3 مه, 2010

World Journal of Sport Sciences 2 (1): 13-20, 2009 ISSN 2078-4724 © IDOSI Publications, 2009 Leptin, Heart Disease and Exercise 1F. Rahmani Nia, Z. Hojjati, N. Rahnama and B. Soltani 1Department of Sport Sciences, University of Guilan, Guilan, Iran 2Department of Sport Sciences, University of Isfahan, Isfahan, Iran 3Cellular and Molecular Research Center, Guilan University of Medical Sciences, Guilan, Iran Abstract: Obesity is a complex disorder characterized by the accumulation of excess adipose tissue. Discovery of the hormone leptin in 1994 catalyzed the field of obesity research by demonstrating the existence of an afferent hormonal signal from adipose tissue to the central nervous system. Leptin the product of the ob gene is a proteohormone with a molecular mass of 16 kDa that is thought to play a key role in the regulation of body weight. Leptin increases energy expenditure by enhancing sympathic nervous activity and lypolysis. It also suppresses appetite by acting on the hypothalamus. In recent years the potential participation of leptin has been reported to increase arterial pressure and heart rate by peripherally or centrally mediated mechanisms. The finding that leptin is linked to heart disease risk, strongly suggests that fat may be important in heart disease risk. Leptin deficiency and resistance to the effects of leptin are each associated with weight gain. Leptin resistance is much more common than leptin deficiency in human obesity. There are receptors for leptin on the endothelium and on vascular smooth muscle cells. Accordingly, leptin can exert receptor mediated influence on vessel tone and growth. In cell culture, leptin stimulates vascular smooth muscle proliferation. Vascular calcification is also accelerate by leptin in experimental models. Additionally, leptin induces oxidative stress in endothelial cells. Accordingly, it is possible that the high level of leptin observed in obesity could contribute to its adverse effects on cardiovascular health. Diet and exercise have been shown to reduce leptin levels regardless of weight loss. Exercise training induced reduction in leptin levels have been attributed to alterations in energy balance, improvements in insulin sensitivity alterations in lipid metabolism and unknown factors. This article considers leptin function and the impact that exercise has on blood leptin concentrations. Key words: Leptin % Risk factor % Exercise INTRODUCTION from lifestyle factors such as diet and satiety may be predominantly responsible for the recent dramatic Obesity is an increasing prevalent metabolic disorder increase in the prevalence of obesity [1, 2]. Lack of affecting not only the developed but also developing exercise and poor diet are the primary causes of clinical countries [1]. In fact obesity can be described as the obesity in developed countries [4]. «New World Syndrome» that is one of the most severe In the United States, despite the fact that problems for the modern day health industry. Its consumption of fat has been reduced dramatically over prevalence has been rose in all age groups in the world the last thee decades, a decrease in incidence of obesity [2]. Statistical data reveals that the problem of obesity has has not occurred [1]. This is likely attributable to increased from 12-20% in men and from 16-25% in women maintenance of food intake with an increase in total [2, 3]. Resent studies suggest that nearly 15-20% of the calories and also reduced physical activity. middle aged European population are obese [2, 4]. In USA Obesity, in simple terms, may be defined as a state of alone it is responsible for as many as 300000 premature imbalance between calories ingested versus calories deaths each years [2].The cause of obesity are varied expenditure which would lead to excessive or abnormal fat and have both central and peripheral origins [4]. The accumulation. Body mass index (BMI) s a measure of pathogenesis of obesity is multi-factorial incorporating weight corrected for height and which reflects the total both genetics and lifestyle, while heredity explains 30% body fat and has been the most accepted parameters for to 70% of obesity cases (Table 1) [1, 5]. The contribution defining over weight [5]. Corresponding Author: Z. Hojjati, Department of Sport Sciences, University of Guilan, Guilan, Iran 13 World J. Sport Sci., 2 (1): 13-20, 2009 Table 1: Some important causes and precautionary measures of obesity Causes Sedentary life style Food availability High fat diet Hereditary Drug induced weight gain Table 2: Obesity-associated diseases and risk factors Main disease Related disease Management Physical activity Diet control Behavioral therapy Medication Surgery Cardiovascular diseases (CVD) Respiratory diseases Metabolic disorders Gastrointestinal disorders Malignancies Miscellaneous Hypertension, Coronary heart disease, Cereberovascular disease, Varicose veins, Deep venous thrombosis Breathless, sleep apnea, Hypoventilation syndrome Hyperlipidemia. Diabetes mellitus, Insulin resistance, Menstrual irregularities Fatty liver and cirrhosis, Hemorrhoids, Hernia, Colorectal cancer, Gallstones Brest cancer, Endometrial cancer, Prostate cancer, Cervical caancer Pregnancy stress, Arthritis and bone mass BMI = weight (kg)/hight (m ) There is a very good correlation between BMI and the percentage of body fat in large populations [2]. Percent Body Fat = 1.2(BMI) + 0.23 (age)-10.8 (gender)-5.4 Where, Gender = «1» for men and «0» for women times higher in women than in men even when adjusted for age and BMI [13]. Adipose tissue is the major source of leptin expression, however, other sites have been identified, including skeletal muscle, mammary, epithelium, heart, the fondues of the stomach, liver, gastric epithelium [11, 14] and the brain [12, 15]. It appears that leptin is not stored in any significant quantities. No large storage organelles for leptin have been found in adipocytes [12, 16]. And, studies looking at the kinetics of leptin synthesis and secretion in response to known secretagogues found no Obesity and Diseases: The metabolic effects of obesity evidence of leptin release from stored sytolitic pools [12]. have made this highly prevalent disease one of the most Thus, increases in leptin release are due to an increase in common risk factors for diabetes, hypertension and leptin expression. The leptin receptor (with long and short other cardiovascular diseases and osteoarthritis [2, 6, 7]. isoforms) is a member of the cytokine family of receptors Epidemic logical studies underlined that Obesity and is expressed in a variety of tissues including the represents a significant risk for the development of hypothalamic nuclei [15, 17]. Neurons in the arcuate, cancer (Table 2) [4, 8]. ventromedial and dorsomedial hypothalamic nuclei that In addition, uncorrected obesity dramatically are sensitive to leptin express neuropeptides/ enhanced the propensity of other metabolic disorders neurotransmitters that are associated with central such as hyperlipidemia, hyperuricemia and low plasma regulation of energy balance [11, 12, 18]. high-density lipoprotein cholesterol (HDL), collectively known as the metabolic syndrome [2, 3, 5, 7, 9]. Numerous factors alter leptin synthesis and secretion including genetics, various nutrients, sex hormones, insulin, catecholamines, fat free mass, fat stores and Leptin and its Functions: Leptin (from Greek leptos-thin) energy balance [12, 19]. was discovered in 1994 following the isolation of the ob Leptin has been implicated in regulating an array of gene [10]. The discovery of leptin has led to numerous physiological processes such as appetite, metabolic rate, experiments to better understand its function [11]. Leptin reproduction and immunity [20, 21]. It is thought that a is a proteohormone with a helical structure similar to major role of leptin is to relay information to signal cytokines and a relative mass of 16 kDa [12]. The traducing receptors in the hypothalamus concerning the circulation leptin concentration is usually proportional to status of energy stores and thus aid in reduced feeding total adipose tissue mass, i.e. increased in obese and [11, 22]. In fact leptin acts on the central nervous system, decreased in lean subjects [8]. Serum leptin levels are 2-3 in particular the hypothalamus, suppressing food intake 14 World J. Sport Sci., 2 (1): 13-20, 2009 and stimulating energy expenditure [18]. In mice, individuals have markedly increased leptin production mutations of the ob gene (and subsequent lack of probably as a consequence of resistance to its function leptin production) cause hyperphagia and early and [32, 35, 36]. However, the widespread distribution of rapid onset of obesity. However, this mutation is quite functioning leptin receptors on vascular cells suggests rare in humans [12]. Obese individuals often have that leptin also plays an important role in vascular increased leptin concentrations and leptin administration physiology [25, 33]. In experimental models, leptin has shows only very limited effects [23]. Recent data have been shown to have angiogenic activity [21], increase indicated that this is likely the results of desensitization oxidative stress in endothelial cells [25] and promote for the leptin signal, a phenomenon now often referred to vascular cell calcification [35] and smooth muscle cell as leptin resistance [24]. Leptin and Heart DiseaseMany proliferation and migration [21]. studies have shown that weight gain is an independent Leptin is also associated with increased heart rate predictor of diabetes mellitus and cardiovascular disease and may contribute to platelet aggregation [31, 37, 38] and a (CVD) in human [7]. Numerous peripheral effects of thrombosis [35]. leptin suggesting its involvement in glucose and lipid Hyperleptinemia, universal in human obese metabolism, angiogenesis and blood pressure regulation population [39], has been deemed an independent risk [8]. factor for cardiovascular disease and, more specifically, a Recent data suggests that hyperleptinemia, predictor of first myocardial infarction and an independent secondary to increased fat cell mass and other factors, risk factor for ischemic and hemorrhagic stroke [22, 39]. may contribute to the development of the insulin resistance syndrome, including increasing blood pressure The Effect of Exercise on Adipose Tissue Leptin [24] through the effect on sympathetic tone, insulin Secretion: Although the precise mechanisms that sensitivity and number of other hormonal interactions underlie leptin secretion are not fully understood, a link [25]. Higher leptin levels in essential hypertension and with negative energy balance, sympathetic activation, noninsulin-dependent diabetes mellitus (NIDDM) may other hormones and metabolites has been observed suggest a possible role for leptin in the development of [11, 40, 41]. atherosclerotic heart disease [7]. The physiological stress of exercise is an obvious Patients with advanced chronic heart failure potential regulator of leptin secretion by adipose tissue. have increased serum concentrations of leptin and its The attendant changes in fuel flux, systemic hormone soluble receptor. Leptin may participate in the catabolic concentrations and energy expenditure may influence cachexia in the course of chronic heart failure [26]. Leptin and C-reactive protein (an inflammatory plasma leptin concentration and presumably, leptin action. There are many investigations that have examined predictor) levels are independently associated in the effects of exercise on leptin. There are several reasons normal human providing further evidence linking why responses and adaptations to exercise may have metabolic and inflammatory cardiovascular disease important ramifications: exercise is Known to effectively mechanisms [27]. The study by Sesso et al. [28] has reduce obesity (fat mass), thus if leptin levels are affected, clearly shown that elevated plasma C-reactive protein this may provide some explanation of how exercise affects (CRP) was associated with the future development of obesity [42]. hypertension in dose-dependent manner. These finding Research on leptin and exercise has in general taken suggest that hypertension may be an inflammatory three traditional approaches: cross-sectional studies, disease that is associated with obesity and the metabolic acute (single-bout) exercise studies and exercise training. syndrome. This could represent a causative pathway Studies investigating large databases have in general by which inflammation predisposes to both arterial reported that the log of plasma leptin is inversely related stiffness and hypertension as well as to cardiovascular to fitness [43, 44], but this relationship is generally not and renal disease [6, 27, 29]. Furthermore, there may independent of adiposity. Exercise alters concentrations be hormonal pathway acting independently of either of certain hormones that may alter leptin concentrations, metabolic or inflammatory disturbances, with the including insulin, cortisol, catecholamines, estrogen, finding that fasting serum leptin levels were testosterone and growth hormone [10, 11]. Additionally, independently associated with arterial distensibility the effects of exercise on leptin concentration may be the [30-32]. The effect of obesity on vascular function may main result of the importance of exercise in heart diseases be mediated by the hormone leptin [33, 34]. Obese prevention and treatment. 15 World J. Sport Sci., 2 (1): 13-20, 2009 Acute Effects of Exercise: The effect of physical exercise suggested that exercise does not alter systemic leptin on leptin concentrations is currently controversial. independent of changes in fat mass [26, 50]. Exceptions Several investigators reported that exercise may result to this include work from the author’s group, suggesting in reductions depending on duration and calorie that plasma leptin maybe reduced in exercise-trained expenditure whereas others have reported no change in females (but not males in an identical training program) leptin concentrations [14]. despite stable fat mass [41, 51] and a study from saris› Elias et al. reported a decline in leptin concentrations group suggesting that an independent effect of exercise in males (age-18-55) after a graded treadmill exercise test on plasma leptin is detectable after 10 months of training to exhaustion [11]. Essig et al. [45] stated lower leptin [44]. It is important to note, that in early studies about concentrations in trained males after 2 separate leptin concentrations neither the acute exercise studies exercise tests, 800 and 1500 kcal treadmill run. These nor the training interventions controlled for energy authors concluded that the decrease in plasma leptin balance and most sampled only a single fasting plasma concentrations after 48 hrs was preceded by a decrease leptin pre-and post intervention. Recently many studies in insulin concentrations. have elegantly demonstrated the care that is necessary Kreamer et al. have demonstrated that 30 min of to study leptin-exercise interventions [11, 52]. Because exercise at 80% of VO2maxis associated with reduced leptin leptin is actually sensitive to negative energy balance concentration in postmenopausal females regardless of (fasting or caloric restriction), then it is important to whether they are on or off hormone replacement therapy, design studies that can distinguish the effects of exercise but the reductions were due to the circadian rhythm of per se from any attendant change in energy balance leptin as determined from the control trial samples from or, perhaps more specifically, energy availability. the same subjects [41]. Nine trained males completed 60 In a study of adolescent female runners, min of running at 70% of VO2max (energy expenditure Kraemer et al. [41] measured resting and post maximal 882.7±14.4 kcal). It showed that leptin concentrations were exercise leptin concentrations over the course of a significantly lower immediately after exercise, 24 and 48 short track season. Resting leptin levels were not hrs during recovery [43]. Responses did not appear to be modified over the 7 weeks, nor were the acute responses related to changes in insulin or glucose concentration. to intense exercise despite a significant reduction in Blood samples were also collected from the same subjects skin folds. Additionally short term training (60 min at after a short term maximal exercise test (energy 75% of VO2max during 7 successive days) does not expenditure 197.5±11.5 kcal) and leptin levels did not modify leptin concentrations in healthy young and decrease immediately after or at 24 or 48 hrs post exercise. older males [53]. Many researchers have reported that acute aerobic Merino et al. reported leptin concentrations were exercise does not alter leptin concentrations [15, 46, 47]. decreased after 3 weeks of a military training. The fat Zoladz et al. [48] studied the responses of leptin in 8 mass in this study was not measured, but the body weight healthy men following two incremental exercises. The remained stable [14]. maximal incremental exercise was performed in the fed Unal et al. [54] measured leptin concentrations in state however the sub-maximal incremental exercise test trained young male athletes (from different sports) and up to 150 W was performed in a fasted state; the authors in healthy sedentary subjects. They noted a significant reported no significant changes in leptin concentrations. lower leptin after exercise and concluded that regular Kraemer in a review study indicated that generally exercise, by reducing fat percentage, suppresses serum short-term exercises (< 60 min) and exercises that leptin levels. generated energy expenditure lower than 800 kcal do Frank et al. [29] reported that regular, moderate not modify the concentrations of leptin [11]. In fact exercise decreases fasting insulin and leptin exercises of very long duration that generate a sufficient concentrations in overweight / obese postmenopausal energy imbalance suppress the amplitude of the diurnal women and that the adoption of regular/ moderate rhythm of leptin [14]. It still needs to be determined intensity exercise may be particularly useful among post how the hormones and the metabolites affecting the menopausal women who gain mass over time. secretion of leptin work together and can lower the Finally, these findings suggest that by following concentration of leptin under certain conditions, but the recommendations of $30 min of moderate intensity not in others [49]. physical activity on most, or preferably all, days of the week [29], women may achieve a more desirable metabolic Effects of Training: Similar to the majority of acute profile, especially with respect to carbohydrate and lipid exercise studies, exercise training interventions have metabolism. 16 World J. Sport Sci., 2 (1): 13-20, 2009 Barbeau [55] indicated that the 8-month physical and insulin action. Leptin concentration declined by 36% training doses prescribed to obese teenagers did not in the group that weight. result in significant group differences in mean change in Changes in leptin levels were not related to alteration leptin, although there was large variability in individual in resting metabolic rate or plasma catecholamines. response. The change in leptin was inversely associated However, the authors speculated that weight loss in the with baseline leptin and change in cardiovascular fitness. resistance training/weight loss subjects might mediate an They reported also: diet, physical activity level, visceral increase in insulin action reported in the study [46]. adiposity and glucose concentrations were not associated with leptin, neither at baseline nor in response to physical Effect of Caloric Restriction: Many studies have shown training over the 8-month intervention period, regardless that serum leptin levels in humans decline with weight of group membership, youths who hat the lowest increase loss [14]. Considine et al. for example, found that leptin in cardiovascular fitness tended to have the highest fell 53% in obese subjects who lost approximately 10% of increase in leptin. initial body weight in 8-12 weeks by consuming an 800 kcal/day leptin falls not only with long-term reductions in Effects of Resistance Exercise: Information regarding body weight (and fat) but also is response to short-term the response of serum leptin to a single bout of resistance decreases in energy intake [61]. Two human studies of exercise is limited. In contrast to continuous running of fasting, one of 36 hrs and the other of 52 hrs, found that moderate intensity, heavy resistance exercise is a potent leptin declined by 35 and 72%, respectively [62]. Such nonoxidative stimulus that produces differential neural, reductions are likely to be associated with a series of metabolic and neuroendocrine responses [56]. One study neurohormonal events that ultimately increase appetitive reports reduced 24-hr serum leptin in diabetic not in behavior and decrease energy expenditure in an effort to healthy individuals [40] and other reports reduction of restore energy balance [7]. Leptin levels increase rapidly serum leptin levels 9-13 hrs post-exercise in healthy lean when caloric restriction is terminated [61]. Thus plasma men [57]. There is an early study [58] concerning leptin leptin deceases markedly during short-term total fasting levels in trained men with low fat mass plus large increase not in proportion to the loss in fat mass and returns to of muscle. The findings indicated that leptin correlated baseline concentrations with refeeding [13]. Furthermore, with BMI in overweight subjects, but this correlation was after a fast, refeeding a diet providing energy intakes not observed either in athletes or in controls. The authors considerably below requirements increases leptin concluded: 1) regardless of the high BMI characteristics concentrations and energy expenditure even with of body builders, no correlation was observed with leptin ongoing fat mobilization [9]. 2) trained state induced by resistance exercise does not Klein et al. reported that compared with lean influence leptin production independently of variations in women, the fasting-induced decline in leptin production body composition [58]. blunted in women with upper body obesity. The altered Fatouros et al. [59] reported a decrease in plasma decline in attenuated decline in plasma insulin may be leptin concentration after resistance training (6 months, responsible for many of the alterations in the metabolic 3 days/week, 10 exercises/three sets) in fifty inactive men. response to fasting associated with obesity [51]. These authors noted that this decrease was accompanied by reduce skinfold sum and BMI. Reseland et al. [63] concluded that long-term diet and exercise interventions may have direct effects on Zeferides et al. [19] examined the acute effects of plasma leptin concentration beyond the effect expected maximum strength, muscular hypertrophy and strengthen due to changes in fat mass. Additionally the role of leptin endurance resistance exercise protocols on serum leptin. in normalizing several starvation-induced neuroendocrine The main findings of the study indicated that in normal changes may have important implications for the individuals the three resistance exercise protocols elicit pathophysiology and treatment of eating disorders and comparable serum leptin response and that a single bout obesity. of heavy resistance exercise protocols has on serum leptin compared with resting session. Then it appeared that differences in the configuration of the intensity, total work and rest interval among resistance training protocols do CONCLUSION The work of Hilton and Loucks is elegant and not affect acute serum leptin responses as they affect informative. The studies are useful in that they provide other hormonal responses. Ryan et al. [60] studied effects evidence of the limitation of studied using a single fasting of 16 weeks of resistance trining in obese postmenopausal blood sample to assess diet/exercise effects on systemic females with and without weight loss, on plasma leptin leptin. Both studies also make it clear that careful 17

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یعقوب مهر نهاد ؛ روزنامه نگار و فعال مدنی که به جرم ابراز عقیده صب� امروز ( 115/5/87 ) به دار آویخته شد
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از پیش بیش باد به خویش اتکای زن

غیر از صدای مرد نیاید ز نای مرد

باید که هم زنای زن آید صدای زن

هر جا زن است نیز همانجاست جای مرد

هرجاست مرد نیز همانجاست جای زن

ما را خرد یگانه خداوند باد و باد

 باد او رهنمای مرد و همو رهنمای زن

پرسیدن ، آستانه آگاه گشتن است

شادا سگا لش زن و چون و چرای زن

بادا جهان چنانکه نبیند به هیچ روی

نه زن جفای مرد و نه مردی جفای زن

زیرا بقای زن بود اندر بقای مرد

همچون بقای مرد که اندر بقای زن

بادا هماره شاد  دلِ زن گرای مرد

وز غم بدور باد ، دل مرد زای زن

خواهند یافت آدم و حوا بهشت خویش

گر مرد هم به راه رود پا به  پای زن



5 ژوئیه, 2008

اگر انسان همه چیز است ، اگر هیچ ،

منش بی عشق نشناسم مگر هیچ ؛

همه عشق و همه عشق و همه عشق ،

دگر هیچ و دگر هیچ و دگر هیچ  .

( دکتر اسماعیل خوئی )


تنها به عنوان یکی از میلیونها جوان ایرانی ، عَلَفَک که جزئی ساده و کوچک  از دنیای مجازی صفحات به هم پیچیده در اینترنت محسوب می شود را ایجاد کردم ؛ شاید بتواند مخاطبی هر چند اندک ، حتی موردی یافته  و یا لااقل باز گو کننده حرفهای فرو خورده ام باشد …