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The severity of metabolic syndrome is usually determined according to static variables (blood glucose, insulin level, body mass index etc.) The most important classification is dynamic and prognostic classification which can be used to determine the ability to decrease elevated metabolite and hormone levels or to lose weight. Different mathematical approaches were used to determine these phenomena: 1. Mathematical modelling e.g. (Bergman minimal model or glycation model). 2. Predictive calculations using multiple regression (using static and dynamic parameters to determine weight loss in obesity treatment). 3. One day starvation test (finding very variable hormone and metabolic changes in obese patients). We can conclude There are 3 types of metabolic parameters: A. Static (basic) description, B. Functional (actual) description, C. Dynamic-stability describing variables. Mathematical modelling is a complicated method needing many blood samples. It is very invasive for patients and it is difficult to be repeated. Predictive importance can have also repeated measured metabolic data which are able to classify the stability (fixation) of metabolic state. Some basic parameters and simple dynamic tests like one day starvation test can be used in prognostic classification of patients who are able to change their fixed metabolic state.
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PMID:Classification of metabolic patients using dynamic variables. 1072 67

Obesity and starvation have opposing affects on normal physiology and are associated with adaptive changes in hormone secretion. The effects of obesity and starvation on thyroid hormone, GH, and cortisol secretion are summarized in Table 1. Although hypothyroidism is associated with some weight gain, surveys of obese individuals show that less than 10% are hypothyroid. Discrepancies have been reported in some studies, but in untreated obesity, total and free T4, total and free T3, TSH levels, and the TSH response to TRH are normal. Some reports suggest an increase in total T3 and decrease in rT3 induced by overfeeding. Treatment of obesity with hypocaloric diets causes changes in thyroid function that resemble sick euthyroid syndrome. Changes consist of a decrease in total T4 and total and free T3 with a corresponding increase in rT3. untreated obesity is also associated with low GH levels; however, levels of IGF-1 are normal. GH-binding protein levels are increased and the GH response to GHRH is decreased. These changes are reversed by drastic weight reduction. Cortisol levels are abnormal in people with abdominal obesity who exhibit an increase in urinary free cortisol but exhibit normal or decreased serum cortisol and normal ACTH levels. These changes are explained by an increase in cortisol clearance. There is also an increased response to CRH. Treatment of obesity with very low calorie diets causes a decrease in serum cortisol explained by a decrease in cortisol-binding proteins. The increase in cortisol secretion seen in patients with abdominal obesity may contribute to the metabolic syndrome (insulin resistance, glucose intolerance, dyslipidemia, and hypertension). States of chronic starvation such as seen in anorexia nervosa are also associated with changes in thyroid hormone, GH, and cortisol secretion. There is a decrease in total and free T4 and T3, and an increase in rT3 similar to findings in sick euthyroid syndrome. The TSH response to TRH is diminished and, in severe cases, thyroid-binding protein levels are decreased. In regards to GH, there is an increase in GH secretion with a decrease in IGF-1 levels. GH responses to GHRH are increased. The [table: see text] changes in cortisol secretion in patients with anorexia nervosa resemble depression. They present with increased urinary free cortisol and serum cortisol levels but without changes in ACTH levels. In contrast to the findings observed in obesity, the ACTH response to CRH is suppressed, suggesting an increased secretion of CRH. The endocrine changes observed in obesity and starvation may complicate the diagnosis of primary endocrine diseases. The increase in cortisol secretion in obesity needs to be distinguished from Cushing's syndrome, the decrease in thyroid hormone levels in anorexia nervosa needs to be distinguished from secondary hypothyroidism, and the increase in cortisol secretion observed in anorexia nervosa requires a differential diagnosis with primary depressive disorder.
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PMID:Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion. 1205 88

The aim of this study was to compare the postprandial leptin response in rats with and without metabolic syndrome induced by a fructose-enriched diet. The effect of aging and the association between variations in metabolic substrates was also evaluated. Oral glucose tolerance test (OGTT) and fasting/re-feeding test were used to evaluate the responses of leptin and to explore the dynamic relationship between endogenous leptin and metabolic substrates, including glucose, insulin and triglycerides (TG). At the 7th week, plasma leptin was unchanged in control rats after oral glucose loading. However, plasma leptin levels increased in fructose-fed rats with insulin resistant OGTT curves. At the 11th month, plasma leptin level was reduced during starvation and returned to the level prior to starvation during re-feeding in control rats. In contrast, the starvation-induced reduction in leptin showed a potentially larger rebound effect during re-feeding in fructose-fed rats. Analysis of covariance demonstrated that there alone was no interactive effect of dietary manipulation between leptin and TG, suggesting that fructose diet-induced insulin resistance-related metabolic syndrome may concomitantly elevate leptin and TG. Furthermore, multiple regression analysis suggests TG was the primary correlative determinant of endogenous leptin concentration. Our data showed that there are different patterns of leptin response to OGTT and fasting/re-feeding tests in rats with and without metabolic syndrome. The results suggest that these effects may be related to a TG-mediated impairment of leptin function and a protective mechanism to reduce lipid-induced tissue damage in patients with metabolic syndrome.
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PMID:Plasma leptin response to oral glucose tolerance and fasting/re-feeding tests in rats with fructose-induced metabolic derangements. 1643 85

Over the last 50 years there has been a major epidemic of obesity and associated co-morbidities, the so-called 'metabolic syndrome', mostly in the western world but with an increasingly global dimension. The development of such chronic diseases has a strong genetic component, yet the timescale of their increase cannot reflect a population genetic change. Consequently, the most accepted model is that obesity and its sequelae are a result of a gene-environment interaction, an ancient genetic selection to deposit fat efficiently that is maladaptive in modern society. Why we have this genetic predisposition has been a matter of much speculation. Following the seminal contribution of Neel, there has been a broad consensus that over evolutionary time we have been exposed to regular periods of famine, during which fatter individuals would have enjoyed a selective advantage by their greater survival. Consequently, individuals with genes promoting the efficient deposition of fat during periods between famines ('thrifty genes') would be favoured. In the modern environment this genetic predisposition prepares us for a famine that never comes, and an epidemic of obesity with all the attendant chronic illnesses follows. In this review I present details of the evidence supporting the famine hypothesis and then show that this idea has five fundamental flaws. In essence, famines are a relatively modern phenomenon and occur only about once every 100-150 years. Consequently, most human populations have only experienced at most 100 famine events in their evolutionary history. Famines involve increases in total mortality that only rarely exceed 10% of the population. Moreover, most people in famines die of disease rather than starvation and the age distribution of mortality during famine would not result in differential mortality between lean and obese individuals. A simple genetic model shows that famines provide insufficient selective advantage over an insufficient time period for a thrifty gene to have any penetration in the modern human population. Over the 40 or so years since Neel proposed the thrifty gene hypothesis, no convincing candidates for these genes have been discovered. My analysis suggests that perhaps it is time to call off the search.
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PMID:Thrifty genes for obesity and the metabolic syndrome--time to call off the search? 1678 74

Although the brain constitutes only 2% of the body mass, its metabolism accounts for 50% of total body glucose utilization. This delicate situation is aggravated by the fact that the brain depends on glucose as energy substrate. Thus, the contour of a major problem becomes evident: how can the brain maintain constant fluxes of large amounts of glucose to itself in the presence of powerful competitors as fat and muscle tissue. Activity of cortical neurons generates an "energy on demand" signal which eventually mediates the uptake of glucose from brain capillaries. Because energy stores in the circulation (equivalent to ca. 5 g glucose) are also limited, a second signal is required termed "energy on request"; this signal is responsible for the activation of allocation processes. The term "allocation" refers to the activation of the "behavior control column" by an input from the hippocampus-amygdala system. As far as eating behavior is concerned the behavior control column consists of the ventral medial hypothalamus (VMH) and periventricular nucleus (PVN). The PVN represents the central nucleus of the brain's stress systems, the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). Activation of the sympatico-adrenal system inhibits glucose uptake by peripheral tissues by inhibiting insulin release and inducing insulin resistance and increases hepatic glucose production. With an inadequate "energy on request" signal neuroglucopenia would be the consequence. A decrease in brain glucose can activate glucose-sensitive neurons in the lateral hypothalamus (LH) with the release of orexigenic peptides which stimulate food intake. If the energy supply of the brain depends on activation of the LH rather than on increased allocation to the brain, an increase in body weight is evitable. An increase in fat mass will generate feedback signals as leptin and insulin, which activate the arcuate nucleus. Activation of arcuate nucleus in turn will stimulate the activity of the PVN in a way similar to the activation by the hippocampus-amydala system. The activity of PVN is influenced by the hippocampal outflow which in turn is the consequence of a balance of low-affinity and high-affinity glucocorticoid receptors. This set-point can permanently be displaced by extreme stress situations, by starvation, exercise, hormones, drugs or by endocrine-disrupting chemicals. Disorders in the "energy on request" process will influence the allocation of energy and in so doing alter the body mass of the organism. In this "selfish brain theory" the neocortex and the limbic system play a central role in the pathogenesis of diseases, such as anorexia nervosa, obesity and diabetes mellitus type II. From these considerations it appears that the primary disturbance in obesity is a displacement of the hippocampal set-point of the system. The resulting permanent activation of the feedback system must result in a likewise permanent activation of the sympatico-adrenal system, which induces insulin resistance, hypertension and the other components of the metabolic syndrome. Available therapies for treatment of the metabolic syndrome (blockade of alpha- and beta-adrenergic receptors, insulin and insulin secretagogues) interfere with mechanisms, which must be considered compensatory. This explains why these therapies are disappointing in the long run. New therapeutic strategies based on the "selfish brain theory" will be discussed.
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PMID:The selfish brain: competition for energy resources. 1687 72

It is well recognized that investigation into the relationship between early life programming and subsequent neurological disorders may have powerful implications for understanding the human vulnerability to psychopathology. The present article will propose that schizophrenia may be adaptively programmed by early environmental adversity permitting physiological and behavioral characteristics that would have created a fitness advantage in the ancestral environment under conditions of nutritional scarcity and severe environmental stress. This proposition will be analyzed in terms of phenotypic plasticity theory which explains how and why specific environmental stressors can alter normal gene expression resulting in an alternative phenotype that is better suited for an adverse environment. The primary neurophysiological symptoms of schizophrenia can be induced in animals through exposure to prenatal and postnatal stressors, and that schizophrenia itself is known to be associated with exposure to stress during development, supports the view that the "disorder" may represent a predictive, adaptive response to adversity. In fact, maternal malnutrition, maternal stress, multiparity, short birth interval and stress provoking postnatal events are well recognized epidemiological risk factors for schizophrenia that may represent cues for the initiation of epigenetic programming. Behavioral and physiological characteristics of schizophrenia will be analyzed and interpreted as protective in the context of environmental hardship. For instance, the hypometabolic areas of the schizophrenic brain--the hippocampus and the frontal lobes--are the same areas that are known to become adaptively hypometabolic in response to starvation, stress and variations in ecological rigor in birds and mammals. Individuals with schizophrenia are also highly genetically inclined to develop the metabolic syndrome, which is widely thought to allow developmentally deprived mammals to conserve energy under poor circumstances. It is well known that schizophrenia features an up-regulated hypothalamic-pituitary-adrenal axis and an exaggerated stress response--both alterations thought to represent predictive, adaptive responses to stress in mammals--which may have increased attentiveness to the environment and created a defensive, vigilance-based behavioral strategy. The habituation deficits characteristic of schizophrenia--which can be induced in other mammals through stress--may represent a cognitive strategy that alerts the organism to salient, potentially informative stimuli and that permits it to be more impulsive and vigilant. Inability to calm instinctual drives, ignore arousing stimuli, and inhibit transient desires are all core characteristics of the disorder, which predict social and vocational disabilities in modern times, but may have amounted to a robust, selfish strategy in prehistoric times.
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PMID:Schizophrenia and phenotypic plasticity: schizophrenia may represent a predictive, adaptive response to severe environmental adversity that allows both bioenergetic thrift and a defensive behavioral strategy. 1732 Oct 61

The incidence of the metabolic syndrome, type 2 diabetes and cardio- and cerebrovascular disease is increasing in the Western world. The adipocyte derived protein adiponectin is thought to have a protective role against these conditions. But why is it so? Is it reasonable to believe that we have adiponectin to gain protection from welfare related diseases? Humans have had a far deadlier foe throughout history than obesity and sedentariness and that is starvation. During starvation, the body is catabolic in order to provide fuel. Catabolism is also seen in patients with advanced cardiac or renal failure, type 1 diabetes and anorexia. These subjects have higher adiponectin levels than controls. In this article, I will put forward the hypothesis that the adiponectin system evolved in order to help us to survive periods of malnourishment.
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PMID:Adiponectin: saving the starved and the overfed. 1750 73

A model of the origin of modern humans through several population bottlenecks caused by glacial cycles and cold-arid periods was used as a frame for describing occurrence of unique physiological characteristics. Occurrence of regular evening food sharing among the hominid group members improved their chances of finding food the next day. It allowed slow emergence of a gracile and energy efficient phenotype. Improving chances of group survival in the harsh environment included these traits: - The menstrual cycle occurrence in the common ancestor of human and great apes. - Single pregnancies only in women with sufficient fat reserves. Ovulations stop during the food shortage seasons, or longer periods of starvation and during lactation. - Women prone to obesity sooner become pregnant, passing the obesity trait as an advantage. - Seldom pregnancies separated by several years of anovulation made a strong pressure toward the longevity of women and man. - Menopausis improved the group survival through preventing pregnancy of women to old to deliver and raise children without significant risks. The modern times food abundance results in high incidences of adiposity, diabetes and metabolic syndrome. Continuos ovulations from puberty to menopausis except during seldom pregnancies and lactations is considered responsible for the occurrence of estrogen induced breast and endometrial cancers. The combination of longevity with decades of androgen secretion is the main cause of prostate cancer.
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PMID:Human adiposity, longevity and reproduction features as consequences of population bottlenecks. 1797 25

An intragastric D-glucose tolerance test was performed, after overnight starvation, in female rats depleted in long-chain polyunsaturated omega3 fatty acids (omega3D rats) and control rats of same age and gender. The plasma D-glucose and insulin concentrations, insulinogenic index, and HOMA for insulin resistance were all higher, after overnight starvation, in omega3D rats than in control animals. Over the 120-minute period following the intragastric administration of D-glucose, the area under the curve for the same four variables was also higher in omega3D rats than in control animals. In addition to visceral obesity, liver steatosis, hypertension, and cardiac hypertrophy, the omega3D rats thus display further features of the metabolic syndrome, namely glucose intolerance and insulin resistance, despite hyperinsulinemia.
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PMID:Glucose intolerance associated to insulin resistance and increased insulin secretion in rats depleted in long-chain omega3 fatty acids. 1799 38

Forkhead transcription factors FoxOs are conserved beyond species and regulated by insulin signaling pathway. FoxOs have diverse functions on differentiation, proliferation and cell survival. In calorie restriction (CR) or starvation, FoxOs are in nucleus, active transcriptionally, and increase hepatic glucose production, decrease insulin secretion, increase food intake and cause degradation of skeletal muscle for supplying substrates for glucose production. However, even in insulin resistance due to excessive calorie intake, FoxOs are active and causes type 2 diabetes and hyperlipidemia. The understanding of molecular mechanism how FoxOs affect glucose or lipid metabolism will shed light on the novel therapy of type 2 diabetes and the metabolic syndrome.
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PMID:The FoxO transcription factors and metabolic regulation. 1802 95


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