Background: Atherogenic dyslipidemia, which is frequently associated with type 2 diabetes (T2D) and insulin resistance, contributes to the development of vascular complications. Statin therapy is the primary approach to dyslipidemia management in T2D, however, the role of non-statin therapy remains unclear. Ezetimibe reduces cholesterol burden by inhibiting intestinal cholesterol absorption. Fibrates lower triglyceride levels and increase high-density lipoprotein cholesterol (HDL-C) levels via peroxisome proliferator- activated receptor alpha agonism. Therefore, when combined, these drugs effectively lower non-HDL-C levels. Despite this, few clinical trials have specifically targeted non-HDL-C, and the efficacy of triple combination therapies, including statins, ezetimibe, and fibrates, has yet to be determined. Methods: This is a multicenter, prospective, randomized, open-label, active-comparator controlled trial involving 3,958 eligible participants with T2D, cardiovascular risk factors, and elevated non-HDL-C (≥100 mg/dL). Participants, already on moderate-intensity statins, will be randomly assigned to either Ezefeno (ezetimibe/fenofibrate) addition or statin dose-escalation. The primary end point is the development of a composite of major adverse cardiovascular and diabetic microvascular events over 48 months. Conclusion This trial aims to assess whether combining statins, ezetimibe, and fenofibrate is as effective as, or possibly superior to, statin monotherapy intensification in lowering cardiovascular and microvascular disease risk for patients with T2D. This could propose a novel therapeutic approach for managing dyslipidemia in T2D.

Diabetic heart disease is a growing and important public health risk. Apart from the risk of coronary artery disease or hypertension, diabetes mellitus (DM) is a well-known risk factor for heart failure in the form of diabetic cardiomyopathy (DiaCM). Currently, DiaCM is defined as myocardial dysfunction in patients with DM in the absence of coronary artery disease and hypertension. The underlying pathomechanism of DiaCM is partially understood, but accumulating evidence suggests that metabolic derangements, oxidative stress, increased myocardial fibrosis and hypertrophy, inflammation, enhanced apoptosis, impaired intracellular calcium handling, activation of the renin-angiotensin-aldosterone system, mitochondrial dysfunction, and dysregulation of microRNAs, among other factors, are involved. Numerous animal models have been used to investigate the pathomechanisms of DiaCM. Despite some limitations, animal models for DiaCM have greatly advanced our understanding of pathomechanisms and have helped in the development of successful disease management strategies. In this review, we summarize the current pathomechanisms of DiaCM and provide animal models for DiaCM according to its pathomechanisms, which may contribute to broadening our understanding of the underlying mechanisms and facilitating the identification of possible new therapeutic targets.

Diabetic heart disease is a growing and important public health risk. Apart from the risk of coronary artery disease or hypertension, diabetes mellitus (DM) is a well-known risk factor for heart failure in the form of diabetic cardiomyopathy (DiaCM). Currently, DiaCM is defined as myocardial dysfunction in patients with DM in the absence of coronary artery disease and hypertension. The underlying pathomechanism of DiaCM is partially understood, but accumulating evidence suggests that metabolic derangements, oxidative stress, increased myocardial fibrosis and hypertrophy, inflammation, enhanced apoptosis, impaired intracellular calcium handling, activation of the renin-angiotensin-aldosterone system, mitochondrial dysfunction, and dysregulation of microRNAs, among other factors, are involved. Numerous animal models have been used to investigate the pathomechanisms of DiaCM. Despite some limitations, animal models for DiaCM have greatly advanced our understanding of pathomechanisms and have helped in the development of successful disease management strategies. In this review, we summarize the current pathomechanisms of DiaCM and provide animal models for DiaCM according to its pathomechanisms, which may contribute to broadening our understanding of the underlying mechanisms and facilitating the identification of possible new therapeutic targets.

The global burden of diabetes mellitus and its related complications are currently increasing. Diabetes mellitus affects the heart through various mechanisms including microvascular impairment, metabolic disturbance, subcellular component abnormalities, cardiac autonomic dysfunction, and a maladaptive immune response. Eventually, diabetes mellitus can cause functional and structural changes in the myocardium without coronary artery disease, a disorder known as diabetic cardiomyopathy (DCM). There are many diagnostic tools and management options for DCM, although it is difficult to detect its development and effectively prevent its progression. In this review, we summarize the current research regarding the pathophysiology and pathogenesis of DCM. Moreover, we discuss emerging diagnostic evaluation methods and treatment strategies for DCM, which may help our understanding of its underlying mechanisms and facilitate the identification of possible new therapeutic targets.
Coronary Artery Disease ; Diabetes Mellitus ; Diabetic Cardiomyopathies* ; Heart ; Heart Failure ; Myocardium

Critically ill patients often experience hyperglycemia, which may be associated with increased morbidity and mortality. In 2001, van den Berghe et al. suggested significant benefit of normalization of blood glucose level in critically ill patients using intensive intravenous insulin therapy. Subsequent multicenter randomized studies, however, demonstrated adverse effects of tight glucose control. Therefore, while the need for glucose control in critically ill patients is generally accepted, the treatment thresholds for initiation of insulin therapy or target glucose values are still undetermined. Furthermore, occurrence of a hypoglycemic event during intensive insulin therapy is known to be an independent predictor of clinical outcome, and glycemic variability is an important variable of glucose management in the critically ill patients. Novel technological approaches such as a continuous glucose monitoring system (CGMS) might help to overcome some problems of tight glucose control by reducing the risk of hypoglycemia and minimizing glycemic variability.
Blood Glucose ; Critical Illness* ; Glucose ; Humans ; Hyperglycemia ; Hypoglycemia ; Insulin ; Intensive Care Units ; Mortality

OBJECTIVE: There are still a limited number of studies assessing the prevalence of metabolic syndrome in the community. The aim of this study is to investigate the prevalence and gender-related characteristics of metabolic syndrome in Korean community. METHODS: A total of 417 community subjects (mean age was 60.7+/-13.6 years, 35.3% were men) who attended the routine check-up were analyzed. National Cholesterol Education Program-Adult Treatment Panel (NCEP-ATP) III clinical guideline was used to define metabolic syndrome. RESULTS: Metabolic syndrome was diagnosed in 38.1% of study subjects. The prevalence of metabolic syndrome was not different between men and women (men 39.0% vs. women 37.5%, p=0.766). The positive association between age and the prevalence of metabolic syndrome was more pronounced in women (chi2=17.52, p for trend<0.001) than men (chi2=2.38, p for trend=0.123). In young age group (<50 years), the prevalence of metabolic syndrome was higher in men than in women (34.7% vs. 11.7%, p=0.042). This gender difference was not observed in older group (> or =50 years). The most prevalent factor of metabolic syndrome was hypertriglyceridemia (49.9%) and hypertension (47.6%) in both genders. Among metabolic syndrome components, central obesity (40.5% vs. 25.2%, p=0.002) and hypertriglyceridemia (54.5% vs. 41.8%, p=0.015) were more prevalent in women than in men, and the prevalence of other components were similar between genders. CONCLUSIONS: In the community, metabolic syndrome was highly prevalent in middle-aged and elderly Korean adult. Age related change in the prevalence of metabolic syndrome was gender specific. Age and gender effects should be considered for the effective control of metabolic syndrome in the community.
Adult ; Aged ; Cholesterol ; Education ; Female ; Humans ; Hypertension ; Hypertriglyceridemia ; Male ; Obesity, Abdominal ; Prevalence*

Pregnancy-induced osteoporosis is a rare disorder characterized by fragility fracture and low bone mineral density (BMD) during or shortly after pregnancy, and its etiology is still unclear. We experienced a case of a 39-year-old woman who suffered from lumbago 3 months after delivery. Biochemical evidence of increased bone resorption is observed without secondary causes of osteoporosis. Radiologic examination showed multiple compression fractures on her lumbar vertebrae. We report a case of patient with pregnancy-induced osteoporosis improved her clinical symptom, BMD and bone turnover marker after teriparatide therapy.
Adult ; Bone Density ; Bone Resorption ; Female ; Fractures, Compression ; Humans ; Low Back Pain ; Lumbar Vertebrae ; Osteoporosis* ; Pregnancy ; Teriparatide*

No abstract available.
Obesity ; Tea

Autophagy is necessary for the degradation of long-lasting proteins and nonfunctional organelles, and is activated to promote cellular survival. However, overactivation of autophagy may deplete essential molecules and organelles responsible for cellular survival. Lifelong calorie restriction by 40% has been shown to increase the cardiac expression of autophagic markers, which suggests that it may have a cardioprotective effect by decreasing oxidative damage brought on by aging and cardiovascular diseases. Although cardiac autophagy is critical to regulating protein quality and maintaining cellular function and survival, increased or excessive autophagy may have deleterious effects on the heart under some circumstances, including pressure overload-induced heart failure. The importance of autophagy has been shown in nutrient supply and preservation of energy in times of limitation, such as ischemia. Some studies have suggested that a transition from obesity to metabolic syndrome may involve progressive changes in myocardial inflammation, mitochondrial dysfunction, fibrosis, apoptosis, and myocardial autophagy.
Aging ; Apoptosis ; Autophagy ; Cardiovascular Diseases ; Fibrosis ; Heart ; Heart Failure ; Inflammation ; Ischemia ; Nutritional Status ; Obesity ; Organelles ; Proteins ; Starvation

Diabetic mastopathy is an unusual fibroinflammatory breast lesion that is characteristically presented in premenopausal women with long-standing diabetes with multiple microvascular complications. This patient was a 49-year-old postmenopausal woman with diabetic nephropathy, neuropathy, and retinopathy. Although palpable mass was detected on the left breast, an ultrasonography could not distinguish it from breast cancer. Excisional biopsy was conducted. Histological findings indicated diabetic mastopathy with keloid-like fibrosis, perivascular lymphocytic infiltration, and lymphocytic lobulitis without evidence of malignancy. After excision, there has been no recurrence until now.
Biopsy ; Breast ; Breast Neoplasms ; Diabetic Nephropathies ; Female ; Fibrosis ; Humans ; Middle Aged ; Recurrence