<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13(4)</volume><submitter>Yoshiji S</submitter><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Previous studies suggested that β-cell function markers such as fasting and postprandial serum C-peptide and C-peptide increment (FCPR, PCPR, and ΔCPR, respectively) may be useful in estimating glycemic response to glucagon-like peptide-1 receptor agonists. However, it remains elusive whether baseline glycemic control confounds these markers. Here we aimed to identify the least confounded β-cell function markers and investigate whether these markers could predict glycemic response to dulaglutide.&lt;h4>Methods&lt;/h4>We evaluated FCPR, PCPR, and ΔCPR levels in patients with type 2 diabetes who initiated dulaglutide treatment after a standardized meal tolerance test (MTT). We first investigated the confounding effects of baseline HbA1c on β-cell function markers using Pearson's correlation test. Then, we evaluated the association between each β-cell function marker and glycemic response (HbA1c change 0-6 months) to dulaglutide using generalized linear model and logistic regression analysis with adjustment for baseline HbA1c.&lt;h4>Results&lt;/h4>In 141 patients, baseline HbA1c was significantly inversely correlated with PCPR and ΔCPR (P &lt; 0.01 for both) but not with FCPR (r = 0.02; P = 0.853), suggesting that FCPR was the marker least confounded by baseline glycemic control. Of all patients, 59 continued dulaglutide for at least 6 months without initiating any additional glucose-lowering medications. Mean ± SE HbA1c change 0-6 months was - 1.16 ± 0.17% (P &lt; 0.001 vs. baseline). The β-cell function markers were significantly associated with HbA1c change 0-6 months in the generalized linear model. FCPR was also a significant predictor for achieving a reduction in HbA1c of at least 1% (P = 0.044) with an area under the receiver operating characteristic curve of 0.83 (sensitivity = 0.81 and specificity = 0.79).&lt;h4>Conclusion&lt;/h4>Fasting and meal-induced C-peptide levels are associated with glycemic response to dulaglutide, among which FCPR is least confounded by baseline glycemic control, suggesting its utility as a marker for glycemic response to dulaglutide.</pubmed_abstract><journal>Diabetes therapy : research, treatment and education of diabetes and related disorders</journal><pagination>733-746</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8991285</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Exploring a Suitable Marker of Glycemic Response to Dulaglutide in Patients with Type 2 Diabetes: A Retrospective Study.</pubmed_title><pmcid>PMC8991285</pmcid><pubmed_authors>Hasebe M</pubmed_authors><pubmed_authors>Hamasaki A</pubmed_authors><pubmed_authors>Fujikawa J</pubmed_authors><pubmed_authors>Honjo S</pubmed_authors><pubmed_authors>Iwasaki K</pubmed_authors><pubmed_authors>Seno Y</pubmed_authors><pubmed_authors>Iwasaki Y</pubmed_authors><pubmed_authors>Yoshiji S</pubmed_authors><pubmed_authors>Shibue K</pubmed_authors><pubmed_authors>Keidai Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Exploring a Suitable Marker of Glycemic Response to Dulaglutide in Patients with Type 2 Diabetes: A Retrospective Study.</name><description>&lt;h4>Introduction&lt;/h4>Previous studies suggested that β-cell function markers such as fasting and postprandial serum C-peptide and C-peptide increment (FCPR, PCPR, and ΔCPR, respectively) may be useful in estimating glycemic response to glucagon-like peptide-1 receptor agonists. However, it remains elusive whether baseline glycemic control confounds these markers. Here we aimed to identify the least confounded β-cell function markers and investigate whether these markers could predict glycemic response to dulaglutide.&lt;h4>Methods&lt;/h4>We evaluated FCPR, PCPR, and ΔCPR levels in patients with type 2 diabetes who initiated dulaglutide treatment after a standardized meal tolerance test (MTT). We first investigated the confounding effects of baseline HbA1c on β-cell function markers using Pearson's correlation test. Then, we evaluated the association between each β-cell function marker and glycemic response (HbA1c change 0-6 months) to dulaglutide using generalized linear model and logistic regression analysis with adjustment for baseline HbA1c.&lt;h4>Results&lt;/h4>In 141 patients, baseline HbA1c was significantly inversely correlated with PCPR and ΔCPR (P &lt; 0.01 for both) but not with FCPR (r = 0.02; P = 0.853), suggesting that FCPR was the marker least confounded by baseline glycemic control. Of all patients, 59 continued dulaglutide for at least 6 months without initiating any additional glucose-lowering medications. Mean ± SE HbA1c change 0-6 months was - 1.16 ± 0.17% (P &lt; 0.001 vs. baseline). The β-cell function markers were significantly associated with HbA1c change 0-6 months in the generalized linear model. FCPR was also a significant predictor for achieving a reduction in HbA1c of at least 1% (P = 0.044) with an area under the receiver operating characteristic curve of 0.83 (sensitivity = 0.81 and specificity = 0.79).&lt;h4>Conclusion&lt;/h4>Fasting and meal-induced C-peptide levels are associated with glycemic response to dulaglutide, among which FCPR is least confounded by baseline glycemic control, suggesting its utility as a marker for glycemic response to dulaglutide.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2025-04-22T01:45:55.745Z</modification><creation>2025-04-05T20:04:56.393Z</creation></dates><accession>S-EPMC8991285</accession><cross_references><pubmed>35285007</pubmed><doi>10.1007/s13300-022-01231-1</doi></cross_references></HashMap>