Mobilization Of Fat Stores Research Articles

Life's Simple 7 1/2 for Women.

Life's Simple 7 1/2 for Women.

Coelomocytes Regulate Starvation-Induced Fat Catabolism and Lifespan Extension through the Lipase LIPL-5 in Caenorhabditis elegans

SummaryDietary restriction is known to extend the lifespan and reduce fat stores in most species tested to date, but the molecular mechanisms linking these events remain unclear. Here, we found that bacterial deprivation of Caenorhabditis elegans leads to lifespan extension with concomitant mobilization of fat stores. We find that LIPL-5 expression is induced by starvation and that the LIPL-5 lipase is present in coelomocyte cells and regulates fat catabolism and longevity during the bacterial deprivation response. Either LIPL-5 or coelomocyte deficiency prevents the rapid mobilization of intestinal triacylglycerol and enhanced lifespan extension in response to bacterial deprivation, whereas the combination of both defects has no additional or synergistic effect. Thus, the capacity to mobilize fat via LIPL-5 is directly linked to an animal’s capacity to withstand long-term nutrient deprivation. Our data establish a role for LIPL-5 and coelomocytes in regulating fat consumption and lifespan extension upon DR.

The Circulatory and Metabolic Responses to Hypoxia in Humans - With Special Reference to Adipose Tissue Physiology and Obesity.

Adipose tissue metabolism and circulation play an important role in human health. It is well-known that adipose tissue mass is increased in response to excess caloric intake leading to obesity and further to local hypoxia and inflammatory signaling. Acute exercise increases blood supply to adipose tissue and mobilization of fat stores for energy. However, acute exercise during systemic hypoxia reduces subcutaneous blood flow in healthy young subjects, but the response in overweight or obese subjects remains to be investigated. Emerging evidence also indicates that exercise training during hypoxic exposure may provide additive benefits with respect to many traditional cardiovascular risk factors as compared to exercise performed in normoxia, but unfavorable effects of hypoxia have also been documented. These topics will be covered in this brief review dealing with hypoxia and adipose tissue physiology.

The effect of a vegetarian versus conventional hypocaloric diet on serum concentrations of persistent organic pollutants in patients with type 2 diabetes

Background and aimsThe aim of this study was to explore the effect of a vegetarian versus conventional diet on the serum levels of persistent organic pollutants (POPs) in patients with T2D after 12 weeks of dietary intervention and to assess their relationships with metabolic parameters. Methods and resultsMen and women with T2D were randomly assigned to follow either a vegetarian diet without fish or meat (n = 37) or an isocaloric conventional antidiabetic diet (n = 37). Both diets were energy restricted (minus 500 kcal/day). All foods were provided to the participants. At randomization (week 0) and 12 weeks, the meal test was performed to assess the β-cell function and serum levels of 24 POPs. Dioxins and dioxin-like POPs were analyzed by isotope dilution high-resolution gas chromatography (HRGC) and mass spectrometry after cleanup of the silica and carbon columns. Non-dioxin-like POPs were analyzed by gas chromatography with an electron capture detector (GC–ECD). Statistical analyses used were repeated-measures analysis of variance (ANOVA), a multivariate regression model, and Pearson's correlations.We observed a statistically nonsignificant trend toward increases in the serum levels of most POPs in response to both hypocaloric diets with no differences between groups. In the groups combined, the change in serum concentrations of total POPs was correlated to changes in HbA1c (r = +0.34; p < 0.01), fasting plasma glucose (r = +0.41; p < 0.01) levels, and β-cell function measured as insulin secretion at a reference glucose level (r = −0.37; p < 0.01), independent of the changes in body weight and volume of visceral fat. ConclusionShort-term hypocaloric vegetarian and conventional diets did not reduce the POP levels, possibly due to mobilization of fat stores. Our findings support the relationship between POPs and diabetes, especially β-cell function. Trial registrationClinicalTrials.gov number, NCT00883038, completed.

Associations Among Lactation, Maternal Carbohydrate Metabolism, and Cardiovascular Health.

In mammalian reproductive physiology, lactation follows pregnancy; growing evidence suggests that disruption of this physiology affects a woman's lifetime risk of metabolic disease. These differences may reflect lactation-induced mobilization of fat stores and modulation of maternal stress reactivity. In addition, confounders may play a role: women who breastfeed for long durations are more likely to engage in other healthy behaviors, and obesity and insulin resistance may interfere with breastfeeding physiology. These findings underscore the importance of evidenced-based care to enable women to achieve their infant feeding goals.

Global deletion of MGL in mice delays lipid absorption and alters energy homeostasis and diet-induced obesity

Monoacylglycerol lipase (MGL) is a ubiquitously expressed enzyme that catalyzes the hydrolysis of monoacylglycerols (MGs) to yield FFAs and glycerol. MGL contributes to energy homeostasis through the mobilization of fat stores and also via the degradation of the endocannabinoid 2-arachidonoyl glycerol. To further examine the role of MG metabolism in energy homeostasis, MGL(-/-) mice were fed either a 10% (kilocalories) low-fat diet (LFD) or a 45% (kilocalories) high-fat diet (HFD) for 12 weeks. Profound increases of MG species in the MGL(-/-) mice compared with WT control mice were found. Weight gain over the 12 weeks was blunted in both diet groups. MGL(-/-) mice were leaner than WT mice at both baseline and after 12 weeks of LFD feeding. Circulating lipids were decreased in HFD-fed MGL(-/-) mice, as were the levels of several plasma peptides involved in glucose homeostasis and energy balance. Interestingly, MGL(-/-) mice had markedly reduced intestinal TG secretion following an oral fat challenge, suggesting delayed lipid absorption. Overall, the results indicate that global MGL deletion leads to systemic changes that produce a leaner phenotype and an improved serum metabolic profile.

Purifying selection on leptin genes in teleosts may be due to poikilothermy.

Leptin is a key harmone in regulating food intake, immune function and energy metabolism in vertebrates. Since it was first cloned in mouse (Zhang et al. 1994) , the leptin gene has received much attention and people started to research its function in energy homoeostasis and reproductive regulation (Campfiled et al. 1995). A large number of researchers have discovered that leptin is present in several fishes and it plays a similar role in regulation of food intake and energy metabolism in fishes as in mammals (Copeland et al. 2011). Although evidence of positive selection on the leptin gene has been documented in primates, seals and chiropterans (Yu et al. 2011), studies on evolution of leptin gene in fishes are fewer. Leptin, the product of the ob gene, was discovered in 1950 (Coleman 2010). The discovery was followed by intense research into the properties and physiological action of leptin. In initial studies, people considered that the primary functions of leptin were its influence on metabolic rate and mobilization of fat stores (Minokoshi and Kahn 2003). With further research, we now know that leptin is pleiotropic, exerting effects on reproduction, immune function, capillary growth and bone remodelling (Friedman 2009). In mammals, leptin acts on the hypothalamus which sends further signals to the brain, leading the brain to regulate food intake and metabolism (Pelleymounter et al. 1995). To our knowledge, mutations in the leptin genes were associated with a large number of hormonal and metabolic alterations (Kennedy 1953). Deficiency of leptin can cause obesity and diabetes in humans and mice (Strobel et al. 1998). Leptin genes of some fishes have been cloned and people have started to study their structure and biological functions of the protein (Murashita et al. 2008; Aguilar et al. 2010). Although leptin genes of several several species of teleosts have been cloned (Kurokawa et al. 2005; Huising et al. 2006; Ronnestad et al. 2010), physiological function of the

Selected Metabolic and Hormonal Profiles during Maintenance of Spontaneous Ovarian Cysts in Dairy Cows

Information is lacking regarding the relationship between metabolic and hormonal profiles and the maintenance of spontaneous ovarian cyst disease in dairy cows. For this reason, the concentrations of non-esterified fatty acids (NEFA), insulin-like growth factor I (IGF-I) and cortisol (C) were investigated during the spontaneous course of ovarian cyst disease in dairy cows (n=6) between the 7th and 16th weeks post-partum (PP). The control group consisted of normally cycling cows (n=6). Blood samples were collected twice a day, and plasma was analysed using different techniques. Progesterone and 15-ketodihydro-PGF(2α) plasma profiles were investigated to confirm the ovulatory or anovulatory conditions of the cows. Cortisol plasma levels were not significantly different among sampling times within each group or between the two groups. NEFA plasma levels were significantly higher in cycling cows compared to cystic cows at the 16th week PP (p<0.01), but with rather low values, indicating by now sparse mobilization of fat stores. Insulin-like growth factor I plasma concentrations were higher in cystic cows during the 8th, 10th, 11th (p<0.01) and 16th week PP (p<0.05), indicating that the presence of ovarian cysts coincides with increased IGF-I levels. These results suggest no influence of cortisol and NEFA levels in cysts maintenance, while a possible involvement of IGF-I can be suspected not only in the pathogenesis, as already known, but also in the maintenance of spontaneous cystic ovarian disease in cattle.

Resveratrol suppresses body mass gain in a seasonal non-human primate model of obesity

BackgroundResveratrol, a natural polyphenolic compound, was shown to protect rodents against high-fat-diet induced diabesity by boosting energy metabolism. To the best of our knowledge, no data is yet available on the effects of resveratrol in non-human primates. Six non-human heterotherm primates (grey mouse lemurs, Microcebus murinus) were studied during four weeks of dietary supplementation with resveratrol (200 mg/kg/day) during their winter body-mass gain period. Body mass, spontaneous energy intake, resting metabolic rate, spontaneous locomotor activity and daily variations in body temperature were measured. In addition, the plasma levels of several gut hormones involved in satiety control were evaluated.ResultsResveratrol reduced the seasonal body-mass gain by concomitantly decreasing energy intake by 13% and increasing resting metabolic rate by 29%. Resveratrol supplementation inhibited the depth of daily torpor, an important energy-saving process in this primate. The daily amount of locomotor activity remained unchanged. Except for an increase in the glucose-dependent insulinotropic polypeptide, a gut hormone known to promote mobilization of fat stores, no major change in satiety hormone plasma levels was observed under resveratrol supplementation.ConclusionsThese results suggest that in a non-human primate, resveratrol reduces body-mass gain by increasing satiety and resting metabolic rate, and by inhibiting torpor expression. The measured anorectic gut hormones did not seem to play a major role in these observations.

The N-terminal Region of Comparative Gene Identification-58 (CGI-58) Is Important for Lipid Droplet Binding and Activation of Adipose Triglyceride Lipase

In mammals, excess energy is stored in the form of triacylglycerol primarily in lipid droplets of white adipose tissue. The first step of lipolysis (i.e. the mobilization of fat stores) is catalyzed by adipose triglyceride lipase (ATGL). The enzymatic activity of ATGL is strongly enhanced by CGI-58 (comparative gene identification-58), and the loss of either ATGL or CGI-58 function causes systemic triglyceride accumulation in humans and mice. However, the mechanism by which CGI-58 stimulates ATGL activity is unknown. To gain insight into CGI-58 function using structural features of the protein, we generated a three-dimensional homology model based on sequence similarity with other proteins. Interestingly, the model of CGI-58 revealed that the N terminus forms an extension of the otherwise compact structure of the protein. This N-terminal region (amino acids 1-30) harbors a lipophilic tryptophan-rich stretch, which affects the localization of the protein. (1)H NMR experiments revealed strong interaction between the N-terminal peptide and dodecylphosphocholine micelles as a lipid droplet-mimicking system. A role for this N-terminal region of CGI-58 in lipid droplet binding was further strengthened by localization studies in cultured cells. Although wild-type CGI-58 localizes to the lipid droplet, the N-terminally truncated fragments of CGI-58 are dispersed in the cytoplasm. Moreover, CGI-58 lacking the N-terminal extension loses the ability to stimulate ATGL, implying that the ability of CGI-58 to activate ATGL is linked to correct localization. In summary, our study shows that the N-terminal, Trp-rich region of CGI-58 is essential for correct localization and ATGL-activating function of CGI-58.

Lipid metabolism, begging behaviour and nestling obesity in a pelagic seabird

Summary 1. Several alternative explanations have been proposed to account for the evolution of nestling obesity in a variety of avian groups. These predict quite different patterns of fat storage, utilization and food solicitation by chicks of different ages, yet surprisingly few studies have measured changes in begging behaviour or use of fat stores during chick development. 2. We tested the applicability of these hypotheses for Manx shearwaters Puffinus puffinus, by direct measurement of changes in plasma lipid metabolites (non‐esterified fatty acids and β‐hydroxybutyrate) and begging behaviour throughout the chick’s development until fledging. 3. Chicks metabolized fat reserves during periods of parental absence throughout their development but there was no evidence that even the poorest fed chicks were close to exhausting these reserves during the period of mass growth. Chicks begged more vigorously during the period of mass loss at the end of the nestling period than at any previous stage of their development, and mobilization of fat stores was also at a maximum during this period in well‐fed chicks, coinciding with a decrease in food provisioning by parents. Increases in lipid metabolite levels occurred at an earlier age in poorly‐fed chicks than in well‐fed chicks and were followed by a marked decline only in poorly‐fed chicks, indicating that they were exhausting their fat stores. 4. These findings are incompatible with several of the proposed explanations for nestling obesity and mainly support the hypothesis that fat stores fuel chicks through a period of several weeks of reduced food provisioning prior to fledging, when parents are unable or unwilling to maintain earlier levels of food provisioning, despite increased solicitation from chicks.

Morphological changes of the rat intestinal lining in relation to body stores depletion during fasting and after refeeding

Intestinal villus atrophy through prolonged fasting was studied according to two different metabolic phases reached by fasting animals and characterized by (a) the mobilization of fat stores as body fuel and (b) an increase in protein catabolism for energy expenditure. The mechanisms involved in the rapid jejunal restoration after refeeding were also determined. Mucosal structural atrophy during fasting proved to worsen over the two phases due mainly to the retraction of the lacteals in the lamina propria, as observed through the immunolocalization of aquaporin 1 in the endothelial cells of the lymphatic vessels and the detachment of the basal membrane of the epithelial lining at the tip of the villi. Microvilli surface area is preserved through fasting, and apical PepT1 expression increases during both metabolic fasting phases. Refeeding after both fasting phases induces an increase in FATP4 accompanied by a rapid lipid uptake by the enterocytes at the tip of the villi and a rapid extension of the lamina propria due to inflated lymphatic vessels. These mechanisms were more prevalent in animals refed after the phase III fast and could be considered as the major processes allowing complete morphological restoration of the jejunum within only 3 days after refeeding.

Changes in body fat distribution in relation to parity in American women: A covert form of maternal depletion

Using data from the Third National Health and Nutrition Examination Survey (NHANES III), conducted from 1988-1994, we investigated the effect of reproduction on the distribution of body fat in well-nourished American women. While women tend to gain weight and fat with succeeding pregnancies, if age and body mass index are controlled, increasing parity is associated with a decrease in hip and thigh circumferences, suprailiac and thigh skinfolds, and body fat estimated from skinfolds, while waist circumference increases, resulting in a relative decrease in lower-body fat. The mobilization of fat stores in the lower body during late pregnancy and lactation may help to meet the special needs of the developing brain for essential fatty acids and energy during the time of peak growth. When fat is regained after the postpartum period, relatively more is stored in central vs. peripheral depots, resulting in a patterned change in body shape with parity.

PYY[3-36] Administration Decreases the Respiratory Quotient and Reduces Adiposity in Diet-Induced Obese Mice

In rodents, weight reduction after peptide YY[3-36] (PYY[3-36]) administration may be due largely to decreased food consumption. Effects on other processes affecting energy balance (energy expenditure, fuel partitioning, gut nutrient uptake) remain poorly understood. We examined whether s.c. infusion of 1 mg/(kg x d) PYY[3-36] (for up to 7 d) increased metabolic rate, fat combustion, and/or fecal energy loss in obese mice fed a high-fat diet. PYY[3-36] transiently reduced food intake (e.g., 25-43% lower at d 2 relative to pretreatment baseline) and decreased body weight (e.g., 9-10% reduction at d 2 vs. baseline) in 3 separate studies. Mass-specific metabolic rate in kJ/(kg x h) in PYY[3-36]-treated mice did not differ from controls. The dark cycle respiratory quotient (RQ) was transiently decreased. On d 2, it was 0.747 +/- 0.008 compared with 0.786 +/- 0.004 for controls (P < 0.001); light cycle RQ was reduced throughout the study in PYY[3-36]-treated mice (0.730 +/- 0.006) compared with controls (0.750 +/- 0.009; P < 0.001). Epididymal fat pad weight in PYY[3-36]-treated mice was approximately 50% lower than in controls (P < 0.01). Fat pad lipolysis ex vivo was not stimulated by PYY[3-36]. PYY[3-36] decreased basal gallbladder emptying in nonobese mice. Fecal energy loss was negligible ( approximately 2% of ingested energy) and did not differ between PYY[3-36]-treated mice and controls. Thus, negative energy balance after PYY[3-36] administration in diet-induced obese mice results from reduced food intake with a relative maintenance of mass-specific energy expenditure. Fat loss and reduced RQ highlight the potential for PYY[3-36] to drive increased mobilization of fat stores to help meet energy requirements in this model.

Changes in mammary fat pad composition and lipolytic capacity throughout pregnancy

Changes in rat mammary fat pad during pregnancy were assessed by studying differences in the morphology and composition of the pad and in the levels of proteins involved in the accumulation and mobilization of fat stores. During pregnancy, the mammary fat pad weight had increased 1.8-fold by day 20, as compared with control rats. DNA content had increased two-fold by day 13 and remained stable until day 20. Protein content showed a two-fold increase on day 20, compared with control rats. As pregnancy advanced, both the percentage of mammary gland cells with respect to the whole mammary fat pad and the size of the adipocytes increased. The specific content of the different elements of the lipolytic pathway, viz. (alpha(2A)-adrenergic receptor (AR), beta(3)-AR, cAMP-dependent protein kinase and hormone-sensitive lipase (HSL)) underwent a decrease as pregnancy progressed, although adenylate cyclase increased greatly. The lipoprotein lipase (LPL) content per gram of tissue increased with pregnancy and the HSL-to-LPL ratio reflected a continuous increase in the triglyceride storage throughout pregnancy. Thus, the mammary fat pad undergoes extensive morphological, compositional and metabolic transformation during pregnancy, attributable to the development of the mammary gland. The various elements of the lipolytic pathway and LPL undergo major changes during the development of the mammary gland focused towards the increase of fat stores and allowing the accumulation of lipid droplets in the epithelial mammary cells and an increase in adipocyte size.

Endocrine response to fasting in the overwintering captive raccoon dog (Nyctereutes procyonoides)

The raccoon dog (Nyctereutes procyonoides) is an omnivorous canid utilizing the passive wintering strategy in the boreal climate. Farmed raccoon dogs (n=12) were randomly assigned into two study groups on 26 November 2003. Between 3 December 2003 and 27 January 2004, half of the animals were fasted for 8 weeks and plasma weight-regulatory hormone concentrations determined on 26 November and 30 December 2003 and on 27 January 2004. The plasma peptide YY, ghrelin, and growth hormone (GH) concentrations increased due to food deprivation, while the T4 and Acrp30 concentrations decreased. Furthermore, the plasma GH concentrations were higher in the fasted raccoon dogs than in the fed animals, which had higher plasma insulin, glucagon, and T4 concentrations. However, fasting had no effect on the plasma leptin concentrations. The results confirm previous findings with unchanged leptin levels in fasting carnivores. Increased GH levels probably contribute to increased lipolysis and mobilization of fat stores. Ghrelin can also enhance lipolysis by increasing the GH levels. The decreased levels of T4 may reduce the metabolic rate. The plasma dopamine concentrations decreased due to fasting unlike observed previously in rats. Together with the unaffected adrenaline, noradrenaline, and cortisol concentrations, this suggests that food deprivation in winter does not cause stress to the raccoon dog but is an integral part of its natural life history.

Effects of fasting and refeeding on jejunal morphology and cellular activity in rats in relation to depletion of body stores

Background: Intestinal mucosa atrophy following a period of starvation characterized by the mobilization of fat stores for energy expenditure (phase II) worsen after a long fast marked by an increase in protein catabolism (phase III). However, the morphology of the jejunum is completely restored after 3 days of refeeding. The aim of this study was to determine the mechanisms involved in the rapid jejunal restoration following the critical phase III. Methods: Jejunal structure was observed through conventional and environmental scanning electron microscopy, whilst cellular dynamics were studied using classical optic microscopy tools and immunohistochemistry. Results: Mucosal structural atrophy during fasting proved to worsen over the two phases. During phase II, apoptosis is still present at the tip of the villi, the number of mitosis in crypts showed a 30% decrease and a transient drop in cell migration is observed. During phase III, however, an 85% rise in mitosis was noticed along with an increase in cell migration and the disappearance of apoptotic cells at the villus tips. This increased cell renewal continues after food ingestion. Conclusions: Starved rats appeared to be in a phase of energy sparing in phase II, with depressed cellular events in the intestinal mucosa. In phase III, however, the preservation of functional cells and the early increase in crypt cell proliferation should prepare the mucosa to refeeding and could explain why jejunal repairs are complete after 3 days of refeeding following either phase II or phase III.

Energy budgets of lactating and non‐reproductive Brown Long‐Eared Bats (Plecotus auritus) suggest females use compensation in lactation

1. The energy budgets of lactating and non‐reproductive female Brown Long‐Eared Bats fed primarily on noctuid moths (≈ 27·2 kJ g–1) were constructed and compared in flight enclosures in captivity. 2. The average dry food consumption of non‐reproductive individuals was 1·8 g bat–1 day–1 (gross energy intake = 48 kJ day–1). The average food consumption throughout days 10–35 of lactation was 2·0 g bat–1 day–1 (gross energy intake = 53 kJ day–1). Lactating females obtained six times more energy from increased food consumption than from mobilization of fat stores, compared with non‐reproductive bats. 3. Milk export, calculated using the difference in water turnover between lactating and non‐reproductive bats (measured using 2H turnover) averaged 2·6 ml bat–1 day–1 (22·9 kJ day–1). This was similar to the average milk intake of sucklings estimated from 3H turnover (22·9 kJ day–1). 4. Energy available for respiration from food and mobilization of fat stores was 18·2 kJ day–1 for lactating females compared with 36·8 kJ day–1 for non‐reproductive females. In comparison, respiratory daily energy expenditure (DEE) of lactating and non‐reproductive bats, measured by doubly labelled water (DLW), was 21·3 kJ day–1 and 23·6 kJ day–1, respectively. Hence, there was a discrepancy between respiratory DEE (measured by DLW) and net available energy estimates for non‐reproductive bats but not for lactating bats. 5. Respiratory DEE for lactating bats was equal to or less than that of non‐reproductive females, suggesting they used compensatory mechanisms in their energy budgets in lactation.

Effects of dietary energy level and source on foetal development and energy balance in concurrently pregnant and lactating primiparous rabbit does

AbstractThe aim of this experiment was to study the effects of dietary energy level and source on foetal growth and survival and mobilization of body stores in concurrently pregnant and lactating primiparous rabbit does. Does were given a moderate-energy diet (≍9·9 MJ digestible energy (DE) per kg dry matter (DM); group M, no. = 23) or a high-energy diet (-12·2 MJ DE per kg DM). In this latter case, additional energy came from starch (group S, no. = 23) or starch and fat (group F, no. = 22). Primiparous rabbit does were mated within 12 h after parturition and were slaughtered on day 28 of gestation-lactation. During the first 21 days, the DE intake and milk production were higher in the group F than in the groups S and M (P &lt; 0·05). On day 28 of pregnancy, the weight of adipose tissues and liver, as well as the lipid content of the carcass, were higher in the groups S and F than in the group M (P &lt; 0·05). Foetal survival and weight were similar in the three groups. These results indicate that increased energy level of the diet did not improve foetal survival or growth in concurrently pregnant and lactating primiparous does. On the contrary, it could reduce the mobilization offat stores, especially if the energy source is starch.

Short-term changes in energy metabolism after 1 month of a regular oral diet in severely malnourished cirrhotic patients

Malnutrition in patients with liver cirrhosis is currently associated with abnormal fuel metabolism. The aim of this study was to evaluate changes in energy production and substrate oxidation rates in a group of 26 nonanorectic severely malnourished cirrhotic patients in stable clinical condition after 1 month of an oral diet. Child-Pugh score, nutritional status, energy expenditure, rates of nutrient oxidation, and plasma levels of intermediary metabolites in the postabsorptive phase were assessed before and after 1 month of oral nutrition. Upon entry onto the study, caloric and protein intakes were 40.1 ± 2.0 kcal/kg and 1.44 ± 0.8 g/kg, respectively. The Child-Pugh score did not change during the study, whereas nutritional status improved as shown by increased muscular midarm circumference, ([MMAC] P < .02), height-creatinine index ( P < .05), triceps skinfold thickness ([TST] P < .01), and fat mass ( P < .001). Inflammatory state improved during the study, as shown by the decrease of C-reactive protein ([CRP] P < .01) and orosomucoid ( P < .001). The ratio of caloric intake to resting energy expenditure (REE) increased (1.53 ± 0.06 v 1.66 ± 0.07, P < .05), as well as the rates of glucose oxidation ([Gox] 73.6 ± 9.9 v 128.1 ± 10.3 mg/min, P < .001) and urine nitrogen excretion (6.69 ± 0.47 v 7.96 ± 0.48 g/d, P < .02). On the other hand, the rate of lipid oxidation (Lox) decreased (67.3 ± 3.9 v 47.3 ± 4.9 mg/min, P < .001) and was correlated with the decrease of free fatty acid (FFA) levels ( P < .05). These results show that a regular oral diet may improve nutritional status in malnourished cirrhotic patients, provided caloric intake is well adapted to energy requirements. Improvement of nutritional status is related to the change in energy metabolism, showing a normalization of carbohydrate storage while mobilization of fat stores is reduced.