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PubMed1995

[Experimental types of hypertension--models for essential hypertension in the human?].

Since the pathogenesis of essential hypertension is multifactorial, the causal therapy of primary arterial hypertension remains a great challenge. At a given genetic predisposition, the manifestation of hypertension depends critically on lifestyle factors. It is thus essential to study the molecular consequences of various deleterious lifestyle factors. We demonstrated by radiotelemetric measurements that an increased caloric intake raises both systolic and diastolic blood pressure as well as heart rate in spontaneously hypertensive rats (SHR). This model is comparable to hyperkinetic hypertension in hypertensive persons which, if it persists, will lead to established hypertension. Overfeeding also results in the characteristic metabolic derangements (hyperinsulinemia, hypertriglyceridemia) of insulin resistant hypertensive persons. The enhanced sympathetic outflow of the brain can be potentiated by lifestyle factors such as high sodium intake and psychological stress. In contrast to sodium intake, psychological stress (e.g. schedule-induced stress) is difficult to mimic in animal experiments. In view of the recent progress in the characterization of imidazoline receptors in the rostral ventrolateral medulla and the development of antihypertensive drugs with a high selectivity (moxonidine) for imidazoline receptors, efforts should be made to elucidate key regulatory mechanisms involved in brain insulin sensitivity and appetite regulation. Such an approach could help in pharmacologically reducing the influence of deleterious lifestyle factors at a given genetic predisposition.

Animals↗
PubMed1995

Weighing the options: criteria for evaluating weight-management programs. The Committee to Develop Criteria for Evaluating the Outcomes of Approaches to Prevent and Treat Obesity.

The United States is experiencing an epidemic of obesity among both adults and children. Approximately 35 percent of women and 31 percent of men age 20 and older are considered obese, as are about one-quarter of children and adolescents. While government health goals for the year 2000 call for no more than 20 percent of adults and 15 percent of adolescents to be obese, the prevalence of this often disabling disease is increasing rather than decreasing. Obesity, of course, is not increasing because people are consciously trying to gain weight. In fact, tens of millions of people in this country are dieting at any one time; they and many others are struggling to manage their weight to improve their appearance, feel better, and be healthier. Many programs and services exist to help individuals achieve weight control. But the limited studies paint a grim picture: those who complete weight-loss programs lose approximately 10 percent of their body weight, only to regain two-thirds of it back within 1 year and almost all of it back within 5 years. These figures point to the fact that obesity is one of the most pervasive public health problems in this country, a complex, multifactorial disease of appetite regulation and energy metabolism involving genetics, physiology, biochemistry, and the neurosciences, as well as environmental, psychosocial, and cultural factors. Unfortunately, the lay public and health-care providers, as well as insurance companies, often view it simply as a problem of willful misconduct--eating too much and exercising too little. Obesity is a remarkable disease in terms of the effort required by an individual for its management and the extent of discrimination its victims suffer. While people often wish to lose weight for the sake of their appearance, public health concerns about obesity relate to this disease's link to numerous chronic diseases that can lead to premature illness and death. The scientific evidence summarized in Chapter 2 suggests strongly that obese individuals who lose even relatively small amounts of weight are likely to decrease their blood pressure (and thereby the risk of hypertension), reduce abnormally high levels of blood glucose (associated with diabetes), bring blood concentrations of cholesterol and triglycerides (associated with cardiovascular disease) down to more desirable levels, reduce sleep apnea, decrease their risk of osteoarthritis of the weight-bearing joints and depression, and increase self-esteem. In many cases, the obese person who loses weight finds that an accompanying comorbidity is improved, its progression is slowed, or the symptoms disappear. Healthy weights are generally associated with a body mass index (BMI; a measure of whether weight is appropriate for height, measured in kg/m2) of 19-25 in those 19-34 years of age and 21-27 in those 35 years of age and older. Beyond these ranges, health risks increase as BMI increases. Health risks also increase with excess abdominal/visceral fat (as estimated by a waist-hip ratio [WHR] > 1.0 for males and > 0.8 for females), high blood pressure (> 140/90), dyslipidemias (total cholesterol and triglyceride concentrations of > 200 and > 225 mg/dl, respectively), non-insulin-dependent diabetes mellitus, and a family history of premature death due to cardiovascular disease (e.g., parent, grandparent, sibling, uncle, or aunt dying before age 50). Weight loss usually improves the management of obesity-related comorbidities or decreases the risks of their development. The high prevalence of obesity in the United States together with its link to numerous chronic diseases leads to the conclusion that this disease is responsible for a substantial proportion of total health-care costs. We estimate that today's health-care costs of obesity exceed $70 billion per year.(ABSTRACT TRUNCATED AT 400 WORDS)

Body Weight↗
PubMed1996

[Leptin--a new way to diet?].

The relatively constant level of body fat in the adult mammal is explained by the lipostat theory as follows: A factor is released from adipose tissue in amounts that reflect total body fat content. This factor is then registered by the hypothalamic centres that regulate appetite. The theory has gained particular support from parabiotic experiments in genetically fat mice, amongst whom the so-called ob/ob mice appear to produce too little of the factor, whilst signal transduction to the satiety centre appears to be defective in the so-called db/db mice. The two genetic defects have recently been clarified, and it has been shown that the normal ob gene nodes for a protein called leptin. Leptin is released from adipose tissue, and its plasma concentration reflects total body fat. The normal db-gene codes for a hypothalamic receptor for leptin. These crucial discoveries have greatly supported the correctness of the lipostat theory. At present, extensive investigations of the roles of leptin and the leptin receptor in human adiposity are in progress.

Adipose Tissue↗
PubMed1996

[Leptin--a new weight-loss agent?].

The relatively constant level of body fat in the adult mammal is explained by the lipostat theory as follows: A factor is released from adipose tissue in amounts that reflect total body fat content. This factor is then registered by the hypothalamic centres that regulate appetite. The theory has gained particular support from parabiotic experiments in genetically fat mice, amongst whom the so-called ob/ob mice appear to produce too little of the factor, whilst signal transduction to the satiety centre appears to be defective in the so-called db/db mice. The two genetic defects have recently been clarified, and it has been shown that the normal ob gene nodes for a protein called leptin. Leptin is released from adipose tissue, and its plasma concentration reflects total body fat. The normal db-gene codes for a hypothalamic receptor for leptin. These crucial discoveries have greatly supported the correctness of the lipostat theory. At present, extensive investigations of the roles of leptin and the leptin receptor in human adiposity are in progress.

Adipose Tissue↗
PubMed1997

[Prevalence and significance of carbohydrate craving in Austria].

Among disorders of appetite and eating frequent craving of carbohydrate containing snacks between meals is well known. Excessive carbohydrate consumption causes increased caloric intake and may lead to overweight and risks of obesity regarding metabolism and vascular remodelling. Up to now prevalence and consequences of that disorder have never been studied in the Austrian population. Hence we investigated by questionnaires and interviews eating habits in samples of 1058 women and 942 men of the Austrian population. Evaluation showed that carbohydrate craving is a more or less serious problem for about 30% of Austrians. Women, especially those with overweight, were affected more frequently than men. In the whole population sample investigated there was a seasonal variation with a tendency to increased carbohydrate craving in fall and winter. This was, however, not significant for overweight women, they probably eat their snacks over the whole year. A subgroup of males reported craving of snacks containing sausage or meat instead of carbohydrate. Craving of carbohydrate is considered the consequence of a decrease of serotonin in appetite regulating neurons and centers of the brain. Treatment of craving by drugs inhibiting the re-uptake of serotonin into afferant neurons is discussed. Medication of this type is, however, hampered by cardiovascular side effects observed with fenfluramines.

Adolescent↗
PubMed2006

The CART (cocaine- and amphetamine-regulated transcript) system in appetite and drug addiction.

CART (cocaine- and amphetamine-regulated transcript) peptides are neuromodulators that are involved in feeding, drug reward, stress, cardiovascular function, and bone remodeling. CART peptides are abundant but discretely distributed in the brain, pituitary and adrenal glands, pancreas, and gut. High expression of CART in discrete hypothalamic nuclei associated with feeding has led to behavioral and pharmacological studies that strongly support an anorectic action of CART in feeding. Subsequent studies on humans and transgenic animals provide additional evidence that CART is important in the regulation of appetite as mutations in the CART gene are linked to eating disorders, including obesity and anorexia. The expression of CART in the mesolimbic dopamine circuit has lead to functional studies demonstrating CART's psychostimulant-like effects on locomotor activity and conditioned place preference in rats. These and other findings demonstrated that CART modulates mesolimbic dopamine systems and affects psychostimulant-induced reward and reinforcing behaviors. The link between CART and psychostimulants was substantiated by demonstrating alterations of the CART system in human cocaine addicts. CART seems to regulate the mesolimbic dopamine system, which serves as a common mechanism of action for both feeding and addiction. Indeed, recent studies that demonstrated CART projections from specific hypothalamic areas associated with feeding to specific mesolimbic areas linked to reward/motivation behaviors provide evidence that CART may be an important connection between food- and drug-related rewards. Given the enormous public health burden of both obesity and drug addiction, future studies exploring the pharmacotherapies targeting CART peptide represent an exciting and challenging research area.

Animals↗
PubMed1994

Appetite and the regulation of body composition.

Stability of body composition requires that energy intake equals energy expenditure when integrated over prolonged periods. As recent human studies have failed to demonstrate active changes in energy expenditure with changes in body composition, it is likely that energy intake is continually adjusted to preserve a constant total adipose tissue mass. If adipose tissue mass is regulated directly, then there must be some input reflecting this quantity to the central nervous system for the purpose of making corrective changes in appetite when total body fat content fluctuates. The nature of this input has been examined in a variety of animal experiments involving induced weight change, lipectomy, plasma transfer from obese or satiated animals to hungry animals, and parabiosis between obese and lean animals. The bulk of evidence suggests that the plasma level of one or more currently unidentified stable circulating molecules increases in proportion to total body fat content and augments the effect of meal-related satiety signals in the central nervous system. The implications of this adipose tissue-related satiety factor for the pathogenesis of obesity, and the possible nature of the factor are discussed.

Animals↗
PubMed1995

Food intake and the menstrual cycle: a retrospective analysis, with implications for appetite research.

The biological regulation of appetite is currently an important topic in nutrition, since hyperphagia has been implicated as the prime cause of obesity. Cyclical fluctuations in food intake occur in women across the menstrual cycle, with a periovulatory nadir and a peak in the luteal phase. These alterations in food intake, in response to ovarian steroid hormone changes may be more than 2.5 MJ/day, with the mean reported changes shown in 19 separate studies of 1.0 MJ/day. Hormonal induced fluctuations in food intake could, therefore, contribute to energy imbalance and consequent weight gain. Further, in nutrition studies involving women subjects where the menstrual cycle phase is not controlled, hormonally induced changes in food selection and intake may mask the often considerably smaller changes in response to experimental variables in appetite research.

Appetite↗
PubMed2005

Anorectics on trial: a half century of federal regulation of prescription appetite suppressants.

Beginning with the passage of the Federal Food, Drug, and Cosmetic Act in 1938 and escalating with the 1962 Kefauver-Harris amendments, increasing pressure has been placed on pharmaceutical manufacturers to demonstrate that a drug's benefits outweigh its risks. Nowhere has the question of risk versus benefit come under greater scrutiny than with anorectics. After the approval in the 1940s and 1950s of a number of amphetamine and amphetamine-like compounds for the treatment of obesity, the U.S. Food and Drug Administration struggled to define the efficacy and safety of these agents. Labeling restrictions on duration of use and warnings about abuse and addiction ultimately contributed to the reduced use of anorectics. That trend continued until the mid-1990s, when the off-label use of fenfluramine plus phentermine (fen-phen) and the approval of dexfenfluramine gave rise to widespread, long-term use of anorectics to treat obesity. The adverse effects that came to be associated with fenfluramine and dexfenfluramine, leading to their eventual withdrawal from the market, gave pause to regulators, physicians, patients, and drug companies alike. Sibutramine, the latest anorectic to enter the market, is now the focus of a landmark trial that is examining, for the first time, whether drug-induced weight loss reduces the risk for fatal and nonfatal cardiovascular disease.

Appetite Depressants↗
PubMed1998

Adrenal steroid regulation of central angiotensin II receptor subtypes and oxytocin receptors in rat brain.

The neuropeptides angiotensin II (AngII) and oxytocin (OT) play important but opposing roles in the regulation of sodium appetite in the rat, AngII as a stimulatory peptide and OT as an inhibitory peptide. Adrenal steroids increase the density of AngII receptors in brain following in vivo administration, although the neuroanatomical and subtype specificity have not been thoroughly examined. Furthermore, previous studies demonstrate that adrenalectomy (ADX) leads to a reduction in OT receptors, although regions associated with sodium appetite remain to be examined. In the present study, quantitative receptor autoradiography was used to locate regions where perturbations in circulating adrenal steroids affect the density of oxytocin receptors and the angiotensin receptor subtypes AT1 and AT2. The results show that ADX results in a small, but significant decrease in AT1 expression in the paraventricular nucleus of the hypothalamus, subfornical organ, and the area postrema. That this effect is reversed by either aldosterone or low-dose corticosterone replacement suggests that occupancy of the mineralocorticoid receptor is responsible for the steroid effect. No changes were observed in AT2 or OT receptors in nuclei associated with sodium appetite, indicating that perturbations in adrenal steroids did not affect these receptors in brain regions implicated in the control of salt appetite.

Aldosterone↗
PubMed1977

The role of physical activity in the control of obesity.

An exercise programme is an important part of the management of the obese patient. Exercise may increase both the specific dynamic action of food and the post-exercise metabolic rate, in addition to its direct caloric cost. Moderate daily exercise aids regulation of the appetite and may reduce the voluntary caloric intake of otherwise sedentary persons. Post-prandial activity may utilize more calories; therefore an adequate breakfast and avoidance of late night eating may be effective in weight control. A better tolerated and more nutritious diet may be allowed, and lean body weight better preserved, by combining exercise with a dietary programme. Regular exercise may also reduce some of the more serious life-threatening complications of obesity and poor dietary habits, allowing greater freedom in the pursuit of other pleasures.

Adolescent↗
PubMed1984

Opioids, feeding, and anorexias.

This review summarizes recent work that focuses on the role of endogenous opioids (EOs) and opiate receptors in the control of food intake. Although the anorexic effect of opiate antagonists are now well accepted, the exact EO, site(s), and mechanism(s) of action remain to be established. However, accumulating evidence suggests that dynorphin, an endogenous ligand for kappa-type opiate receptors, is an important regulator (stimulant) of appetite. The roles of other EOs, such as beta-endorphin, are less clear. EOs appear to be involved in maintaining normal feeding behavior and are likely responsible for the overconsumption of fat in genetically obese and stressed subjects. Opiate antagonists block overconsumption of palatable foods, thus offering a promising approach to weight reduction for some overweight individuals. Anorexias may follow from a deficiency of kappa-type opioid activity, and surprisingly, can also result from excess opioid activity. Indeed, opiate antagonists of the mu type (naloxone) can enhance eating and weight gain in certain anorexic conditions. Therefore, it appears that excess opioid agonist activity may result in hyperphagia or anorexia (depending on the opiate receptor type). Finally, opiate antagonists may help normalize both types of pathological feeding states.

Animals↗
PubMed1996

[Neuroendocrine disorders in anorexia nervosa--primary or secondary?].

Anorexia nervosa is associated with multiple endocrine abnormalities. Hypothalamic neuropeptides and monoamines are involved in the regulation of human appetite, and they are changed in several ways in anorexia nervosa. But it remains to be clarified whether these alterations are secondary or etiologic. Feeding behaviour in anorexia nervosa is characterised by a strong ambivalence and not by loss of appetite. Hypothalamic amenorrhea is a diagnostic criterion, and is not only secondary as it often precedes the weight loss and persists for a long time after weight and motor activity have returned to normal. Hypersecretion of corticotropin releasing hormone seems to be secondary to starvation, but at the same time it may keep up and intensify the anorexia, physical hyperactivity and amenorrhea. Low production of insulinlike growth factor-I and high growth hormone secretion reflects the nutritional deprivation. In conclusion most of the neuroendocrine abnormalities are secondary to weight loss, but some of them seem to participate in a circulus vitiosus and maintain the emaciated state.

Anorexia Nervosa↗
PubMed1991

Effects of naloxone on ad libitum intake and plasma insulin, glucose, and free fatty acids in maintenance-fed sheep.

The dose-dependent effects of naloxone on feed intake, and plasma chemicals (insulin, glucose, FFA) purportedly involved in feed intake regulation, were determined in 16-hr fasted sheep that were lean and chronically fed maintenance. Dorset ewes (n = 5) were treated with 0 (saline), 0.3, 1 or 3 mg/kg of naloxone in a generalized randomized block experiment with at least 7 d between successive doses. Feed intakes and plasma insulin, glucose and FFA were determined frequently during 24 hr of ad libitum intake after each naloxone treatment. The 0.3, 1 and 3 mg/kg doses of naloxone reduced (P less than 0.01) the 4-hr feed intake by 30, 40, and 60% respectively, whereas the initial feed intake (10 min) was decreased (P less than 0.05) 45% only by 3 mg/kg naloxone. However, total 24-hr intakes were similar across all doses because intakes between 4 and 24 hr of feeding in sheep treated with 0.3 (839 g), 1.0 (802 g) and 3.0 (1330 g) mg/kg naloxone exceeded (P less than 0.01) that in saline-treated sheep (391 g). Feeding-induced changes in plasma insulin, glucose and FFA concentrations were independent of naloxone treatment, suggesting that endorphinergic control of feed intake may not involve coincidental changes in plasma insulin, glucose and FFA levels which are thought to play a role in systemic regulation of appetite in animals. The endorphinergic regulation of appetite in sheep may involve the central nervous system, rather than peripheral opiate mechanisms that utilize blood-borne signals. Further, the ability of naloxone to suppress appetite in sheep appears inversely related to the duration of fasting or severity of negative energy balance.

Animals↗