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1Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea
2Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
3Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
4Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea
Copyright © 2023 Korean Endocrine Society
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
The Namgok Award is the highest scientific award of the Korean Endocrine Society, and is given to honor an individual who has made excellent contributions to progress in the field of endocrinology and metabolism. The Namgok Award is named after the pen name of Professor Hun Ki Min, who founded the Korean Endocrine Society in 1982. Professor Young Min Cho received the Namgok Award at the 10th Seoul International Congress of Endocrinology and Metabolism of the Korean Endocrine Society in October 2022.
CONFLICTS OF INTEREST
Young Min Cho received research grants from Daewoong Pharmaceuticals and Sanofi, and consultation fees from LG Chemical.
Design | Intervention | Methods of measurement | No. | HbA1c | Duration of diabetes | Main results (control vs. intervention, if indicated) | |
---|---|---|---|---|---|---|---|
Insulin [10] | Single arm, non-controlled | Intensive insulin therapy, 4 wk | Hyperglycemic clamp (glucose level at 15 mM) with saline, GLP-1, or GIP infusion | 8 | 8.60% | 4.5 yr | Late-phase insulin response (nmol/L×min) |
Saline: 2.7±0.7 vs. 4.9±3.4 (P<0.05) | |||||||
GLP-1: 6.0±2.3 vs. 20.4±12.5 (P<0.05) | |||||||
GIP: 2.7±0.9 vs. 15.2±4.9 (P<0.05) | |||||||
Sulfonylurea [9] | Single arm, non-controlled | Glyburide, 1 mo | Hyperglycemic clamp (glucose level at 5.4 mM above fasting) with GIP infusion | 5 | NA | <3 mo | Insulin during hyperglycemic clamp: 99±29 vs. 156±41 pM (P<0.05) |
Insulin during GIP infusion: 123±37 vs. 283±80 pM (P<0.05) | |||||||
Metformin [36] | Animal study | Metformin, 4 wk | GLP-1 receptor expression in the pancreatic β-cells of Goto-Kakizaki rats | - | - | - | Expression level: 26.1%±2.1% vs. 45.4%±3.3%, P<0.001 |
DPP-4 inhibitor [37] | Randomized, double-blind, placebo-controlled | Sitagliptin, 12 wk | Hyperglycemic clamp (glucose level at 15 mM) with saline, GLP-1, or GIP infusion | 25 | 7.80% | 5.0 yr | AUC of insulin (pmol/L×120 min) |
Saline: 15.4±3.0 vs. 21.2±3.0 (nonsignificant) | |||||||
GIP: 20.7±3.8 vs. 31.2±6.4 (P<0.05) | |||||||
GLP-1: 52.5±11.1 vs. 95.3±27.0 (nonsignificant) | |||||||
Phlorizin [38] | Animal study | Phlorizin, 4 wk | GLP-1 and GIP receptor expression in the pancreatic β-cells of pancreatectomized hyperglycemic rats and Zucker diabetic fatty rats | - | - | - | Phlorizin treatment restored GLP-1 and GIP receptor expression in pancreatectomized hyperglycemic rat |
Phlorizin treatment restored GIP receptor expression in Zucker diabetic fatty rat | |||||||
SGLT2 inhibitor [11] | Single arm, non-controlled | Dapagliflozin, 8 wk | Hyperglycemic clamp (glucose level at 15.5 mM) with sequential GLP-1 and GIP infusion | 19 | 7.80% | 10.2 yr | C-peptide response (nmol/L×min) |
C-peptide response to hyperglycemia: 10.9±6.5 vs. 16.6±9.2, P=0.009 | |||||||
C-peptide response to GLP-1: 83.6±42.1 vs. 106.6±45.7, P=0.011 | |||||||
C-peptide response to GIP: 82.5±58.4 vs. 101.9±50.3, P=0.087 |
Design | Intervention | Methods of measurement | No. | HbA1c | Duration of diabetes | Main results (control vs. intervention, if indicated) | |
---|---|---|---|---|---|---|---|
Insulin [10] | Single arm, non-controlled | Intensive insulin therapy, 4 wk | Hyperglycemic clamp (glucose level at 15 mM) with saline, GLP-1, or GIP infusion | 8 | 8.60% | 4.5 yr | Late-phase insulin response (nmol/L×min) |
Saline: 2.7±0.7 vs. 4.9±3.4 (P<0.05) | |||||||
GLP-1: 6.0±2.3 vs. 20.4±12.5 (P<0.05) | |||||||
GIP: 2.7±0.9 vs. 15.2±4.9 (P<0.05) | |||||||
Sulfonylurea [9] | Single arm, non-controlled | Glyburide, 1 mo | Hyperglycemic clamp (glucose level at 5.4 mM above fasting) with GIP infusion | 5 | NA | <3 mo | Insulin during hyperglycemic clamp: 99±29 vs. 156±41 pM (P<0.05) |
Insulin during GIP infusion: 123±37 vs. 283±80 pM (P<0.05) | |||||||
Metformin [36] | Animal study | Metformin, 4 wk | GLP-1 receptor expression in the pancreatic β-cells of Goto-Kakizaki rats | - | - | - | Expression level: 26.1%±2.1% vs. 45.4%±3.3%, P<0.001 |
DPP-4 inhibitor [37] | Randomized, double-blind, placebo-controlled | Sitagliptin, 12 wk | Hyperglycemic clamp (glucose level at 15 mM) with saline, GLP-1, or GIP infusion | 25 | 7.80% | 5.0 yr | AUC of insulin (pmol/L×120 min) |
Saline: 15.4±3.0 vs. 21.2±3.0 (nonsignificant) | |||||||
GIP: 20.7±3.8 vs. 31.2±6.4 (P<0.05) | |||||||
GLP-1: 52.5±11.1 vs. 95.3±27.0 (nonsignificant) | |||||||
Phlorizin [38] | Animal study | Phlorizin, 4 wk | GLP-1 and GIP receptor expression in the pancreatic β-cells of pancreatectomized hyperglycemic rats and Zucker diabetic fatty rats | - | - | - | Phlorizin treatment restored GLP-1 and GIP receptor expression in pancreatectomized hyperglycemic rat |
Phlorizin treatment restored GIP receptor expression in Zucker diabetic fatty rat | |||||||
SGLT2 inhibitor [11] | Single arm, non-controlled | Dapagliflozin, 8 wk | Hyperglycemic clamp (glucose level at 15.5 mM) with sequential GLP-1 and GIP infusion | 19 | 7.80% | 10.2 yr | C-peptide response (nmol/L×min) |
C-peptide response to hyperglycemia: 10.9±6.5 vs. 16.6±9.2, P=0.009 | |||||||
C-peptide response to GLP-1: 83.6±42.1 vs. 106.6±45.7, P=0.011 | |||||||
C-peptide response to GIP: 82.5±58.4 vs. 101.9±50.3, P=0.087 |
HbA1c, hemoglobin A1c; GLP-1, glucagon-like peptide-1; GIP, glucose-dependent insulinotropic polypeptide; NA, not available; DPP-4, dipeptidyl peptidase-4; AUC, area under the curve; SGLT2, sodium-glucose co-transporter 2.