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Biomedical subjects

A M Sharma

Publications and source records attributed to A M Sharma.

At least 37 records · Page 2Linked to original sources
PubMed2003

[Management of diabetes and hypertension: how do primary care physicians judge their performance?].

With regard to the management of hypertension and diabetes, HYDRA reveals that doctors report multiple problems in their everyday practice. Being confronted with an average of 73 patients a day, with almost every second having either diabetes or hypertension, frequently associated with multiple comorbid conditions, the core obstacle is the time factor. Doctors do not have sufficient time to perform diagnostic tests and especially no time for non-drug interventions of any type. Further available treatment guidelines are only used in 1 out of 2 doctors. Further they seem not to affect doctors performance significantly.

Adult↗
PubMed2003

[Hypertension, diabetes mellitus and comorbidity in primary care].

Almost every second patient seeing a primary care doctor suffers from arterial hypertension and about every fifth has diabetes mellitus. These diseases often occur at the same time. They are associated in more than 80% of the cases with other severe concomitant and subsequent diseases (heart attack, stroke, renal failure, neuropathy etc.). The magnitude especially of subsequent and concomitant diseases, the dimension of the personal suffering and the immense diagnostic and therapeutic challenges for the doctors have been massively underestimated so far. The article informs about the prevalence of the above disease, and structure of the problem. Before the background of an extremely high patient load seen by German General Physicians, the mainstay challenge is highlighted how to achieve further improvements of the quality of care on the basis of scientific guidelines alone, without a concomitant change in the system structure.

Adolescent↗
PubMed2003

Obesity and cardiovascular risk.

In most industrialized countries, 40-60% of the population is now overweight or obese. Obesity has recently been recognized as a major modifiable risk factor for cardiovascular disease, second only to cigarette smoking. Excess weight and obesity markedly increase the risk for hypertension, diabetes, coronary artery disease and congestive heart failure in both men and women. Populations most severely affected include the poor, the uneducated and certain racial and ethnic groups. Obesity is currently classified based on body mass index (BMI), but measurement of waist circumference as an important determinant of cardiovascular and metabolic risk is receiving increasing acceptance. For moderate overweight and obesity, interventions include dietary modification, increasing physical activity, behavior therapy and pharmacotherapy. Surgery is currently the only viable approach to morbid obesity.

Body Mass Index↗
PubMed2003

Endothelial cell specific molecule-1--a newly identified protein in adipocytes.

Expression of the endothelial cell-specific molecule (ESM)-1 was originally identified in lung and kidney endothelial cells, where its expression is regulated by cytokines. In vitro, ESM-1 interferes with the molecular mechanisms of immune cell migration by binding to adhesion molecules. In this study, we have explored the expression of ESM-1 in isolated human adipocytes and in rat adipose tissue depots. Human primary adipocytes were cultivated after collagenase digestion and used for in vitro incubation studies. Adipocytes were also isolated from different fat depots of Sprague-Dawley rats. Gene expression was quantified by TaqMan RT-PCR using specific human and rat ESM-1 primers. The cellular localisation of ESM-1 was determined by confocal microscopy using a specific antibody. ESM-1 expression in human adipocytes was stimulated by phorbol ester, an activator of protein kinase C, and by retinoic acid, an activator of nuclear receptors. The maximum increase in gene expression was 3.2-fold after 72 h treatment with phorbol ester and 4.6-fold after 72 h treatment with retinoic acid. The highest expression was found in subcutaneous rat adipose tissue - two-fold compared to epididymal and six-fold compared to intrascapular brown adipose tissue. As obesity is related to systemic inflammation (examplified by increased circulating levels of C-reactive protein and interleukin-6), the formation of ESM-1 in adipocytes and its activation by protein kinase C may play a role in the regulation of inflammatory processes.

Adipocytes↗
PubMed2002

Habitual fat intake and basal fat oxidation in obese and non-obese Caucasians.

OBJECTIVE: To examine the relationship between habitual fat intake and basal fat oxidation in obese and non-obese Caucasian men and women. METHODS: Habitual fat intake was assessed by 7-day weighed dietary records and resting fat oxidation was determined after an overnight fast in 132 weight stable non-diabetic subjects (38 males, 94 females). All subjects were characterized for weight, height, waist-to-hip ratio, physical activity, plasma glucose and insulin response to an oral glucose load, plasma catecholamine and leptin levels. Under-reporters, defined according to plausibility of the relationship between energy expenditure and energy intake, were excluded from the analyses. RESULTS: The mean age was 53.1+/-10.6 y (19-72 y) and mean body mass index (BMI) was 30.7+/-5.8 kg/m(2) (19.4-45.8 kg/m(2)). Sixty-eight subjects were obese (BMI>30 kg/m(2)). Univariate regression analysis revealed a significant, albeit modest, relationship between absolute fat intake and BMI (r(2)=0.06; P<or=0.05) but not between fat intake and fat mass (r(2)=0.026; P=0.08). However, multiple regression analysis revealed significant effects of body fat mass (FM) and sex on basal fat oxidation (bFO) explaining 33% of the variation of bFO (P<or=0.0001; radical s.e.=18.0 g/24 h). In univariate regression analysis, habitual fat intake was significantly related to adjusted fat oxidation, explaining 12% of the variation (P<or=0.0001; radical s.e.=11.7 g/24 h). CONCLUSION: Habitual fat intake has a significant, albeit modest, effect on basal fat oxidation, even when adjusted for sex and body FM. The rather modest effect of habitual fat intake on fat oxidation may in part explain the increased propensity to gain FM on a high-fat diet.

Adult↗
PubMed2002

Second International Symposium on Obesity and Hypertension: genetics and molecular mechanisms, 25-27 October 2001, Berlin, Germany.

The 2nd International Symposium on Obesity and Hypertension (ISOH'01) was held on October 28-30, 2001 at the Max Delbrück Center for Molecular Medicine in Berlin-Buch, Germany. The meeting, which consisted largely of invited lectures, presented a state-of-the-art overview of the genetic and molecular mechanisms that link obesity and hypertension. The over 40 oral presentations were supplemented by 85 poster presentations from 27 countries. The meeting was attended by around 250 participants from 48 countries. This paper briefly reviews the contents of the invited lectures presented at this meeting covering topics ranging from genetics, molecular mechanisms, pathophysiology, cardiovascular risk, to the management of patients with obesity-related hypertension. Stimulated by the continuing success of these Symposia the organizers are currently planning to hold a 3rd International Symposium on Obesity and Hypertension (ISOH'03) in Berlin: A tentative date for this meeting has been set for October 23-26, 2003.

Humans↗
PubMed2002

Adipose tissue: a mediator of cardiovascular risk.

Two key findings regarding the cardiovascular risks associated with obesity have emerged in recent years: one relates to the importance of visceral obesity as a risk factor for cardiovascular disease, and the other to the recognition that adipose tissue can be regarded as a large endocrine organ that directly contributes to cardiovascular risk by secreting a number of molecules known to modulate vascular, metabolic, inflammatory and other functional aspects of the cardiovascular system. Therefore, abdominal fat deposition, which is characterized by increase in waist circumference, should be the target of clinical intervention in obese individuals.

Adipocytes↗
PubMed2001

Enhanced affective startle modulation in salt-sensitive subjects.

Salt-sensitive normotensive men exhibit an enhanced pressor response to mental stress. Although an enhanced pressor response is associated with higher affective startle modulation in men, an association between salt sensitivity of blood pressure and affective startle modulation has not been studied so far. We studied reactivity to mental stress and startle modulation in 14 salt-sensitive healthy white male students and 14 salt-resistant control subjects, who were well matched for age, body mass index, physical fitness, and family history of hypertension. Subjects performed a computerized information-processing task under time pressure (manometer test), while heart rate and blood pressure were continuously registered. In a separate session, subjects viewed a series of 42 pictures of the International Affective Picture System (IAPS), varying in pleasure and arousal, while acoustic startle probes were administered randomly, and electromyogram activity of the orbicular eye muscle was continuously recorded. Startle modulation was calculated as the difference between startle responses under negative and positive affective stimuli. In contrast to salt-resistant subjects, salt-sensitive subjects showed significantly enhanced startle amplitudes under negative stimuli and diminished amplitudes under positive stimuli. Thus, salt-sensitive subjects displayed a significantly higher startle modulation than did salt-resistant subjects (P<0.05). Subjective ratings of the presented IAPS pictures did not differ between the groups. The increased startle modulation of salt-sensitive subjects suggests an enhanced activity of the central nucleus of the amygdala. This enhanced central nervous responsiveness may contribute to higher sympathetic pressor reactivity and, thus, to the later development of hypertension in salt-sensitive individuals.

Adult↗
PubMed2001

Limited effect of systemic beta-blockade on sympathetic outflow.

Central beta-adrenoreceptors may augment sympathetic outflow. We tested the hypothesis that beta-blockade attenuates central sympathetic outflow by inhibiting central adrenoreceptors. We studied 18 healthy controls (4 female, 14 male; age, 26+/-6 years, body mass index, 23+/-3 kg/m(2)). ECG, brachial, and finger arterial blood pressure, muscle sympathetic nerve activity, and respiration were measured continuously before and during complete beta-blockade. Subjects received a total intravenous dose of 0.21 mg/kg of propranolol in 15 minutes. Spontaneous baroreflex slopes were calculated using the sequence technique (BRSup, BRSdown). The sympathetic baroreflex slope was determined at baseline using phenylephrine and sodium nitroprusside infusions. The subjects underwent cold pressor testing before and during beta-blockade. The R-R interval increased from 861+/-119 ms at baseline to 952+/-141 ms during beta-blockade (P<0.01). Blood pressure was 117+/-9/65+/-8 mm Hg at baseline and 117+/-10/67+/-8 mm Hg during beta-Blockade (P=NS). beta-Blockade did not affect baroreflex sensitivity (BRSup: 21+/-10 versus 28+/-11 ms/mmHg, P<0.1; BRSdown: 17+/-8 versus 20+/-8 ms/mmHg, P=NS). Muscle sympathetic nerve activity increased significantly during beta-blockade (number of bursts/100 beats: 32+/-9 versus 40+/-14, P<0.05), compared with baseline. However, the operating points of the parasympathetic and sympathetic baroreflex during beta-blockade were on the baroreflex curves obtained at baseline. beta-Blockade blunted the heart rate response to cold pressor testing; blood pressure and muscle sympathetic nerve activity responses were similar. Our study demonstrates that propranolol does not cause an acute decrease in sympathetic activity in normotensive young subjects. This, observation is not consistent with an important tonic stimulatory effect of beta-adrenoreceptors in the brain.

Adrenergic beta-Antagonists↗
PubMed2001

[Lowering blood pressure in obese hypertensive patients. Which antihypertensive drugs are suitable].

Current guidelines in the treatment of arterial hypertension do not recommend differential treatment of obesity-associated hypertension. Since optimal blood pressure control in most obese hypertensives requires a combination of blood pressure-lowering substances, careful consideration of the choice of treatment is of particular importance. On the basis of their favorable metabolic properties, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, and low-dose diuretics, should be preferentially employed in the obese. Beta-blockers should not be given to young obese patients with uncomplicated hypertension. Before definitive pronouncements on what constitutes optimal treatment of obese patients can be made, the results of studies looking at hard end points must be available.

Antihypertensive Agents↗
PubMed2001

[Treatment of hypertension in obesity].

BACKGROUND: Hypertension and obesity are common medical conditions independently associated with increased cardiovascular risk. Many large epidemiological studies have demonstrated associations between body mass index and blood pressure, and there is evidence to suggest, that obesity is a causal factor in the development of hypertension in obese subjects. Weight Reduction and maintenance is an essential first step in the treatment of obesity-associated hypertension. Weight reduction may be achieved by behavior modification, diet, and exercise or by the use of anti-obesity medication. However, the long-term outcomes of weight management programs for obesity are generally poor, and most hypertensive patients will require antihypertensive drug therapy. PATHOPHYSIOLOGY: Obese hypertensive patients often have metabolic abnormalities known to be exacerbated by commonly used antihypertensive agents but also obesity per se is often associated with endorgan damage including left ventricular hypertrophy, glomerular hyperfiltration and microalbuminuria, congestive heart failure or sudden cardiac death. Furthermore they have revealed volume expansion, increased cardiac output, and lower total peripheral resistance than lean patients. Hypertension in obese patients appears to be related to both increased sympathetic nervous system activity and activation of the renin-angiotensin system. Where antihypertensive therapy is necessary, the aim should be to use agents based on the hemodynamic and metabolic background and that have benefits beyond blood pressure lowering and improve the conditions most commonly linked with obesity-associated hypertension, such as hyperlipidaemia, Type II diabetes, left ventricular hypertrophy, coronary artery disease, or congestive heart failure. PHARMACOTHERAPY: Based on their favorable metabolic profiles, it would appear that ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, moxonidine and alpha-blockers can lower blood pressure without worsening the metabolic abnormalities, that is just one aspect of the problem. Yet, most guidelines fail to provide specific advice on the pharmacological management of hypertension in obese patients. This may be due to the fact that there are currently no studies that have addressed the efficacy of specific antihypertensive agents in reducing mortality in obese-hypertensive patients. This paper reviews the theoretical reasons for the differential use of the major classes of antihypertensive agents in the pharmacological management of obesity-related hypertension and also considers the potential role of anti-obesity agents.

Antihypertensive Agents↗
PubMed2001

The renin-angiotensin system and natriuretic peptides in obesity-associated hypertension.

Excessive accumulation of adipose tissue is associated with profound alterations in the cardiovascular system. including an increase in systemic blood pressure. It now appears clear that a central feature of obesity-associated hypertension is related to changes in sodium handling that may result from abnormalities in sympathetic nervous system activity, the renin-angiotensin-aldosterone system, natriuretic peptides, and kidney function. In this paper we review the role of these factors in the development of obesity-associated hypertension, thereby focusing on the potential role of adipose tissue in these alterations.

Adipose Tissue↗
PubMed2001

New developments in mechanisms of obesity-induced hypertension: role of adipose tissue.

Hypertension develops in almost 60% of obese individuals. Apart from the recent observation of obesity-associated structural changes in kidney structure that may lead to enhanced tubular sodium reabsorbtion, reports of paracrine and hormonal factors derived from adipose tissue have prompted speculations about the role of adipose tissue in the pathophysiology of obesity-induced hypertension. We summarize recent data on leptin's sympathoexcitatory actions, the possible influence of adipose tissue on atrial natriuretic peptide levels, and the formation of vasoactive substances, such as angiotensin II and nonesterified fatty acids, by adipocytes. The mechanisms discussed herein may contribute to the typical findings in obesity-induced hypertension, including volume expansion, sodium retention, enhanced sympathetic nervous system activity, increased activity of the systemic renin-angiotensin system, low atrial natriuretic peptide levels, and disturbed glucose and insulin metabolism. Together, these data strengthen the hypothesis that adipose tissue is potentially a major regulator of cardiovascular-renal function.

Adipose Tissue↗
PubMed2001

Metabolic and hemodynamic response of adipose tissue to angiotensin II.

OBJECTIVE: Recent studies have revealed the presence of a local renin-angiotensin system in adipose tissue. To examine the possible role of this system in adipose tissue, we performed microdialysis studies on the effect of angiotensin II (Ang II) on blood flow and metabolism in abdominal subcutaneous adipose tissue (aSAT) and femoral subcutaneous adipose tissue (fSAT) in young healthy men. RESEARCH METHODS AND PROCEDURES: Using the microdialysis technique, two different protocols were run perfusion with Ringer's solution + 50 mM ethanol with the subsequent addition of 125, 250, and 500 microg/liter Ang II (n = 8) and Ringers's solution + 50 mM ethanol with the subsequent addition of isoproterenol (1 microM) alone and in combination with 500 microg/liter Ang II (n = 6). Dialysate concentrations of ethanol, glycerol, glucose, and lactate were measured for estimating blood flow (ethanol dilution technique), lipolysis, and glycolysis, respectively. RESULTS: Perfusion with Ang II resulted in a dose-dependent decrease in blood flow (fSAT > aSAT), lipolysis (fSAT > aSAT), and glucose uptake (fSAT = aSAT). Isoproterenol increased blood flow and lipolysis at both sites and those effects could be returned to baseline values by the addition of Ang II in aSAT but not fSAT. DISCUSSION: In conclusion, our data indicate that in addition to its well-known vasoconstricting effect, Ang II inhibits lipolysis in adipose tissue, whereby femoral fat depots seem to be more sensitive to this effect than abdominal depots.

Adipose Tissue↗