XI. STRATEGIES FOR IMPROVING DIABETES CARE D iabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetes care is complex and requires that many issues, beyond glycemic control, be addressed. A large body of evidence exists that supports a range of interventions to improve diabetes outcomes. These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care. While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided. These standards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information, refer to Bode (Ed.): Medical Management of Type 1 Diabetes (1), Burant (Ed): Medical Management of Type 2 Diabetes (2), and Klingensmith (Ed): Intensive Diabetes Management (3). The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes. A grading system (Table 1), developed by the American Diabetes Association (ADA) and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations. The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E.

Standards of Medical Care in Diabetes

Principles and Practice of Structural Equation Modeling (2nd ed.)

https://ipip.ori.org/Goldberg_etal_2006_IPIP_JRP.pdf

The international personality item pool and the future of public-domain personality measures ☆

The classical perception of adipose tissue as a storage place of fatty acids has been replaced over the last years by the notion that adipose tissue has a central role in lipid and glucose metabolism and produces a large number of hormones and cytokines, e.g. tumour necrosis factor-α, interleukin-6, adiponectin, leptin, and plasminogen activator inhibitor-1.

The increased prevalence of excessive visceral obesity and obesity-related cardiovascular risk factors is closely associated with the rising incidence of cardiovascular diseases and type 2 diabetes mellitus. This clustering of vascular risk factors in (visceral) obesity is often referred to as metabolic syndrome. The close relationship between an increased quantity of visceral fat, metabolic disturbances, including low-grade inflammation, and cardiovascular diseases and the unique anatomical relation to the hepatic portal circulation has led to an intense endeavour to unravel the specific endocrine functions of this visceral fat depot. The objective of this paper is to describe adipose tissue dysfunction, delineate the relation between adipose tissue dysfunction and obesity and to describe how adipose tissue dysfunction is involved in the development of diabetes mellitus type 2 and atherosclerotic vascular diseases. First, normal physiology of adipocytes and adipose tissue will be described.

/pdf/adipose-tissue-dysfunction-in-obesity-diabetes-and-vascular-1irley3ao1.pdf

Adipose tissue dysfunction in obesity, diabetes, and vascular diseases

Kinins are proinflammatory peptides that mediate numerous vascular and pain responses to tissue injury. Two pharmacologically distinct kinin receptor subtypes have been identified and characterized for these peptides, which are named B1 and B2 and belong to the rhodopsin family of G protein-coupled receptors. The B2 receptor mediates the action of bradykinin (BK) and lysyl-bradykinin (Lys-BK), the first set of bioactive kinins formed in response to injury from kininogen precursors through the actions of plasma and tissue kallikreins, whereas the B(1) receptor mediates the action of des-Arg9-BK and Lys-des-Arg9-BK, the second set of bioactive kinins formed through the actions of carboxypeptidases on BK and Lys-BK, respectively. The B2 receptor is ubiquitous and constitutively expressed, whereas the B1 receptor is expressed at a very low level in healthy tissues but induced following injury by various proinflammatory cytokines such as interleukin-1beta. Both receptors act through G alpha(q) to stimulate phospholipase C beta followed by phosphoinositide hydrolysis and intracellular free Ca2+ mobilization and through G alpha(i) to inhibit adenylate cyclase and stimulate the mitogen-activated protein kinase pathways. The use of mice lacking each receptor gene and various specific peptidic and nonpeptidic antagonists have implicated both B1 and B2 receptors as potential therapeutic targets in several pathophysiological events related to inflammation such as pain, sepsis, allergic asthma, rhinitis, and edema, as well as diabetes and cancer. This review is a comprehensive presentation of our current understanding of these receptors in terms of molecular and cell biology, physiology, pharmacology, and involvement in human disease and drug development.

https://pharmrev.aspetjournals.org/content/pharmrev/57/1/27.full.pdf

International Union of Pharmacology. XLV. Classification of the Kinin Receptor Family: from Molecular Mechanisms to Pathophysiological Consequences

Context: Visfatin (also known as pre-B cell colony-enhancing factor or PBEF) is a cytokine that is highly expressed in visceral fat and whose blood levels correlate with obesity. Originally isolated as a secreted factor that promotes the growth of B cell precursors and recently found to act as an insulin analog on the insulin receptor, its pathophysiological role in humans remains largely unknown. Objectives: In this study we investigated whether plasma visfatin level is altered in patients with type 2 diabetes mellitus (T2DM). Design and Patients: Plasma visfatin as well as adiponectin and resistin concentrations were measured through ELISA in type 2 diabetic and nondiabetic subjects. Results: A total of 61 patients with T2DM and 59 sex- and age-matched nondiabetic subjects were studied. Plasma visfatin was found to be elevated in patients with T2DM (31.9 ± 31.7 vs. 15.8 ± 16.7 ng/ml, P = 0.002). In contrast, adiponectin was decreased (4.3 ± 2.5 vs. 30.8 ± 10.3 μg/ml, P < 0.001), whereas plasma resistin ...

Elevated Plasma Level of Visfatin/Pre-B Cell Colony-Enhancing Factor in Patients with Type 2 Diabetes Mellitus

There are controversies regarding the association of visfatin with overweight/obesity, type 2 diabetes mellitus, insulin resistance (IR), metabolic syndrome and cardiovascular disease in published articles. A meta-analysis was performed to identify the significance of visfatin in these diseases. We searched for relevant articles in Pubmed, Scopus and SCIE. A total of 1035 articles were surveyed and 46 articles were identified, with 14 reports reporting more than one of our investigated diseases. A total of 13 (n = 644), 19 (n = 2405), 20 (n = 2249), 5 (n = 527) and 5 (n = 851) articles/(participants) were included in each meta-analysis regarding the association of visfatin and overweight/obesity, type 2 diabetes mellitus, insulin resistance, metabolic syndrome and cardiovascular diseases, respectively. Plasma visfatin concentrations were increased in participants diagnosed with overweight/obesity, type 2 diabetes mellitus, metabolic syndrome and cardiovascular diseases, with pooled log odds ratios of 1.164 [95% confidence interval (CI): 0.348 to 1.981, p = 0.005], 1.981 (95% CI: 1.377 to 2.584, p < 0.001), 1.094 (95% CI: 0.678 to 1.511, p < 0.001), and 2.902 (95% CI: 0.924 to 4.879, p < 0.005), respectively. The circulating visfatin level was positively associated with insulin resistance, with a Fisher's z of 0.089 (95% CI: 0.013 to 0.165, p = 0.022). No single study was found to affect the overall result of each analysis by sensitivity testing. No publication bias was found by the Egger test. Our study suggests that the use of visfatin may be promising for predicting obesity, diabetes status, insulin resistance, metabolic syndrome and cardiovascular disease.

Visfatin in overweight/obesity, type 2 diabetes mellitus, insulin resistance, metabolic syndrome and cardiovascular diseases: a meta‐analysis and systemic review

Pathways of empowerment perceptions, health literacy, self-efficacy, and self-care behaviors to glycemic control in patients with type 2 diabetes mellitus.

Objective— Adiponectin, an adipocyte-derived peptide with antiinflammatory and antiatherogenic effects, is known to protect against the initiation and progression of atherosclerosis. In this study, we investigate whether hypoadiponectinemia is present in patients with ischemic cerebrovascular disease (CVD). Methods and Results— In this case-control study, plasma adiponectin concentration was measured by an enzyme-linked immunosorbent assay in type 2 diabetic and nondiabetic subjects with or without ischemic CVD. A total of 534 subjects were studied. The mean plasma level of adiponectin of the 228 patients with ischemic CVD was significantly lower than that of 306 subjects without CVD. When the analysis was stratified according to diabetes status, plasma levels of adiponectin in CVD subjects with or without type 2 diabetes were significantly lower than those of their counterparts. Decreasing concentrations of adiponectin were independently and significantly associated with a higher risk of CVD when concentrations were analyzed by quartile and as a continuous variable. When patients with CVD were subgrouped according to the comorbidity with or without type2 diabetes, the same trend of association between plasma adiponectin and risk of CVD was observed in each group. Conclusion— These data show that there are significantly lower levels of plasma adiponectin in patients with ischemic CVD.

Hypoadiponectinemia Is Associated With Ischemic Cerebrovascular Disease

OBJECTIVE—Because ACE insertion/deletion (I/D) polymorphism has been shown to be associated with diabetes, hypertension, coronary artery diseases, and diabetic nephropathy, and because plasma ACE concentration has been found to be associated with plasma triglyceride and total cholesterol levels in patients with type 2 diabetes, the goal of this study was to investigate whether ACE gene I/D polymorphism is associated with metabolic syndrome in Chinese subjects with type 2 diabetes. RESEARCH DESIGN AND METHODS—A total of 711 patients with type 2 diabetes and 750 control subjects were studied. The ACE I/D polymorphism was determined by PCR. The definition and criteria of metabolic syndrome used in this study matched those proposed in the 1998 World Health Organization classification. RESULTS—Of 711 patients with type 2 diabetes, 534 (75.1%) fulfilled the criteria for metabolic syndrome. The prevalence of metabolic syndrome in control subjects with II, ID, and DD genotype was 9.4, 11.5, and 15.4%, respectively, and in patients with type 2 diabetes, it was 68.6, 79.2, and 86.1%, respectively. The ACE I/D polymorphism was significantly associated with the syndrome in patients with type 2 diabetes (P = 0.001). When pooling the control subjects with diabetic patients, the prevalence of metabolic syndrome in the whole study group with II, ID, and DD genotype was 37.9, 44.5, and 51.0%, respectively, and ACE I/D polymorphism was still significantly associated with metabolic syndrome (P = 0.003). Diabetic patients with DD genotype were also found to have a higher prevalence of dyslipidemia (II/ID/DD = 43.1/53.1/65.8%, P CONCLUSIONS—The ACE I/D polymorphism was found to be associated with metabolic syndrome in Chinese patients with type 2 diabetes. This finding may provide genetic evidence to explain the clustering of metabolic syndrome and suggests that the renin-angiotensin system is involved in the pathophysiology of metabolic derangement in patients with type 2 diabetes.

https://care.diabetesjournals.org/content/diacare/25/6/1002.full.pdf

ACE gene insertion/deletion polymorphism associated with 1998 World Health Organization definition of metabolic syndrome in Chinese type 2 diabetic patients.

Yau-Jiunn Lee

Papers

Elevated Plasma Level of Visfatin/Pre-B Cell Colony-Enhancing Factor in Patients with Type 2 Diabetes Mellitus

Visfatin in overweight/obesity, type 2 diabetes mellitus, insulin resistance, metabolic syndrome and cardiovascular diseases: a meta‐analysis and systemic review

Pathways of empowerment perceptions, health literacy, self-efficacy, and self-care behaviors to glycemic control in patients with type 2 diabetes mellitus.

Hypoadiponectinemia Is Associated With Ischemic Cerebrovascular Disease

ACE gene insertion/deletion polymorphism associated with 1998 World Health Organization definition of metabolic syndrome in Chinese type 2 diabetic patients.