 g of glucose. Over the 4.5-h postprandial period, diabetic subjects had increased mean blood glucose levels (14.1 ± 1.1 vs. 6.2 ± 0.2 mM, P < 0.001) and increased systemic glucose appearance (100.0 ± 6.3 vs. 70.0 ± 3.3 g, P < 0.001). The latter was mainly due to ∼23 g greater endogenous glucose release (39.8 ± 5.9 vs. 17.0 ± 1.8 g, P < 0.002), since systemic appearance of the ingested glucose was increased by only ∼7 g (60.2 ± 1.4 vs. 53.0 ± 2.2 g, P < 0.02). Approximately 40% of the diabetic subjects’ increased endogenous glucose release was due to increased renal glucose release (19.6 ± 3.1 vs. 10.6 ± 2.4 g, P < 0.05). Postprandial systemic tissue glucose uptake was also increased in the diabetic subjects (82.3 ± 4.7 vs. 69.8 ± 3.5 g, P < 0.05), and its distribution was altered; renal glucose uptake was increased (21.0 ± 3.5 vs. 9.8 ± 2.3 g, P < 0.03), whereas muscle glucose uptake was normal (18.5 ± 1.8 vs. 25.9 ± 3.3 g, P = 0.16). We conclude that, in T2DM, 1) both liver and kidney contribute to postprandial overproduction of glucose, and 2) postprandial renal glucose uptake is increased, resulting in a shift in the relative importance of muscle and kidney for glucose disposal. The latter may provide an explanation for the renal glycogen accumulation characteristic of diabetes mellitus as well as a mechanism by which hyperglycemia may lead to diabetic nephropathy.

Pathways for glucose disposal after meal ingestion in humans

2003 ◽  
Vol 284 (4) ◽  
pp. E716-E725 ◽  
Author(s):  
Hans J. Woerle ◽  
Christian Meyer ◽  
Jean M. Dostou ◽  
Niyaz R. Gosmanov ◽  
Nazmul Islam ◽  
...  
Keyword(s):  
Tritiated Water ◽  
Postprandial Glucose ◽  
Systemic Circulation ◽  
Glucose Disposal ◽  
Indirect Pathway ◽  
Postprandial Period ◽  
Glucose Storage ◽  
Meal Ingestion ◽  
And Storage ◽  
Glycogen Formation

To characterize postprandial glucose disposal more completely, we used the tritiated water technique, a triple-isotope approach (intravenous [3-H3]glucose and [14C]bicarbonate and oral [6,6-2H2]glucose) and indirect calorimetry to assess splanchnic and peripheral glucose disposal, direct and indirect glucose storage, oxidative and nonoxidative glycolysis, and the glucose entering plasma via gluconeogenesis after ingestion of a meal in 11 normal volunteers. During a 6-h postprandial period, a total of ∼98 g of glucose were disposed of. This was more than the glucose contained in the meal (∼78 g) due to persistent endogenous glucose release (∼21 g): splanchnic tissues initially took up ∼23 g, and an additional ∼75 g were removed from the systemic circulation. Direct glucose storage accounted for ∼32 g and glycolysis for ∼66 g (oxidative ∼43 g and nonoxidative ∼23 g). About 11 g of glucose appeared in plasma as a result of gluconeogenesis. If these carbons were wholly from glucose undergoing glycolysis, only ∼12 g would be available for indirect pathway glycogen formation. Our results thus indicate that glycolysis is the main initial postprandial fate of glucose, accounting for ∼66% of overall disposal; oxidation and storage each account for ∼45%. The majority of glycogen is formed via the direct pathway (∼73%).

Cranberries improve postprandial glucose excursions in type 2 diabetes

2017 ◽  
Vol 8 (9) ◽  
pp. 3083-3090 ◽  
Author(s):  
Jace Schell ◽  
Nancy M. Betts ◽  
Megan Foster ◽  
R. Hal Scofield ◽  
Arpita Basu
Keyword(s):  
Type 2 Diabetes ◽  
Vascular Complications ◽  
Postprandial Glucose ◽  
Postprandial Hyperglycemia

An overview of the role of dried cranberries in reducing postprandial hyperglycemia and inflammation in type 2 diabetes and the subsequent risks of vascular complications.

scholarly journals The Cre/CysC Ratio can Predict Muscle Composition and is Associated with Glucose Disposal Ability and Macrovascular Disease in Patients with Type 2 Diabetes

2021 ◽  
Author(s):  
Qing Yang ◽  
Mei Zhang ◽  
Peng Sun ◽  
Yanying Li ◽  
Huichao Xu ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Diabetic Complications ◽  
Linear Regression Analysis ◽  
Macrovascular Disease ◽  
Postprandial Glucose ◽  
Glucose Disposal ◽  
Skeletal Muscle Index ◽  
Muscle Composition

Abstract Background: Since the ratio of creatinine to cystatin C (Cre/CysC) can reflect muscle volume, it has been proven to be a predictor of sarcopenia in patients with or without diabetes. Here, we investigated the predictive value of Cre/CysC in skeletal muscle composition and its correlations with glucose disposal ability and diabetic complications in patients with type 2 diabetes.Methods: The skeletal muscle index (SMI) and mean skeletal muscle attenuation (MMA) values of 193 patients with type 2 diabetes were obtained through analyses of CT images at the lumbar 3 level.Results: Serum Cre/CysC was significantly correlated with both the SMI (r =0.375, P < 0.001) and MMA (r = 0.378, P < 0.001). Multiple stepwise linear regression analysis demonstrated that Cre/CysC was the only biochemical predictor of the SMI [b = 0.48, (95% Cl, 0.02 to 0.94) and MMA [b= 0.57, (95% Cl, 0.14 to 1.01). In the diabetic complications analysis, Cre/CysC was negatively correlated with cardiovascular disease (r = -0.190, P = 0.008) and lower extremity arterial disease (r = -0.209, P = 0.004). Moreover, in the 100 g steamed bun test, Cre/CysC was significantly correlated with glucose levels at 60 min (r = -0.162, P = 0.045), 120 min (r = -0.287, P < 0.001) and 180 min (r = -0.313, P < 0.001).Conclusions: Cre/CysC is a valuable predictor of skeletal muscle composition in type 2 diabetes. Patients with higher levels of Cre/CysC may have a better ability to dispose of postprandial glucose and lower risk of macrovascular disease.

23-OR: The Effect of 14-Day Atorvastatin Treatment on Postprandial Glucose Metabolism in Healthy Males—A Link to Why Statin Therapy Increases the Risk of Type 2 Diabetes?

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 23-OR
Author(s):  
MARTIN L. THOMASEN ◽  
DAVID P. SONNE ◽  
MARTIN L. KÅRHUS ◽  
ANDREAS BRØNDEN ◽  
BART STAELS ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Statin Therapy ◽  
Postprandial Glucose ◽  
Atorvastatin Treatment ◽  
Healthy Males

scholarly journals Effects of Sustained Treatment With Lixisenatide on Gastric Emptying and Postprandial Glucose Metabolism in Type 2 Diabetes: A Randomized Controlled Trial

Diabetes Care ◽  
2020 ◽  
Vol 43 (8) ◽  
pp. 1813-1821 ◽  
Author(s):  
Christopher K. Rayner ◽  
Linda E. Watson ◽  
Liza K. Phillips ◽  
Kylie Lange ◽  
Michelle J. Bound ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Randomized Controlled Trial ◽  
Gastric Emptying ◽  
Glucose Metabolism ◽  
Controlled Trial ◽  
Postprandial Glucose ◽  
Randomized Controlled

scholarly journals Effects of Ipragliflozin on Postprandial Glucose Metabolism and Gut Peptides in Type 2 Diabetes: A Pilot Study

2018 ◽  
Vol 9 (1) ◽  
pp. 403-411 ◽  
Author(s):  
Hiroaki Ueno ◽  
Hiroko Nakazato ◽  
Emi Ebihara ◽  
Kenji Noma ◽  
Takahisa Kawano ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Pilot Study ◽  
Glucose Metabolism ◽  
Postprandial Glucose ◽  
Gut Peptides

scholarly journals Effects of sustained treatment with lixisenatide on gastric emptying and postprandial glucose metabolism in type 2 diabetes: a randomized controlled trial

2020 ◽  
Author(s):  
Christopher K. Rayner ◽  
Linda E. Watson ◽  
Liza K. Phillips ◽  
Kylie Lange ◽  
Michelle J. Bound ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Gastric Emptying ◽  
Glucose Metabolism ◽  
Postprandial Glucose ◽  
Oral Glucose ◽  
Continuous Exposure ◽  
Short Acting ◽  
Postprandial Glycemia ◽  
Gastric Emptying Scintigraphy

<i>Objective</i> <p>Slowing of gastric emptying by GLP-1 exhibits tachyphylaxis with continuous exposure. We therefore aimed to establish whether prolonged use of a “short-acting” GLP-1 receptor agonist (GLP-1RA), lixisenatide, achieves sustained slowing of gastric emptying and reduction in postprandial glycemia. </p> <p> </p> <p><i>Research design and methods</i></p> <p>30 patients with metformin-treated type 2 diabetes underwent assessment of gastric emptying (scintigraphy) and glucose metabolism (dual tracer technique) after a 75g glucose drink, before and after 8 weeks’ treatment with lixisenatide (20µg subcutaneously daily) or placebo, in a double-blind randomized parallel design.</p> <p> </p> <p><i>Results</i></p> <p>Gastric retention of the glucose drink was markedly increased after lixisenatide versus placebo (ratio of adjusted geometric means for area under curve (AUC) over 240 min of 2.19 (95% CI 1.82, 2.64; P<0.001), associated with substantial reductions in the rate of systemic appearance of oral glucose (P<0.001) and incremental AUC for blood glucose (P<0.001). Lixisenatide suppressed both glucagon (P=0.003) and insulin (P=0.032), but not endogenous glucose production, over 120 min after oral glucose. Postprandial glucose-lowering over 240 min was strongly related to the magnitude of slowing of gastric emptying by lixisenatide (r = -0.74, P = 0.002) and to the baseline rate of emptying (r = 0.52, P = 0.048), but unrelated to ß-cell function (assessed by ß-cell glucose sensitivity).</p> <p> </p> <p><i>Conclusions</i></p> <p>8 weeks’ treatment with lixisenatide is associated with sustained slowing of gastric emptying and marked reductions in postprandial glycemia and appearance of ingested glucose. Short-acting GLP-1RAs therefore potentially represent an effective long-term therapy for specifically targeting postprandial glucose excursions.</p>

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