State Of Energy Deficit Research Articles

Central angiotensin II has catabolic action at white and brown adipose tissue

Considerable evidence implicates the renin-angiotensin system (RAS) in the regulation of energy balance. To evaluate the role of the RAS in the central nervous system regulation of energy balance, we used osmotic minipumps to chronically administer angiotensin II (Ang II; icv; 0.7 ng/min for 24 days) to adult male Long-Evans rats, resulting in reduced food intake, body weight gain, and adiposity. The decrease in body weight and adiposity occurred relative to both ad libitum- and pair-fed controls, implying that reduced food intake in and of itself does not underlie all of these effects. Consistent with this, rats administered Ang II had increased whole body heat production and oxygen consumption. Additionally, chronic icv Ang II increased uncoupling protein-1 and β(3)-adrenergic receptor expression in brown adipose tissue and β3-adrenergic receptor expression in white adipose tissue, which is suggestive of enhanced sympathetic activation and thermogenesis. Chronic icv Ang II also increased hypothalamic agouti-related peptide and decreased hypothalamic proopiomelanocortin expression, consistent with a state of energy deficit. Moreover, chronic icv Ang II increased the anorectic corticotrophin- and thyroid-releasing hormones within the hypothalamus. These results suggest that Ang II acts in the brain to promote negative energy balance and that contributing mechanisms include an alteration in the hypothalamic circuits regulating energy balance, a decrease in food intake, an increase in energy expenditure, and an increase in sympathetic activation of brown and white adipose tissue.

Pervasiveness Of Anemia In Adolescent Girls Of Low Socio-Economic Group Of The District Of Kurukshetra (Haryana)

During adolescent, due to growth spurt anemia appears to be more for both sexes and risk is high in girls due to onset of menstruation and may continue later during their reproductive life. In the perspective study, one hundred ten adolescent girls between ages 13 -16 years of low socio-economic group of district Kurukshetra (Haryana) were screened out for their hemoglobin level and for nutritional as well as socio-economic status. Data regarding socio-economic status was collected through pre-structured questionnaire cum interview method. Nutritional status was adjudged by their anthropometric measurements (height, weight and BMI) and nutrient intake. Dietary intake of selected subjects was adjudged by 24 hour recall method for three consecutive days and intake of nutrients from the diet was calculated with help of nutritive value of Indian foods. Hemoglobin level of each subject was measured by using Sahil's technique. Out of one hundred ten girls, more than two third (81.81 per cent) girls were suffering from various degree of anemia as their Hb level ranges between 6.6 g/dl to 11.0 g/dl. The dietary data revealed that nutrient intake especially iron intake was very much less than as recommended by ICMR for adolescent girls. Due to low dietary intake, their weight was found less and the subjects were in energy deficit state. Analysis of data further disclosed that prevalence of anemia was directly related to family size and type of family as that affect quality and quantity of food consumption. Thus, inspite of various welfare programmes, it appears from the study that these girls are not benefited from any scheme run by government such as ICDS .

Anabolic neuropeptides

The hypothalamus and other brain regions that control energy homeostasis contain neuronal populations that produce specific neuropeptides which have experimental effects on feeding behavior and body weight. Here, we describe examples of neuropeptides that exert ‘anabolic’ effects, notably stimulation of feeding and increased body weight. Neuropeptide Y (NPY) neurons in the hypothalamic arcuate nucleus (ARC) are inhibited by leptin and insulin, and thus are stimulated in states of energy deficit and fat loss, e.g., underfeeding. NPY neuronal overactivity contributes to enhanced hunger and food-seeking activity under these conditions. The lateral hypothalamic area (LHA) contains specific neuronal populations that affect feeding in different ways. Neurons expressing the appetite-stimulating peptide orexin A are stimulated by starvation (but not food restriction) and by hypoglycemia, but only if food is withheld. Orexin neurons are apparently activated by low glucose but are promptly inhibited by visceral feeding signals, probably mediated via vagal sensory pathway and the nucleus of the solitary tract (NTS); a short-term role in initiating feeding seems most likely. Other LHA neurons express melanin-concentrating hormone (MCH), which transiently increases food intake when injected centrally. MCH neurons may be regulated by leptin, insulin and glucose. Glucose-sensing neurons in the hypothalamus and elsewhere are sensitive to other cues of nutritional state, including visceral satiety signals (transmitted via the vagus) and orexin A. Thus, long- and short-term humoral and neural signals interact with each other to meet diverse nutritional needs, and anabolic neuropeptides are important in the overall integration of energy homeostasis. Clarifying the underlying mechanisms will be essential to understanding normal energy balance and the pathogenesis and treatment of disorders, such as obesity and cachexia.

THE EFFECTS OF CROSS-TRAINING ON ENERGY EXPENDITURE AND UTILIZATION OF OVERWEIGHT WOMEN 476

The purpose of this study was to determine if energy expenditure (EE) or energy utilization (EU) changed in response to cross-training. Twelve overweight women (BMI±SD=28.7±4.4) participated in a diet and exercise study while living in a metabolic research unit. The controlled diet was mildly restricted in energy (8.03±1.05 MJ·d-1). Exercise included a daily 3 mile walk, aerobic workout 5 d·wk-1, and weight training 3 d·wk-1. At the beginning (T0) and after 8 wk of training (T8), EE and EU were studied by indirect calorimetry in this sequence: at rest, following ingestion of a 1 MJ “sports bar”, during 30 min of cycling at 50% peak VO2, and for 1 hr post-exercise. Serial blood samples were obtained coincidentally and analyzed for glucose and insulin. As a result of intervention, body mass decreased by 5%, but fat-free mass decreased by only 1%. At T8, exercise EE increased 7% (p<0.01) due to modest improvements in peak VO2. The increase in EE resulted from higher carbohydrate oxidation (p≤0.01). Also during exercise at T8, plasma glucose levels were lower (T0=3.9mM vs T8=3.6mM, p≤0.01), and insulin levels did not change. These data suggest that the production of glucose during exercise did not keep pace with its utilization. Despite increased exercise EE, post-exercise EE decreased 5-7% (p≤0.01), post-prandial EE decreased 4% (p≤0.05), whereas resting EE did not change. During rest at T8, the respiratory exchange ratio tended to decrease (p=0.06), and carbohydrate oxidation decreased by 16% (p≤0.05). The small decreases in EE, post-prandial and post-exercise, could impact energy balance over time and could be viewed as a compensatory mechanism that conserves energy during a state of energy deficit. Contrary to what we expected, we found no enhancement of fat utilization as a result of cross-training.

Anorexia induced by the parasitic nematode, Nippostrongylus brasiliensis: effects on NPY and CRF gene expression in the rat hypothalamus.

Infections of the gastrointestinal nematode, Nippostrongylus brasiliensis, in the laboratory rat result in a characteristic biphasic anorexia which is followed by hyperphagia once the worm burden has been cleared. Despite the importance of parasite-induced anorexia, relatively little is known of the underlying mechanisms. We have investigated the involvement of the central appetite drive in this anorexia by studying the gene expression of two neuropeptides with opposing actions on energy balance, NPY and CRF. Gene expression was assessed by in situ hybridization at 2, 8 and 16 days post-infection (p.i.) in infected rats, in uninfected controls, and in a group with food intake restricted to match that taken voluntarily by the parasitize animals. The sampling intervals corresponded to each of the two phases of maximum anorexia and the period of compensatory hyperphagia. Surprisingly, we found that increases in NPY gene expression in the hypothalamic arcuate nucleus (ARC) accompany anorexia in rats infected with N. brasiliensis; there was a significant relationship between degree of anorexia and induction of NPY mRNA after 8 days of infection. Furthermore, ARC NPY mRNA levels in parasitized animals were similar to those in pair-fed individuals with food intake restricted to match the infected rats. The number of larvae used to establish the infection affected both the degree of anorexia and the level of NPY mRNA at 8 days p.i. in a dose-dependent manner. NPY gene expression remained elevated in infected rats during at least the initial stages of compensatory hyperphagia. This suggests that animals detect a state of energy deficit during the early stages of the infection, yet do not feed, but become hyperphagic coincident with worm loss. The failure of anorectic parasitized animals to feed in response to activation of the NPYergic system makes this a novel system in which to study the regulation of hypothalamic NPY by physiological challenge. There were no significant differences in CRF gene expression between the groups at any of the sampling intervals.

Polycose and sucrose appetite in rats: Influence of food deprivation and insulin treatment

Rats appear to have two different carbohydrate tastes, a sweet taste for sugars, and a "polysaccharide" taste for starch and starch-derived polysaccharides. The present study explored the possible functional significance of this dual taste system by comparing the effects of food deprivation and insulin treatment on the appetite for sucrose and Polycose. Food deprivation (24 h) produced comparable increases in the 5-min and 30-min intakes of Polycose and sucrose (1-8%) solutions in adult female rats. Polycose and sucrose intakes were also increased to a similar degree by insulin injections (1 unit/kg) during brief (3-min) one-bottle tests. In brief two-bottle tests, however, insulin treatment tended to shift the rat's preference from sucrose to Polycose. Chronic treatment with insulin increased the long-term intake of 30% Polycose and sucrose solutions, with the effect being more pronounced with Polycose. These findings demonstrate that energy deficit states enhance the appetite for Polycose as much as or more than the appetite for sucrose.

Regional Impacts of Rising Energy Prices

The basic argument of this paper is that the regional impact of the rise in energy costs has been less than was widely expected. Energy surplus states have benefited from an income transfer from the energy-deficit states, but the transfer has been much less than the growth in value added by energy producers. The shift away from energy-intensive goods has probably retarded growth in the energy-rich states, and locational patterns had adjusted to regional differences in energy prices long before the energy crisis of 1973-74. Unless these regional differences widen, the rise in the levels of energy prices is not likely to have much impact on industrial location patterns. 12 references, 5 tables

Higher Energy Prices and Resource Endowments in an Export Base Model Context

This paper modifies previous work that has shown that export base employment growth is positively correlated with per capita income growth. Modifications made to the model allow researchers to distinguish between energy surplus and deficit states, sunbelt and non-sunbelt states, and pre-embargo years and post-embargo years.The model confirmed that energy surplus states experienced considerably higher export base employment and real capital expenditure growth rates in post-embargo years than energy deficit states

Absence of increased thermogenesis during short-term overfeeding in normal and overweight women

Dietary thermogenesis was studied under carefully controlled dietary and physical activity plans. Eight females, four normal and four overweight, were kept in a metabolic ward and O2 consumption was measured during three periods. The first (5 days) served as a baseline control, in which the subjects ate ad libitum and retained their usual weight. In the second period (5 days), each subject ate a daily excess averaging about 2,300 kcal superimposed on her normal daily intake in the first period. The subjects were then released and dieted at home. After each subject had lost between 2 and 5 kg., she was called for a third period of 2 days during which she ate the same daily excess as in two matching days in the second period. O2 consumption was measured three times daily: at rest after arising in the morning, and during two daily exercise periods, one before breakfast, and the other after breakfast. Leisure time activity was controlled throughout the experiment. It was found that: 1) There was no increase in O2 consumption during the two overfeeding periods as compared to control, either at rest or during the exercise periods. 2) There was no difference between the normal and overweight subjects in their responses to overfeeding. 3) There was no increased efficiency in energy utilization during overfeeding which followed a state of energy deficit, as compared to overfeeding which followed a state of energy balance. It is suggested that an increased dietary thermogenesis is not a factor in the regulation of energy balance during periods of overeating lasting several days only.