Amelioration of Paget Disease of Bone After Denosumab for Osteopenia.

Background/objective: Denosumab is a monoclonal antibody that inhibits bone resorption and is indicated for the treatment of osteoporosis, bone metastases, and giant cell tumor of bone. We describe a woman with symptomatic Paget disease of the skull whose headaches and monostotic disease of the skull improved after receiving denosumab for concomitant low bone density.

Case Report: A 75-year-old woman presented with unremitting headache of 1 month.

Elderly hypertensives show decreased cognitive performance compared with elderly normotensives.

Background: Essential hypertension has been associated with decreased cognitive performance; however, the literature is conflicting.

Objective: This study aims at comparing cognitive performance between elderly normotensives ("N"; n = 17; age 68 ± 1; blood pressure = 133 ± 3/74 ±2 mmHg) and hypertensives ("H"; n = 28; age 69 ± 1, blood pressure = 148 ± 4/80 ± 1mmHg) with at least 5 years of education.

Methods: The comprehensive neuropsychological assessment was comprised of the Cambridge Cognition-Revised (CAMCOG-R), the Trail Making Test A and B (TMT A and B) and the Rey Auditory Verbal Learning Test (RAVLT).

Maternal high-fat diet programs for metabolic disturbances in offspring despite leptin sensitivity.

A fatty diet during pregnancy in mouse dams causes metabolic abnormalities (similar to metabolic syndrome in humans) in the rodents' offspring. We tested the hypothesis that the offspring of dams fed a high-fat diet during pregnancy and lactation develop metabolic abnormalities and leptin resistance. Pregnant C57BL/6 mice (n = 20) were fed either standard chow (SC; 19% fat) or a high-fat diet (HF; 49% fat).

Dissociation between sympathetic nerve traffic and sympathetically mediated vascular tone in normotensive human obesity.

Obesity increases the risk of hypertension and its cardiovascular complications. This has been partly attributed to increased sympathetic nerve activity, as assessed by microneurography and catecholamine assays. However, increased vasoconstriction in response to obesity-induced sympathoactivation has not been unequivocally demonstrated in obese subjects without hypertension.

Arterial compliance and endothelial function.

Decreased arterial compliance (increased stiffness) correlates with cardiovascular events, possibly due to increased cardiac afterload caused by more rapidly reflected pulse waves. Endothelium-derived mediators regulate vascular tone and structure, both of which can markedly influence arterial stiffness. Thus, increased arterial stiffness may be a mechanism by which endothelial dysfunction predisposes to complications of atherosclerosis.

Role of leptin in the cardiovascular and endocrine complications of metabolic syndrome.

Aim: To review the potential role of leptin, hyperleptinaemia and leptin resistance in the cardiovascular and endocrine complications of metabolic syndrome.

Methods: Review of literature listed in Medline.

Results: Hyperleptinaemia is common in obesity and reflects increased adiposity and leptin resistance.

Emerging drugs for obesity: linking novel biological mechanisms to pharmaceutical pipelines.

Obesity is associated with hypertension, diabetes, dyslipidaemias and metabolic syndrome, and causes substantial morbidity and mortality from cardiovascular and other diseases. The cost to treat obesity and its complications in the US has increased steeply and is currently estimated to be USD 100 billion. Current therapy for obesity is mainly based on changes in lifestyle that often fail.

Effects of aging and atherosclerosis on endothelial and vascular smooth muscle function in humans.

Background: Nitric oxide is an endothelium dependent dilator, which may protect against atherosclerosis. Several studies have shown a decrease in nitric oxide activity with aging, however none have assessed aging and atherosclerosis separately. We tested the hypothesis that aging blunts both basal and receptor-mediated endothelial nitric oxide release in humans.

Loss of leptin actions in obesity: two concepts with cardiovascular implications.

Obesity is associated with increased risk of hypertension and heart disease. Leptin has recently been linked to increased risk of cardiovascular disease. We review briefly here two concepts regarding loss of leptin actions that have potential implications for cardiovascular disease.

Obesity-associated hypertension: new insights into mechanisms.

Obesity is strongly associated with hypertension and cardiovascular disease. Several central and peripheral abnormalities that can explain the development or maintenance of high arterial pressure in obesity have been identified. These include activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system.

Leptin, obesity and cardiovascular disease.

Purpose Of Review: Obesity is a risk factor for cardiovascular diseases. Leptin levels are increased in obesity and leptin exhibits cardiovascular actions that may contribute to increased cardiovascular risk. We review the sympathetic, renal and vascular actions of leptin and their relevance to cardiovascular disease.

Obesity-related hypertension: is there a role for selective leptin resistance?

Obesity is a risk factor for cardiovascular diseases, in particular for hypertension. Serum leptin levels and sympathetic nerve activity are both increased in obesity. Leptin has been demonstrated to increase sympathetic nerve activity.

Impaired skeletal muscle and skin microcirculatory function in human obesity.

Background: Obesity is associated with exaggerated blood pressure and systemic vascular resistance responses to mental stress.

Objective: To test the hypothesis that skin and muscle microvascular dilatation in response to mental stress is blunted in obesity.

Design And Methods: Blood pressure, heart rate and forearm and skin blood flow responses to mental stress were compared in 23 obese and 23 age- and sex-matched lean normotensive individuals.

Selective leptin resistance: a new concept in leptin physiology with cardiovascular implications.

Leptin, an adipocyte secreted hormone, acts in the hypothalamus to inhibit appetite and promote thermogenic metabolism, thereby reducing adiposity and body weight. Leptin has multiple autonomic and cardiovascular actions, including sympathetic activation, increases in endothelium derived nitric oxide (NO), and angiogenesis. The predominant cardiovascular effect of chronic hyperleptinemia is a pressor effect mediated by increased sympathetic activity.

Hemodynamic consequences of neuropeptide Y-induced obesity.

Background: Acute central nervous system administration of neuropeptide Y (NPY) elicits variable hemodynamic responses. Chronic intracerebroventricular (ICV) administration of NPY produces obesity in rats. Obesity has been shown to increase arterial pressure.

The concept of selective leptin resistance: evidence from agouti yellow obese mice.

Leptin, a hormone secreted by adipose tissue, acts to inhibit appetite and promote metabolism, thereby reducing body weight. Leptin also increases sympathetic activity and arterial pressure. Several murine models of obesity, including agouti obese mice, exhibit resistance to the anorexic and weight-reducing effects of leptin.