1.
The effects of short-term continuous subcutaneous insulin infusion treatment on fasting glucagon-like peptide-1 concentrations in newly diagnosed type 2 diabetes.
Huang, X, Li, S, Yang, M, Fu, X, Li, H, Yan, T, Liu, Y, Chen, L, Lan, L, Li, L, et al
Diabetes research and clinical practice. 2018;:246-252
Abstract
OBJECTIVE Early short-term intensive insulin therapy in newly diagnosed type 2 diabetes patients shows benefit in glycemic control and β-cell function. Glucagon-like peptide-1 (GLP-1) plays an important role in glucose metabolism and development of type 2 diabetes. We did a study to observe the changes of GLP-1 and β-cell function after short-term continuous subcutaneous insulin infusion (CSII) treatment. METHODS A total of 66 subjects were enrolled, including 30 normal glucose tolerance controls (NGT) and 36 patients with newly diagnosed type 2 diabetes between October 2015 and July 2016. Fasting plasma glucose (FPG), insulin, and GLP-1 were measured in each subject. The patients underwent CSII treatment for 2 weeks, and then FBG, insulin, and GLP-1 were measured. HOMA-IR and HOMA-B were then calculated. RESULTS All patients achieved target glycemic control in two weeks. HOMA-IR and HOMA-B improved significantly after intensive interventions (p < 0.05). The GLP-1 concentration increased significantly in patients after treatment (p < 0.05). When grouped according to bodyweight and age in all patients, the HOMA-IR changed significantly in overweight and old age subgroups, the HOMA-B increased significantly in normal weight, overweight and middle age subgroups, and the GLP-1 concentration also increased significantly in overweight and middle age subgroups respectively (p < 0.05). CONCLUSION Short-term CSII treatment can obtain glycemic control target and recover β-cell function and GLP-1 secretion in newly diagnosed type 2 diabetes patients. The overweight and middle-aged patients may get more benefit from this treatment.
2.
Gastrointestinal hormone secretion in women with polycystic ovary syndrome: an observational study.
Lin, T, Li, S, Xu, H, Zhou, H, Feng, R, Liu, W, Sun, Y, Ma, J
Human reproduction (Oxford, England). 2015;(11):2639-44
Abstract
STUDY QUESTION Is the secretion of gastrointestinal hormones impaired in patients with polycystic ovary syndrome (PCOS)? SUMMARY ANSWER Gastrointestinal hormone levels were abnormal in patients with PCOS. WHAT IS KNOWN ALREADY The hormones glucagon-like peptide-1 (GLP-1) and peptide tyrosine-tyrosine (PYY) are both involved in signaling satiety. Secretion of GLP-1 and PYY in response to nutrients in the small intestine plays an important role in energy metabolism. Most PCOS patients are overweight or obese, which suggests dysregulation of appetite. STUDY DESIGN, SIZE, DURATION In order to evaluate levels of gastrointestinal hormones in PCOS, a cohort study was undertaken, involving 30 PCOS patients and 29 BMI-matched healthy women recruited from Shanghai Renji Hospital between 1 March 2013 and 30 May 2014. PARTICIPANTS/MATERIALS, SETTING, METHODS After an overnight fast, all participants underwent an oral glucose tolerance test. Blood was sampled frequently for measurement of blood glucose and plasma insulin, total GLP-1 and PYY concentrations. MAIN RESULTS AND THE ROLE OF CHANCE Fasting and postprandial insulin levels were significantly higher in patients with PCOS compared with the healthy controls (P < 0.05). Fasting and postprandial GLP-1 (t = 0 and 30 min; mean ± SEM) were also higher in PCOS group (17.5 ± 1.07 pM versus 14.1 ± 1.16 pM, P < 0.05; 29.7 ± 2.39 pM versus 22.8 ± 2.09 pM, P < 0.05). However, there were no differences in plasma PYY between patients with PCOS and healthy controls either fasting or postprandially. PYY levels were lower in obese PCOS patients than in lean PCOS patients (P < 0.05). LIMITATIONS, REASONS FOR CAUTION The study involved a small number of subjects with PCOS, and examined hormone responses to oral glucose rather than a physiological meal. WIDER IMPLICATIONS OF THE FINDINGS Deficient secretion of GLP-1 and PYY does not contribute to excessive food intake in the pathophysiology of PCOS.