P-35 Study of metabolic control, body weight, body mass index and blood pressure in patients with Type 2 diabetes with insulin resistance with intensified insulin therapy

2008 ◽  
Vol 79 ◽  
pp. S68
Author(s):  
Anil Kumar ◽  
Reddy Iska
2010 ◽  
Vol 63 (9-10) ◽  
pp. 611-615 ◽  
Author(s):  
Branka Koprivica ◽  
Teodora Beljic-Zivkovic ◽  
Tatjana Ille

Introduction. Insulin resistance is a well-known leading factor in the development of metabolic syndrome. The aim of this study was to evaluate metabolic effects of metformin added to sulfonylurea in unsuccessfully treated type 2 diabetic patients with metabolic syndrome. Material and methods. A group of thirty subjects, with type 2 diabetes, secondary sulfonylurea failure and metabolic syndrome were administered the combined therapy of sulfonylurea plus metformin for six months. Metformin 2000 mg/d was added to previously used sulfonylurea agent in maximum daily dose. Antihypertensive and hypolipemic therapy was not changed. The following parameters were assessed at the beginning and after six months of therapy: glycemic control, body mass index, waist circumference, blood pressure, triglycerides, total cholesterol and its fractions, homeostatic models for evaluation of insulin resistance and secretion (HOMA R, HOMA B) and C- peptide. Results. Glycemic control was significantly improved after six months of the combined therapy: (fasting 7.89 vs. 10.61 mmol/l. p<0.01; postprandial 11.12 vs. 12.61 mmol/l. p<0.01, p<0.01; glycosylated hemoglobin 6.81 vs. 8.83%. p<0.01). the body mass index and waist circumference were significantly lower (26.7 vs. 27.8 kg/m2, p<0.01 and 99.7 vs. 101.4 cm for men, p<0.01; 87.2 vs. 88.5 for women, p<0.01). Fasting plasma triglycerides decreased from 3.37 to 2.45 mmol/l (p<0.001) and HOMA R from 7.04 to 5.23 (p<0.001). No treatment effects were observed on blood pressure, cholesterol, and residual insulin secretion. Conclusion. Administration of metformin in type 2 diabetes with metabolic syndrome decreased cardiovascular risk factors by reducing glycemia, triglycerides, BMI, central obesity and insulin resistance.


Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2496-PUB
Author(s):  
ZHANG CHENGHUI ◽  
LI MINGXIA ◽  
WANG SUYUAN ◽  
WU YUNHONG

2018 ◽  
Vol 128 (03) ◽  
pp. 170-181 ◽  
Author(s):  
Rainer Lundershausen ◽  
Sabrina Müller ◽  
Mahmoud Hashim ◽  
Joachim Kienhöfer ◽  
Stefan Kipper ◽  
...  

Abstract Purpose To assess quality of life, glycemic control, and safety/tolerability associated with liraglutide versus insulin initiation in patients with type 2 diabetes in Germany. Methods Liraglutide/insulin-naïve adults with type 2 diabetes and inadequate glycemic control despite using oral antidiabetic medication were assigned to liraglutide (≤1.8 mg daily; n=878) or any insulin (n=382) according to the treating physician’s decision and followed for 52 weeks. The primary objective was to evaluate Audit of Diabetes-Dependent Quality of Life (ADDQoL) scores. Results At baseline, the liraglutide group was younger and had shorter type 2 diabetes duration, lower glycated hemoglobin (HbA1c), higher body mass index, and a lower prevalence of certain diabetes-related complications than the insulin group (all p<0.05). ADDQoL average weighted impact scores improved numerically in both groups from baseline to 52 weeks (mean difference [95% confidence interval], liraglutide vs. insulin: 0.159 [−0.023;0.340]; not significant). Changes in general wellbeing and five ADDQoL domains significantly favored liraglutide (remaining 14 domains, not significant). HbA1c reductions were greater with insulin than liraglutide (−2.0% vs. −1.2%; p<0.01); however, mean HbA1c after 52 weeks was 7.2% in both groups. Compared with insulin, liraglutide significantly decreased body mass index (−1.54 kg/m2 vs. +0.27 kg/m2; p<0.001), systolic blood pressure (−5.03 mmHg vs. −1.03 mmHg; p<0.01) and non-severe hypoglycemia (0.85% vs. 4.55% at 52 weeks; p<0.01). Adverse drug reactions were reported for<3% of patients in both groups. Conclusions Liraglutide improved certain ADDQoL components and reduced body mass index, systolic blood pressure, and non-severe hypoglycemia versus insulin. Both treatments improved glycemic control.


2011 ◽  
Vol 11 (1) ◽  
Author(s):  
Miguel A Salinero-Fort ◽  
Enrique Carrillo-de Santa Pau ◽  
Francisco J Arrieta-Blanco ◽  
Juan C Abanades-Herranz ◽  
Carmen Martín-Madrazo ◽  
...  

2021 ◽  
Author(s):  
Beatriz Teresita Martín-Márquez ◽  
Flavio Sandoval-Garcia ◽  
Mónica Vazquez-Del Mercado ◽  
Erika-Aurora Martínez-García ◽  
Fernanda-Isadora Corona-Meraz ◽  
...  

2016 ◽  
Vol 144 (9-10) ◽  
pp. 497-502
Author(s):  
Teodora Beljic-Zivkovic ◽  
Milica Marjanovic-Petkovic ◽  
Miljanka Vuksanovic ◽  
Ivan Soldatovic ◽  
Dobrila Kanlic ◽  
...  

Introduction. A combination of drugs is required for treatment of obese subjects with diabetes, due to multiple pathogenic mechanisms implicated in the development of both diabetes and obesity. Objective. Assessment of the effect of sitagliptin added to insulin glargine and metformin, in obese subjects with type 2 diabetes. Methods. A total of 23 obese subjects on metformin and insulin glargine participated in the study. Titration of insulin glargine during a one-month period preceded the addition of 100 mg of sitagliptin daily. Body mass index, waist circumference, fasting, and prandial glucose were measured monthly, lipids and hemoglobin A1c (HbA1c) every three months, insulin, c-peptide and glucagon at the start and after six months of treatment. Homeostatic models for insulin secretion (HOMA B) and insulin resistance (HOMA IR) were calculated. Results. Participants were 58.65 ?} 7.62 years of age with a body mass index of 35.06 ?} 5.15 kg/m2, waist circumference of 115.04 ?} 15.5 cm, and the duration of diabetes of 4.11 ?} 2.57 years. With the titration of insulin glargine, target fasting glucose levels were not achieved. Waist circumference and body mass index decreased during three months of sitagliptin treatment, thereafter remaining stable. HbA1c decreased significantly after three and six months of therapy. C-peptide increased significantly, while glucagon level fell. HOMA indexes were unchanged. Conclusion. Sitagliptin can improve diabetes control and induce modest weight loss in obese subjects poorly controlled on insulin glargine and metformin. Titration of insulin glargine to optimal fasting glucose values is a prerequisite of success of this combination therapy.


2001 ◽  
Vol 86 (11) ◽  
pp. 5450-5456 ◽  
Author(s):  
Lidia Maianu ◽  
Susanna R. Keller ◽  
W. Timothy Garvey

Insulin resistance in type 2 diabetes is due to impaired stimulation of the glucose transport system in muscle and fat. Different defects are operative in these two target tissues because glucose transporter 4 (GLUT 4) expression is normal in muscle but markedly reduced in fat. In muscle, GLUT 4 is redistributed to a dense membrane compartment, and insulin-mediated translocation to plasma membrane (PM) is impaired. Whether similar trafficking defects are operative in human fat is unknown. Therefore, we studied subcellular localization of GLUT4 and insulin-regulated aminopeptidase (IRAP; also referred to as vp165 or gp160), which is a constituent of GLUT4 vesicles and also translocates to PM in response to insulin. Subcutaneous fat was obtained from eight normoglycemic control subjects (body mass index, 29 ± 2 kg/m2) and eight type 2 diabetic patients (body mass index, 30 ± 1 kg/m2; fasting glucose, 14 ± 1 mm). In adipocytes isolated from diabetics, the basal 3-O-methylglucose transport rate was decreased by 50% compared with controls (7.1 ± 2.9 vs. 14.1 ± 3.7 mmol/mm2 surface area/min), and there was no increase in response to maximal insulin (7.9 ± 2.7 vs. 44.5 ± 9.2 in controls). In membrane subfractions from controls, insulin led to a marked increase of IRAP in the PM from 0.103 ± 0.04 to 1.00± 0.33 relative units/mg protein, concomitant with an 18% decrease in low-density microsomes and no change in high-density microsomes (HDM). In type 2 diabetes, IRAP overall expression in adipocytes was similar to that in controls; however, two abnormalities were observed. First, in basal cells, IRAP was redistributed away from low-density microsomes, and more IRAP was recovered in HDM (1.2-fold) and PM (4.4-fold) from diabetics compared with controls. Second, IRAP recruitment to PM by maximal insulin was markedly impaired. GLUT4 was depleted in all membrane subfractions (43–67%) in diabetes, and there was no increase in PM GLUT4 in response to insulin. Type 2 diabetes did not affect the fractionation of marker enzymes. We conclude that in human adipocytes: 1) IRAP is expressed and translocates to PM in response to insulin; 2) GLUT4 depletion involves all membrane subfractions in type 2 diabetes, although cellular levels of IRAP are normal; and 3) in type 2 diabetes, IRAP accumulates in membrane vesicles cofractionating with HDM and PM under basal conditions, and insulin-mediated recruitment to PM is impaired. Therefore, in type 2 diabetes, adipocytes express defects in trafficking of GLUT4/IRAP-containing vesicles similar to those causing insulin resistance in skeletal muscle.


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