Single-dose acarbose decreased glucose-dependent insulinotropic peptide and glucagon levels in Chinese patients with newly diagnosed type 2 diabetes mellitus after a mixed meal

Chen, Zhong; Fu, Xiaoying; Kuang, Jian; Ju, Chen; Chen, Hongmei; Pei, Jian-Hao; Yang, Hongjiang

doi:10.1186/s12902-016-0133-7

Cited by 7 publications

(9 citation statements)

References 32 publications

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“…In our study, all carbohydrates suppressed glucagon secretion with no substantial differences between RYGB and control subjects, and glucagon was not enhanced by distal digestion, suggesting that other mechanisms besides co-secretion with GLP-1 from L-cells are involved (64). Secretory responses of C-peptide were considerably lowered by acarbose in both RYGB and control subjects in agreement with previous reports (30,32,33,49). Reduced beta-cell stimulation by glucose and incretin hormones following alpha-glucosidase inhibition may explain this finding.…”

Section: Discussionsupporting

confidence: 92%

“…Judging from the glycemic profiles, alpha-glucosidase inhibition by acarbose effectively suppressed sucrose digestion, but somewhat surprisingly, this did not lead to greater GLP-1 secretion in control subjects, again raising doubt about the idea that delaying glucose absorption to distal sites will enhance GLP-1 secretion. Previous studies in unoperated individuals have observed only slightly increased GLP-1 release when acarbose is ingested with sucrose (29,30), and generally no change when the drug is combined with a mixed meal (32)(33)(34)(35)(36). Given that absorption of glucose is necessary for GLP-1 secretion also in the ileum (18), the simplest explanation for the lack of effect is that the alpha glucosidase activity was inhibited so much that hydrolysis was partially prevented, leading to malabsorption and transfer of some of the sucrose load to the colon.…”

Section: Discussionmentioning

confidence: 89%

“…The enzymatic activity of alpha-glucosidases can be inhibited pharmacologically by administration of acarbose. Acarbose ingested with sucrose has been found to increase GLP-1 release in unoperated individuals (29)(30)(31), while there is little effect when the drug is administered with a mixed meal (32)(33)(34)(35)(36), perhaps because the effect is overshadowed by the stimulatory effects of the other nutrients. Taken together, when digestion of carbohydrates is delayed, proximal absorption is assumed to be inhibited, leading to a more distal digestion and absorption and thereby greater release of GLP-1.…”

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confidence: 99%

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Augmented GLP-1 Secretion as Seen After Gastric Bypass May Be Obtained by Delaying Carbohydrate Digestion

Martinussen

Bojsen‐Møller

Dirksen

et al. 2019

The Journal of Clinical Endocrinology &Amp; Metabolism

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Context: Exaggerated postprandial Glucagon-like Peptide-1 (GLP-1) secretion seems important for weight loss and diabetes remission after Roux-en-Y gastric bypass (RYGB) and may result from carbohydrate absorption in the distal small intestine. Objective: To investigate distal (GLP-1; Peptide YY, PYY) and proximal (Glucosedependent Insulinotropic Polypeptide, GIP) gut hormone secretion in response to carbohydrates hydrolyzed at different rates. We hypothesized that slow digestion restricts proximal absorption, facilitating distal delivery of carbohydrates and thereby enhanced GLP-1 secretion in unoperated individuals, while this may not apply after RYGB. Design: Single-blinded, randomized, crossover study. Setting: Hvidovre Hospital, Denmark. Participants: 10 RYGB-and 10 unoperated matched subjects. Interventions: 4 separate days with ingestion of different carbohydrate loads, either rapidly/proximally digested (glucose+fructose; sucrose) or slowly/distally digested (isomaltulose; sucrose+acarbose). Main outcome measures: GLP-1 secretion (area-under-the-curve above baseline). Secondary outcomes included PYY and GIP. Results: Isomaltulose enhanced secretion of GLP-1 nearly 3-fold (p=0.02) and PYY 9-fold (p=0.08) compared with sucrose in unoperated subjects but had modest effect after RYGB. Acarbose failed to increase sucrose induced GLP-1 secretion in unoperated subjects and diminished the responses by 50% after RYGB (p=0.03). In both groups, GIP secretion was reduced by isomaltulose and even more so by sucrose+acarbose when compared to sucrose intake. Conclusions: GLP-1 secretion depends on the rate of carbohydrate digestion, but in a different manner after RYGB. Enhanced GLP-1 secretion is central after RYGB, but it may also be obtained in unoperated individuals by delaying hydrolysis of carbohydrates, pushing their digestion and absorption distally in the small intestine.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 89%

mentioning

confidence: 99%

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Augmented GLP-1 Secretion as Seen After Gastric Bypass May Be Obtained by Delaying Carbohydrate Digestion

Martinussen

Bojsen‐Møller

Dirksen

et al. 2019

The Journal of Clinical Endocrinology &Amp; Metabolism

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“…a-Glucosidase inhibitors (acarbose and miglitol) reduce levels of both GIP and glucagon (15), delay glucose absorption, and thereby blunt the insulin response to glucose (16). DPP-4 inhibitors are known to increase the early insulin response (by increasing circulating concentrations of active GLP-1), reduce glucagon secretion in a glucose-dependent manner, and therefore reduce both hyper-and hypoglycemia.…”

Section: Commentarymentioning

confidence: 99%

Combined Dipeptidyl Peptidase 4 Inhibitor and α-Glucosidase Inhibitor Treatment in Postprandial Hypoglycemia

Broome

2022

Clinical Diabetes

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“…There are studies that showed that he GIP and glucagon levels decreased after a mixed meal in patients with new diagnosed type 2 diabetics by treatment with single-dose acarbose [36,37] and acarbose decreased GIP and glucagon only in a mixed meal test rather than OGTT. [38] Glitazones Low-dose glitazones given to patients with reactive hypoglycemia associated with IGT are also considered to be effective in the symptoms of reactive hypoglycaemia and the prevention of diabetes. [39,40] As a matter of fact, hyperinsu-linemia and IGT were found in OGTT in 2 cases with hypoglycemic symptoms, and it has been shown that hyperinsulinemic clamp reduces the insulin sensitivity.…”

Section: Alpha Glucosidase Inhibitorsmentioning

confidence: 99%

Postprandial Reactive Hypoglycemia

Altuntaş

2019

Sisli Etfal

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R eactive hypoglycemia (RH) is the condition of postprandially hypoglycemia occurring 2-5 hours after food intake. [1] Many conditions are associated with postprandial hypoglycemia. RH clinically seen in three different forms as follows: idiopathic RH (at 180 min), alimentary (within 120 min) and late RH (at 240-300 min). Earliest change before type 2 diabetes is the loss of first-phase insulin release, which emerges with fasting glucose levels of about 110 mg/dl. Lack of first-phase insulin release, an excellent predictor of both types of diabetes, is thought to be the earliest sign of the adverse effects of hyperglycemia on beta-cells and insulin-sensitive tissues. [2] When the first-phase insulin response decreases, firstly, blood glucose starts to rise after the meal, which leads to late but excessive secretion of the second-phase insulin secretion. Thus, late reactive hypoglycemia occurs. [3] Elevated insulin levels also cause downregulation of the insulin postreceptor on the muscle and fat cells, thus decreasing insulin sensitivity. The cause of the increase in insulin sensitivity in IRH at 3 h is not completely clear. However, there is a decrease in insulin sensitivity in late reactive hypoglycaemia at 4 or 5 hours. Thus, patients with hypoglycemia at 4 or 5 h who have those with a higher number of people with diabetes in the first-degree relative and who have obesity may be more susceptible to diabetes Reactive hypoglycemia (RH) is the condition of postprandially hypoglycemia occurring 2-5 hours after food intake. RH is clinically seen in three different forms as follows: idiopathic RH (at 180 min), alimentary (within 120 min), and late RH (at 240-300 min). When the first-phase insulin response decreases, firstly, blood glucose starts to rise after the meal. This leads to late but excessive secretion of the second-phase insulin secretion. Thus, late reactive hypoglycemia occurs. Elevated insulin levels also cause down-regulation of the insulin post-receptor on the muscle and fat cells, thus decreasing insulin sensitivity. The cause of the increase in insulin sensitivity in IRH at 3 h is not completely clear. However, there is a decrease in insulin sensitivity in late reactive hypoglycaemia at 4 or 5 hours. Thus, patients with hypoglycemia at 4 or 5 h who have a family history of diabetes and obesity may be more susceptible to diabetes than patients with hypoglycemia at 3 h. We believe that some cases with normal glucose tolerance in OGTT should be considered as prediabetes at <55 or 60 mg/dl after 4-5 hours after OGTT. Metformin and AGI therapy may be recommended if there is late RH with IFG. Also Metformin, AGİ, TZD, DPP-IVInhibitors, GLP1RA therapy may be recommended if there is late RH with IGT. As a result, postprandial RH (<55 or 60 mg/dl), especially after 4 hours may predict diabetes. Therefore, people with RH along with weight gain and with diabetes history in the family will benefit from a lifestyle modification as well as the appropriate antidiabetic approach in the prevention of diabetes.

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Single-dose acarbose decreased glucose-dependent insulinotropic peptide and glucagon levels in Chinese patients with newly diagnosed type 2 diabetes mellitus after a mixed meal

Cited by 7 publications

References 32 publications

Augmented GLP-1 Secretion as Seen After Gastric Bypass May Be Obtained by Delaying Carbohydrate Digestion

Augmented GLP-1 Secretion as Seen After Gastric Bypass May Be Obtained by Delaying Carbohydrate Digestion

Combined Dipeptidyl Peptidase 4 Inhibitor and α-Glucosidase Inhibitor Treatment in Postprandial Hypoglycemia

Postprandial Reactive Hypoglycemia

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