Hypertension in obesity.

Obesity and HTN are on the rise in the world. HTN seems to be the most common obesity-related health problem and visceral obesity seems to be the major culprit. Unfortunately, only 31% of hypertensives are treated to goal. This translates into an increased incidence of CVD and related morbidity and mortality. Several mechanisms have been postulated as the causes of obesity-related HTN. Activation of the RAAS, SNS, insulin resistance, leptin, adiponectin, dysfunctional fat, FFA, resistin, 11 Beta dehydrogenase, renal structural and hemodynamic changes, and OSA are some of the abnormalities in obesity-related HTN. Many of these factors are interrelated. Treatment of obesity should begin with weight loss via lifestyle modifications, medications, or bariatric surgery. According to the mechanisms of obesity-related HTN, it seems that drugs that blockade the RAAS and target the SNS should be ideal for treatment. There is not much evidence in the literature that one drug is better than another in controlling obesity-related HTN. There have only been a few studies specifically targeting the obese hypertensive patient, but recent trials that emphasize the importance of BP control have enrolled both overweight and obese subjects. Until we have further studies with more in-depth information about the mechanisms of obesity-related HTN and what the targeted treatment should be, the most important factor necessary to control the obesity-related HTN pandemic and its CVD and CKD consequences is to prevent and treat obesity and to treat HTN to goal.

Ultrastructure of islet microcirculation, pericytes and the islet exocrine interface in the HIP rat model of diabetes.

CONTEXT: The transgenic human islet amyloid polypeptide (HIP) rat model of type 2 diabetes mellitus (T2DM) parallels the functional and structural changes in human islets with T2DM. OBJECTIVE: The transmission electron microscope (TEM) was utilized to observe the ultrastructural changes in islet microcirculation. METHODS: Pancreatic tissue from male Sprague Dawley rats (2, 4, 8, 14 months) were used as controls (SDC) and compared to the 2-, 4-, 8- and 14-month-old HIP rat models. RESULTS: The 2-month-old HIP model demonstrated no islet or microcirculation remodeling changes when compared to the SDC models. The 4-month-old HIP model demonstrated significant pericapillary amyloid deposition and diminution of pericyte foot processes as compared to the SDC models. The 8-month-old model demonstrated extensive islet amyloid deposition associated with pericyte and beta-cell apoptosis when compared with SDC. The 14-month-old HIP model demonstrated a marked reduction of beta-cells and intra-islet capillaries with near complete replacement of islets by amyloidoses. Increased cellularity in the region of the islet exocrine interface was noted in the 4- to 14-month-old HIP models as compared to SDC. In contrast to intra-islet capillary rarefaction there was noticeable angiogenesis in the islet exocrine interface. Pericytes seemed to be closely associated with collagenosis, intra-islet adipogenesis and angiogenesis in the islet exocrine interface. CONCLUSION: The above novel findings regarding the microcirculation and pericytes could assist researchers and clinicians in a better morphological understanding of T2DM and lead to new strategies for prevention and treatment of T2DM.

Polycystic ovarian syndrome.

Polycystic ovarian syndrome (PCOS) is the most common reproductive endocrinopathy of women during their childbearing years. A significant degree of controversy exists regarding the etiology of this syndrome, but there is a growing consensus that the key features include insulin resistance, androgen excess, and abnormal gonadotropin dynamics. Familial and genetic factors cause predisposition to PCOS. Insulin resistance and adiposity put women with PCOS at a higher risk for diabetes, hypertension, dyslipidemia, and cardiovascular disease. Even though the adverse health consequences associated with PCOS are substantial, most women are not aware of these risks. Early recognition and treatment of metabolic sequelae should be the main focus of clinicians. Lifestyle modifications, mainly a balanced diet, weight loss, and regular exercise, are of utmost importance. On the pharmacologic front, various therapies including metformin, thiazolidinediones, and others appear to be very promising in the management of cardiometabolic aspects of PCOS.