Restoration of weight and nutritional status are key elements in the treatment of anorexia nervosa (AN). This review aims to describe issues related to the caloric requirements needed to gain and maintain weight for short and long-term recovery for AN inpatients and outpatients.We reviewed the literature in PubMed pertaining to nutritional restoration in AN between 1960–2012. Based on this search, several themes emerged: 1. AN eating behavior; 2. Weight restoration in AN; 3. Role of exercise and metabolism in resistance to weight gain; 3. Medical consequences of weight restoration; 4. Rate of weight gain; 5. Weight maintenance; and 6. Nutrient intake.A fair amount is known about overall caloric requirements for weight restoration and maintenance for AN. For example, starting at 30–40 kilocalories per kilogram per day (kcal/kg/day) with increases up to 70–100 kcal/kg/day can achieve a weight gain of 1–1.5 kg/week for inpatients. However, little is known about the effects of nutritional deficits on weight gain, or how to meet nutrient requirements for restoration of nutritional status.This review seeks to draw attention to the need for the development of a foundation of basic nutritional knowledge about AN so that future treatment can be evidenced-based.

This article is available online at http://www.jlr.org family, its importance for purposes of this review is minimal.). KBs have been dubbed "metabolism's ugly duckling" because, in the mid-19th century, they were fi rst discovered in large quantities in the urine of patients succumbing to diabetic ketoacidosis. Thus, it is not surprising that physicians of the era considered KBs to be toxic byproducts of impaired carbohydrate metabolism. It took almost half a century for medical scientists to understand that KBs are normal metabolites manufactured by the liver in increasing amounts when dietary sources of carbohydrate and glucogenic amino acids are in short supply ( 1 ). Unfortunately, some physicians still fail to distinguish between the safe "physiological" hyperketonemia that occurs in healthy individuals during fasting or adherence to a ketogenic diet (KD), and the pathological, out-of-control hyperketonemia associated with insulin-defi cient diabetes.When Owen et al. ( 2 ) reported that during a prolonged fast KBs can provide 60% or more of the brain's daily energy requirement (thereby sparing ‫ف‬ 80 g/day of glucose that otherwise would have been derived largely from breakdown of the body's limited protein stores), it was finally acknowledged that, as in Hans Christian Andersen's 1843 fairy tale, the creature fi rst thought to be an ugly duckling was turning out to be an emerging swan. It became evident that the ketogenic response to starvation is an indispensable metabolic adaptation designed by nature to preserve strength and prolong life during times when food is unavailable ( 3 ) .It is now known that (in nondiabetic individuals), owing to the blood's effi cient buffering capacity, plasma KB Abstract Ketone bodies (KBs ), acetoacetate and ␤ -hydroxybutyrate ( ␤ HB), were considered harmful metabolic by-products when discovered in the mid-19th century in the urine of patients with diabetic ketoacidosis. It took physicians many years to realize that KBs are normal metabolites synthesized by the liver and exported into the systemic circulation to serve as an energy source for most extrahepatic tissues. Studies have shown that the brain (which normally uses glucose for energy) can readily utilize KBs as an alternative fuel. Even when there is diminished glucose utilization in cognition-critical brain areas, as may occur early in Alzheimer's disease (AD), there is preliminary evidence that these same areas remain capable of metabolizing KBs. Because the ketogenic diet (KD) is diffi cult to prepare and follow, and effectiveness of KB treatment in certain patients may be enhanced by raising plasma KB levels to у 2 mM, KB esters, such as 1,3-butanediol monoester of ␤ HB and glyceryl-tris-3-hydroxybutyrate, have been devised. When administered orally in controlled dosages, these esters can produce plasma KB levels comparable to those achieved by the most rigorous KD, thus providing a safe, convenient, and versatile new approach to the study and potential treatment of a variety of diseases, including epilepsy, ...

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The mechanism whereby overfeeding with diet containing medium chain triglyceride (MCT) results in diminished body weight and fat was studied. Fifteen male Sprague-Dawley rats were fitted under anesthesia with gastrostomy tubes and divided into two groups. One group was fed MCT diet, the other an isocaloric diet containing long chain triglyceride (LCT) in excess (150%) of spontaneous calorie intake. Both diets, fed for 6 wk, derived 50% of calories from fat. Basal and norepinephrine (25 micrograms/100 g) stimulated 02 consumption and CO2 production, as well as metabolic rate were measured. After the rats were killed, total dissectible fat and fat cell size and number were determined. MCT rats gained 15% less weight than LCT controls (p less than 0.001). Total dissectible fat was significantly lower (p less than 0.001) in MCT group, as was mean adipocyte size (p less than 0.001). Resting and maximal norepinephrine-stimulated 02 consumptions were 39.7 and 22.1% higher in MCT than in LCT group, respectively. Resting and norepinephrine-stimulated metabolic rates were 38.8 and 22.2% higher in MCT than LCT fed rats, respectively. Overfeeding MCT diet results in decreased body fat related to increased metabolic rate and thermogenesis.

The study was designed to determine whether overfeeding rats with a diet containing medium-chain triglyceride (MCT) as the major fat source (45% of calories) would impede the expected gain in weight and body fat as compared to rats overfed with isocaloric amounts of diet containing long-chain triglyceride (LCT). For 6 wk rats were fed either MCT diet or LCT diet twice daily via a gastrostomy tube. MCT-fed rats gained 20% less weight (P less than 0.001) and possessed fat depots weighing 23% less (p less than 0.001) than LCT)-fed rats. Mean adipocyte size was smaller (p less than 0.005) in MCT- than in LCT-fed rats. Weights of carcass protein and water were similar for both groups as were concentrations of serum insulin and levels of physical activity. The decreased deposition of fat in the MCT-fed rats may have resulted from obligatory oxidation of MCT-derived fatty acids in the liver after being transported there via the portal vein, leaving almost no MCT derivatives for incorporation into body fat. MCT may have potential for dietary prevention of human obesity.

The worldwide increase in the incidence of obesity is a consequence of a positive energy balance, with energy intake exceeding expenditure. The signalling systems that underlie appetite control are complex, and the present review highlights our current understanding of key components of these systems. The pattern of eating in obesity ranges from over-eating associated with binge-eating disorder to the absence of binge-eating. The present review also examines evidence of defects in signalling that differentiate these sub-types. The signalling network underlying hunger, satiety and metabolic status includes the hormonal signals leptin and insulin from energy stores, and cholecystokinin, glucagon-like peptide-1, ghrelin and peptide YY3-36 from the gastrointestinal tract, as well as neuronal influences via the vagus nerve from the digestive tract. This information is routed to specific nuclei of the hypothalamus and brain stem, such as the arcuate nucleus and the solitary tract nucleus respectively, which in turn activate distinct neuronal networks. Of the numerous neuropeptides in the brain, neuropeptide Y, agouti gene-related peptide and orexin stimulate appetite, while melanocortins and a-melanocortin-stimulating hormone are involved in satiety. Of the many gastrointestinal peptides, ghrelin is the only appetite-stimulating hormone, whereas cholecystokinin, glucagon-like peptide-1 and peptide YY3-36 promote satiety. Adipose tissue provides signals about energy storage levels to the brain through leptin, adiponectin and resistin. Binge-eating has been related to a dysfunction in the ghrelin signalling system. Moreover, changes in gastric capacity are observed, and as gastric capacity is increased, so satiety signals arising from gastric and post-gastric cues are reduced. Understanding the host of neuropeptides and peptide hormones through which hunger and satiety operate should lead to novel therapeutic approaches for obesity; potential therapeutic strategies are highlighted.

Given that resting metabolic rate (RMR) is related largely to the amount of fat-free mass (FFM), the hypothesis was that strength training, which stimulates muscle hypertrophy, would help preserve both FFM and RMR during dieting. In a randomized controlled intervention trial, moderately obese subjects (aged 19-48 y) were assigned to one of three groups: diet plus strength training, diet plus aerobic training, or diet only. Sixty-five subjects (25 men and 40 women) completed the study. They received a formula diet with an energy content of 70% of RMR or 5150 +/- 1070 kJ/d (x +/- SD) during the 8-wk intervention. They were seen weekly for individual nutritional counseling. Subjects in the two exercise groups, designed to be isoenergetic, trained three times per week under supervision. Those in the strength-training group performed progressive weight-resistance exercises for the upper and lower body. Those in the aerobic group performed alternate leg and arm cycling. After 8 wk, the mean amount of weight lost, 9.0 kg, did not differ significantly among groups. The strength-training group, however, lost significantly less FFM (P < 0.05) than the aerobic and diet-only groups. The strength-training group also showed significant increases (P < 0.05) in anthropometrically measured flexed arm muscle mass and grip strength. Mean RMR declined significantly, without differing among groups. Peak oxygen consumption increased the most for the aerobic group (P = 0.03). In conclusion, strength training significantly reduced the loss of FFM during dieting but did not prevent the decline in RMR.

The role of the stomach in regulating appetite in bulimia nervosa was examined. Subjects were nine normal and nine bulimic women of similar age, height, and weight. Gastric capacity was estimated by filling a balloon in the stomach. The mean stomach capacity of bulimic subjects was significantly larger than that of normal subjects, as revealed by the larger balloon volume tolerated (P less than 0.01) and by the larger volume needed to produce a 5 cm H2O increase in intragastric pressure (P = 0.07). The intake of a liquid meal was also significantly larger for the bulimic subjects. Gastric-emptying rate of a liquid meal was significantly delayed in the bulimic subjects during the initial 5-15 min. In all subjects, test-meal intake correlated significantly with gastric capacity (r = 0.53). In the bulimic subjects, self-reported binge intake (J) also correlated significantly with gastric capacity (r = 0.75). Binge eating in bulimic subjects may enlarge gastric capacity, which could then promote even larger binges through positive feedback.