Weight Loss, Glycemic Control, and Changes in Cardiovascular Biomarkers in Patients With Type 2 Diabetes Receiving Incretin Therapies or Insulin in a Large Cohort Database

Horton, Edward S.; Silberman, C; Davis, Keith L.; Berria, Rachele

doi:10.2337/dc09-2062

Cited by 137 publications

(146 citation statements)

References 22 publications

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“…It has been reported that the anti-diabetic peptides glucagon-like peptide 1 (GLP-1) and exendin 1-39 amide show beneficial effects in reducing cholesterol and triglycerides in diabetic subjects (Klonoff et al 2008, Rizzo et al 2009, Horton et al 2010. GLP-1, an incretin with insulinotropic and insulin-independent anti-diabetic properties (Creutzfeldt 2001), exerts insulin-3-like effects upon glucose metabolism in the liver, the skeletal muscle, and fat, apparently through a specific receptor different from that cloned in the pancreas (Valverde et al 1994, Delgado et al 1995, Villanueva-Peñacarrillo et al 1995, Yang et al 1998, Villanueva-Peñacarrillo et al 2001b, Sancho et al 2005, Arnés et al 2008.…”

Section: Introductionmentioning

confidence: 99%

GLP-1 and exendin-4 can reverse hyperlipidic-related osteopenia

Nuche-Berenguer¹,

Lozano²,

Gutiérrez‐Rojas³

et al. 2011

Journal of Endocrinology

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Increased fat mass contributes to bone deterioration. Glucagon-like peptide 1 (GLP-1) and its related peptide exendin 1-39 amide (Ex-4), two lipid-lowering peptides, exert osteogenic effects in diabetic states. We examined the actions of 3-day administration of GLP-1 or Ex-4 on bone remodeling markers and on bone mass and structure in hyperlipidic (HL) and hypercaloric rats. Wistar rats on a hyperlipidemic diet for 35 days were subcutaneously administered GLP-1 (0 . 86 nmol/kg per h), Ex-4 (0 . 1 nmol/kg per h), or saline (control) by continuous infusion for 3 days. After killing, tibiae were removed for total RNA and protein isolation, as well as femurs and L1-L4 vertebrae for bone mass and quality assessment. Body weight and plasma insulin were unaltered in HL rats, which showed osteopenia (by dual-energy X-ray absorptiometry), associated with hyperglycemia, hypertriglyceridemia, and hypercholesterolemia. GLP-1 or Ex-4 administration decreased the levels of glucose, triglycerides, and total cholesterol in plasma but increased osteocalcin (OC) gene expression and the osteoprotegerin (OPG)/receptor activator of NF-kB ligand (RANKL) ratio -at the expense of an augmented OPG -above corresponding control values in the tibia. Each tested peptide similarly reversed the decreased femoral and vertebral bone mass in these rats, whereas the deteriorated trabecular structure in the vertebrae improved associated with normalization of bone remodeling. These findings demonstrate that GLP-1 and Ex-4 are similarly efficient in reversing the bone alterations in this HL rat model, which has proven to be useful for studying the fat-bone relationships.

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Section: Introductionmentioning

confidence: 99%

GLP-1 and exendin-4 can reverse hyperlipidic-related osteopenia

Nuche-Berenguer¹,

Lozano²,

Gutiérrez‐Rojas³

et al. 2011

Journal of Endocrinology

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“…Most of the clinical trials, in line with animal studies, have reported a reduction of blood pressure after chronic treatment of GLP-1R agonists [148][149][150][151]. This may be explained, at least in part, by the ability of GLP-1 analogs to upregulate anti-oxidative enzymes and inhibit NFkB-mediated inflammatory signaling on endothelial cells [152,153], and to reduce oxidative stress by suppressing MAPK signaling pathways in peripheral lymphocytes of type 2 diabetic patients [154].…”

Section: How Conventional Diabetic Treatments May Ameliorate Endothelmentioning

confidence: 90%

Targeting endothelial metaflammation to counteract diabesity cardiovascular risk: Current and perspective therapeutic options

Potenza

Nacci

Salvia

et al. 2017

Pharmacological Research

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Abstract:The association of obesity and diabetes, termed "diabesity", defines a combination of primarily metabolic disorders with insulin resistance as the underlying common pathophysiology. Cardiovascular disorders associated with diabesity represent the leading cause of morbidity and mortality in the Western world. This makes diabesity, with its rising impacts on both health and economics, one of the most challenging biomedical and social threats of present century. The emerging comprehension of the genes whose alteration confers inter-individual differences on risk factors for diabetes or obesity, together with the potential role of genetically determined variants on mechanisms controlling responsiveness, effectiveness and safety of anti-diabetic therapy underlines the need of additional knowledge on molecular mechanisms involved in the pathophysiology of diabesity. Endothelial cell dysfunction, resulting from the unbalanced production of endothelialderived vascular mediators, is known to be present at the earliest stages of insulin resistance and obesity, and may precede the clinical diagnosis of diabetes by several years. Once considered as a mere consequence of metabolic abnormalities, it is now clear that endothelial dysfunctional activity may play a pivotal role in the progression of diabesity. In the vicious circle where vascular defects and metabolic disturbances worsen and reinforce each other, a low-grade, chronic, and 'cold' inflammation (metaflammation) has been suggested to serve as the pathophysiological link that binds endothelial and metabolic dysfunctions. In this paradigm, it is important to consider how traditional antidiabetic treatments (specifically addressing metabolic dysregulation) may directly impact on inflammatory processes or cardiovascular function. Indeed, not all drugs currently available to treat diabetes possess the same anti-inflammatory potential, or target endothelial cell function equally. Perspective strategies pointing at reducing metaflammation or directly addressing endothelial dysfunction may disclose beneficial consequences on metabolic regulation. This review focuses on existing and potential new approaches ameliorating endothelial dysfunction and vascular inflammation in the context of diabesity.

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“…5,[19][20][21][22] This report adds to the available literature exploring the use of large EMR databases to investigate questions related to the clinical care of patients with diabetes. 10,[23][24][25][26] There is no protocol-based implementation strategy for glycemic management in this population, meaning that this investigation reflects individual rather than protocol-driven practice. This provides data that extend beyond those limited to 1 particular insurance plan, where therapeutic interventions and data collection strategies may be more homogeneous.…”

Section: Discussionmentioning

confidence: 99%

Use of an Electronic Medical Record (EMR) to Identify Glycemic Intensification Strategies in Type 2 Diabetes

Korytkowski

Brooks

Lombardero

et al. 2014

J Diabetes Sci Technol

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Background: Current treatment guidelines for type 2 diabetes (T2D) recommend individualized intensification of therapy for glycated hemoglobin (A1C) ≥ 7% in most patients. The purpose of this investigation was to explore the ability of an electronic medical record (EMR) to identify glycemic intensification strategies among T2D patients receiving pharmacologic therapy. Methods: Patient records between 2005 and 2011 with documentation of A1C and active prescriptions for any diabetes medications were queried to identify potential candidates for intensification based on A1C ≥ 7% while on 1-2 oral diabetes medications (ODM). Patients with follow-up A1C values within 1 year of index A1C were grouped according to intensification with insulin, GLP-1 receptor agonists (GLP-1RA), a new class of ODM, or no intensification. Changes in A1C and continuation of intensification therapy were determined. Results: A total of 4921 patients meeting inclusion criteria were intensified with insulin (n = 416), GLP-1RA (n = 68), ODM (n = 1408), or no additional therapy (n = 3029). Patients receiving insulin had higher baseline (9.3 ± 2.0 vs 8.3 ± 1.2 vs 8.3 ± 1.3 vs 7.6 ± 1.0%, P < .0001) and follow-up A1C (8.1 ± 1.6 vs 7.5 ± 1.2 vs 7.6 ± 1.3 vs 7.2 ± 1.1%, P < .0001) despite experiencing larger absolute A1C reductions (−1.2 ± 2.1 vs −0.8 ± 1.4 vs −0.7 ± 1.4 vs −0.3 ± 1.1%, P < .0001). Patients receiving GLP-1RA were more obese at baseline (BMI: 33.6 ± 7.1 vs 37.7 ± 6.1 vs 33.7 ± 6.8 vs 32.9 ± 7.1 kg/m 2 , P < .0001) and follow-up (BMI: 33.9 ± 7.3 vs 36.6 ± 6.1 vs 33.8 ± 7.0 vs 32.4 ± 7.0 kg/m 2 , P < .0001) despite experiencing more absolute weight reduction. Insulin was the most and GLP-1RA the least likely therapy to be continued. Conclusions: An EMR allows identification of prescribing practices and compliance with T2D treatment guidelines. Patients receiving intensification of glycemic medications had baseline A1C >8% suggesting that treatment recommendations are not being followed.

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Weight Loss, Glycemic Control, and Changes in Cardiovascular Biomarkers in Patients With Type 2 Diabetes Receiving Incretin Therapies or Insulin in a Large Cohort Database

Cited by 137 publications

References 22 publications

GLP-1 and exendin-4 can reverse hyperlipidic-related osteopenia

GLP-1 and exendin-4 can reverse hyperlipidic-related osteopenia

Targeting endothelial metaflammation to counteract diabesity cardiovascular risk: Current and perspective therapeutic options

Use of an Electronic Medical Record (EMR) to Identify Glycemic Intensification Strategies in Type 2 Diabetes

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