Excessive Fat Deposition Research Articles

Dairy and weight loss hypothesis

Obesity research has established that the positive energy balance that underlies excess body fat deposition has a multifactorial origin. In practical terms, this implies that beyond the effects of sedentariness and suboptimal macronutrient composition, numerous environmental factors and genotypes have the potential to induce a significant imbalance in the natural matching between energy intake and expenditure. This is potentially the case for variations in calcium intake and/or dairy food, which have been shown to be related to fluctuations in energy balance and the risk of overweight. In a recent clinical trial, Zemel et al.1 contributed to a more specific description of this relationship by demonstrating that calcium as well as dairy supplementation can accentuate body weight loss during dietary restriction in obese individuals characterized by low-to-very-low calcium consumption at baseline. In accordance with the multifactorial nature of obesity, this study indirectly suggests that calcium/dairy supplementation probably does not represent a solution for all obese individuals; rather, it could constitute a part of the solution for some persons, particularly low-level calcium consumers. Clearly, this message was not considered in a paper published recently by Lanou and Barnard.2 The authors reported a survey of the literature that was …

Childbearing May Increase Visceral Adipose Tissue Independent of Overall Increase in Body Fat

To examine whether childbearing is associated with increased visceral adiposity and whether the increase is proportionally larger than other depots. This prospective study examined changes in adiposity assessed via computed tomography (CT) and dual-energy X-ray absorptiometry among 122 premenopausal women (50 black, 72 white) examined in 1995-1996 and again in 2000-2001. During the 5-year interval, 14 women had one interim birth and 108 had no interim births. Multiple linear regression models estimated mean (95% confidence interval (CI)) 5-year changes in anthropometric and adiposity measures by interim births adjusted for age, race, and changes in total and subcutaneous adiposity. We found no significant differences between one interim birth and no interim births for 5-year changes in weight, BMI, total body fat, subcutaneous adipose tissue, or total abdominal adipose tissue. Visceral adipose tissue increased by 40 and 14% above initial levels for 1 birth and 0 birth groups, respectively. Having 1 birth vs. 0 births was associated with a greater increase in visceral adipose tissue of 18.0 cm2 (4.8, 31.2), P<0.01; gain of 27.1 cm2 (14.5, 39.7) vs. 9.2 cm2 (4.8, 13.6), and a borderline greater increase in waist girth of 2.3 cm (0, 4.5), P=0.05; gain of 6.3 cm (4.1, 8.5) vs. 4.0 cm (3.2, 4.8), controlling for gain in total body fat and covariates. Pregnancy may be associated with preferential accumulation of adipose tissue in the visceral compartment for similar gains in total body fat. Further investigation is needed to confirm these findings and determine whether excess visceral fat deposition with pregnancy adversely affects metabolic risk profiles among women.

Effects of Monoclonal Antibody Against Adipocyte-Specific Membrane Protein on Lipid Metabolism in Pigs

This study was to investigate the regulation of monoclonal antibodies against adipocyte membrane proteins (McAb) on lipid metabolism in pigs. Forty Landrace x Saba pigs were randomly divided into eight groups; the control group was given 10 mL saline and the treat groups were given monoclonal antibody against adipocyte-specific membrane protein with 0.1, 0.5, and 1.0 mg kg −1 body weight at 15 and 60 kg body weight, respectively, by intraperitoneal injection. The results showed that McAb could increase, significantly, serum lipoprotein lipase activity and reduce serum nonesterified fatty acid (NEFA) content. Meanwhile, McAb increased content of serum lipid, triglyceride (TG), cholesterol (CHO), high density lipoprotein (HDL), and low density lipoprotein (LDL) both at 15 and 60 kg body weight. However, McAb affected more significantly the lipid metabolism at 15 kg body weight than at 60 kg body weight. Moreover, this effect of McAb on lipid metabolism exhibited dose-dependent effect. These results suggested that this monoclonal antibody increased lipase activity, promoted lipolysis, and utilization of lipid so that McAb could be applied to restrain excessive fat deposition in porcine production through the regulation of fat metabolism.

Efficacy of pioglitazone in familial partial lipodystrophy of the Dunnigan type: a case report

A 25 year old woman consulted for a severe acanthosis nigricans and central distribution of fat. Her masculine type morphology was associated with muscular appearance of the limbs and excess fat deposits in the face and neck. Biological testing confirmed glucose intolerance associated with a severe insulin resistance, hypertriglyceridemia and polycystic ovary syndrome. The detection of a heterozygous missense mutation in LAMIN A/C gene at position 482 confirmed the diagnosis of Familial Partial Lipodystrophy (FPLD2). Due to a deterioration of clinical and metabolic status, 15 and then 30 mg per day of pioglitazone were added to her previous treatment with metformin, bezafibrate and omega-3 fatty acids. Metabolic status improved rapidly after 3 months and continued thereafter. Weight remained stable, body mass composition and waist circumference improved. After 18 months of treatment, glycaemia and triglycerides levels normalized, hepatic enzymes and liver echographic features improved. Insulin sensitivity improved dramatically with a HOMA % S value of 73% with metformin and of 98.2% when pioglitazone was added. Leptin levels increased from 6.6 to 10.2 μg/ml. We report a very rapid and good efficacy of pioglitazone added to metformin without side effects in FPLD2. If confirmed on more patients, early use of pioglitazone in association with metformin could be proposed in FPLD2.

Adipose tissue expandability and the metabolic syndrome

Adipose tissue expandability and the metabolic syndrome

Lipomatous hypertrophy of the interatrial septum associated with fatty replacement of the ventricular myocardium: A case report

Lipomatous hypertrophy of the interatrial septum (LHIS) is a rare benign entity characterized by the excessive fat deposition in the interatrial septum with typical sparing of the fossa ovalis. We report a case of a 61-year-old woman with an incidentally found LHIS associated with fatty replacement of the ventricular myocardium and epicardial mediastinal lipomatosis diagnosed by computed tomography (CT) and MRI.

Effects of the Monoclonal Antibody against Porcine 40 kDa Adipocyte-specific Plasma Membrane Protein on Adipocytes and Carcass Composition

The effects of the mouse monoclonal antibody against 40 kDa adipocyte-specific plasma membrane protein on porcine adipocytes and carcass composition were investigated in vitro and in vivo. Results revealed that the in vitro complement-mediated cytotoxicity of this monoclonal antibody can lead to adipocyte lysis, remarkable reduction of adipocyte lipid accumulation (P<0.01), and significant decrease of well-differentiated fat cells (P<0.01). Treatment of adipocytes with this antibody alone in vitro did not induce cell lysis, but could lead to noticeable reduction of well-differentiated cells and lipid accumulation (P<0.05) at the pre-adipocyte stage. In vivo, pigs injected with 0.5 mg/kg or 1.0 mg/kg of antibody showed smaller adipocyte sizes (P<0.01) and reduced lipid accumulation of adipocytes (P<0.01). Our results also indicated that pigs intraperitoneally or subcutaneously immunized with 0.5 mg/kg of monoclonal antibody at 15 kg or 1.0 mg/kg antibody at 60 kg had a higher lean meat percentage (P<0.05), larger loin eye area (P<0.05), lower fat meat percentage (P<0.05), less backfat thickness (P<0.05) and smaller leaf fat weight (P<0.05) than the control pigs, but other carcass traits such as caul fat weight, heart weight, liver weight, spleen weight, kidney weight, lung weight, and dressing percentage were not significantly affected. These results suggested that this monoclonal antibody could be applied to restrain excessive fat deposition in porcine production.

Absence of the proapoptotic Bax protein extends fertility and alleviates age-related health complications in female mice

The menopausal transition in human females, which is driven by a loss of cyclic ovarian function, occurs around age 50 and is thought to underlie the emergence of an array of health problems in aging women. Although mice do not undergo a true menopause, female mice exhibit ovarian failure long before death because of chronological age and subsequently develop many of the same age-associated health complications observed in postmenopausal women. Here we show in mice that inactivation of the proapoptotic Bax gene, which sustains ovarian lifespan into advanced age, extends fertile potential and minimizes many age-related health problems, including bone and muscle loss, excess fat deposition, alopecia, cataracts, deafness, increased anxiety, and selective attention deficit. Further, ovariectomy studies show that the health benefits gained by aged females from Bax deficiency reflect a complex interplay between ovary-dependent and -independent pathways. Importantly, and contrary to popular belief, prolongation of ovarian function into advanced age by Bax deficiency did not lead to an increase in tumor incidence. Thus, the development of methods for postponing ovarian failure at menopause may represent an attractive option for improving the quality of life in aging females.

The major facilitator superfamily member Slc37a2 is a novel macrophage- specific gene selectively expressed in obese white adipose tissue

A marked degree of macrophage infiltration of white adipose tissue (WAT) occurs in obesity and may link excess adiposity with the chronic inflammatory state underlying metabolic syndrome and other comorbidities of obesity. Excess deposition of fat in the intra-abdominal vs. subcutaneous WAT depots is a key component of metabolic syndrome. Through construction and differential screening of a murine ob/ob WAT cDNA library, we identified Slc37a2, a novel sugar transporter of the major facilitator superfamily, to be twofold enriched in intra-abdominal vs. subcutaneous fat. We find Slc37a2 is a macrophage-enriched transcript. In murine tissues, Slc37a2 transcript is restricted to spleen, thymus, and obese WAT. It is also readily detected in the RAW264.7 macrophage cell line and increases 46-fold during macrophage differentiation of THP-1 human monocytes. Compared with wild-type mice, Slc37a2 transcript is increased epididymal ninefold in ob/ob WAT and assessment of expression of the macrophage marker emr1 indicated upregulation of Slc37a2 transcript in macrophages populating ob/ob WAT. Studies with PNGase F and tunicamycin reveal the Slc37a2 protein is posttranslationally modified by addition of N-linked glycans. Slc37a2 protein migrates as heterogeneous species of approximately 50-75 kDa and its ectopic expression in mammalian cells results in the appearance of large intracellular vacuoles. We postulate that the function of this macrophage-specific putative sugar transporter is central to the metabolism of the macrophage population specifically present in obese WAT.

Mitochondrial function: use it or lose it

Type 2 diabetes is a progressive metabolic disorder that develops as a result of both environmental and undefined genetic factors [1]. While the precise molecular aetiology of this disorder remains elusive, there is general consensus that type 2 diabetes has several hallmark features: (1) a breakdown in lipid and carbohydrate metabolism, reflected by elevated levels of circulating metabolites and culminating in excessive deposition of fat in various tissues [2]; (2) skeletal muscle insulin resistance [3]; and (3) coordinated defects in oxidative metabolism [4–6]. In conjunction with these altered metabolic states is the impaired insulin signalling observed in muscle of patients with type 2 diabetes [7]. At present, it is unclear whether these (and other) defects are a consequence of the diabetic state or are instrumental in its development. Unravelling this puzzle is made more difficult because these impairments do not occur in isolation but typically co-exist in the same individual.

Sleep Apnea / Hypopnea Syndrome – A Review

The sleep apnoea/hyperpnoea syndrome is characterized by repeated upper airway narrowing or collapse during sleep. These episodes are accompanied by hypoxemia, surges in blood pressure, brief arousal from sleep and pronounced snoring. The signs and symptoms of OSAS may be recognizable in the practice of Dental and Oral Maxillofacial surgery. Common findings in the medical history include day time sleepiness, snoring, hypertension, and type 2 diabetes mellitus. Common clinical findings include male gender, obesity, increased neck circumference, excessive fat deposition in the palate, tongue (macroglossia) and pharynx, a long soft palate, a small recessive maxilla and mandible, and calcified carotid artery atheroma on panoramic and lateral cephalometric radiograph. After confirmation of the diagnosis by a physician, Dental surgeons and Oral maxillofacial surgeons can participate in the management of the disorder by fabricating mandibular advancement appliances that enlarge the retroglossal space by anterior displacement of tongue, and performing corrective upper airway surgery that prevents recurrent airway obstruction respectively.

Chronological Approach of Diet‐induced Alterations in Muscle Mitochondrial Functions in Rats

Mitochondrial dysfunction might predispose individuals to develop insulin resistance. Our objective was to determine whether mitochondrial dysfunction or insulin resistance was the primary event during high-fat (HF) diet. Rats were fed an HF diet for 0, 3, 6, 9, 14, 20, or 40 days and compared with control. Soleus and tibialis muscle mitochondrial activity were assessed using permeabilized fiber technique. Insulin [area under the curve for insulin (AUC(I))] and glucose [area under the curve for glucose (AUC(G))] responses to intraperitoneal glucose tolerance test as well as fasting plasma non-esterified fatty acids (NEFAs), triglyceride, and glycerol concentrations were determined. AUC(I) and AUC(G) were altered from Day 6 (p < 0.01 vs. Day 0). In soleus, oxidative phosphorylation (OXPHOS) activity was transiently enhanced by 26% after 14 days of HF diet (p < 0.05 vs. Day 0) conjointly with 62% increase in NEFA concentration (p < 0.05 vs. Day 0). This was associated with normalized AUC(G) at Day 14 and with a decline of plasma NEFA concentration together with stabilization of intra-abdominal adiposity at Day 20. Prolongation of HF diet again caused an increase in plasma NEFA concentration, intra-abdominal adiposity, AUC(I), and AUC(G). At Day 40, significant decrease in OXPHOS activity was observed in soleus. Mitochondria first adapt to overfeeding in oxidative muscle limiting excess fat deposition. This potentially contributes to maintain glucose homeostasis. Persistent overfeeding causes insulin resistance and results in a slow decline in oxidative muscle OXPHOS activity. This shows that the involvement of mitochondria in the predisposition to insulin resistance is mainly due to an inability to face prolonged excess fat delivery.

ApoO, a Novel Apolipoprotein, Is an Original Glycoprotein Up-regulated by Diabetes in Human Heart

Obesity is an independent risk factor for cardiac failure. Obesity promotes excessive deposition of fat in adipose and nonadipose tissues. Intramyocardial lipid overload is a relatively common finding in nonischemic heart failure, especially in obese and diabetic patients, and promotes lipoapoptosis that contributes to the alteration of cardiac function. Lipoprotein production has been proposed as a heart-protective mechanism through the unloading of surplus cellular lipids. We previously analyzed the heart transcriptome in a dog nutritional model of obesity, and we identified a new apolipoprotein, regulated by obesity in heart, which is the subject of this study. We detected this new protein in the following lipoproteins: high density lipoprotein, low density lipoprotein, and very low density lipoprotein. We designated it apolipoprotein O. Apolipoprotein O is a 198-amino acid protein that contains a 23-amino acidlong signal peptide. The apolipoprotein O gene is expressed in a set of human tissues. Confocal immunofluorescence microscopy colocalized apolipoprotein O and perilipins, a cellular marker of the lipid droplet. Chondroitinase ABC deglycosylation analysis or cell incubation with p-nitrophenyl-beta-d-xyloside indicated that apolipoprotein O belongs to the proteoglycan family. Naringenin or CP-346086 treatments indicated that apolipoprotein O secretion requires microsomal triglyceride transfer protein activity. Apolipoprotein O gene expression is up-regulated in the human diabetic heart. Apolipoprotein O promoted cholesterol efflux from macrophage cells. To our knowledge, apolipoprotein O is the first chondroitin sulfate chain containing apolipoprotein. Apolipoprotein O may be involved in myocardium-protective mechanisms against lipid accumulation, or it may have specific properties mediated by its unique glycosylation pattern.

Gastrostomy feeding in cerebral palsy: too much of a good thing?

The study by Sullivan et al. (p 877) aimed to measure energy balance and body composition in children with severe cerebral palsy (CP) who were fed either orally or by gastrostomy tube. The authors show that feeding by gastrostomy tube, using a commercial formula, may lead to disproportionate (excess) fat deposition in these children. They note that while caloric supplementation of children with eating impairments is associated with weight gain, the nutritional composition of a diet for this group of children has yet to be determined.

A History of Obesity, or How What Was Good Became Ugly and Then Bad

Chronic food shortage and malnutrition have been the scourge of humankind from the dawn of history. The current worldwide epidemic of obesity, now recognized as a public health crisis, is barely a few decades old. Only after the technological advances of the eighteenth century did a gradual increase in food supply became available. The initial effect of these advances in improved public health and amount, quality, and variety of food was increased longevity and body size. These early favorable outcomes of technological advances notwithstanding, their incremental effect since the Second World War has been an overabundance of easily accessible food, coupled with reduced physical activity, that accounts for the recent increased prevalence of obesity. Obesity as a chronic disease with well-defined pathologic consequences is less than a century old. The scarcity of food throughout most of history had led to connotations that being fat was good, and that corpulence and increased "flesh" were desirable as reflected in the arts, literature, and medical opinion of the times. Only in the latter half of the nineteenth century did being fat begin to be stigmatized for aesthetic reasons, and in the twentieth century, its association with increased mortality was recognized. Whereas early reports listed obesity as a risk factor for mortality from "chronic nephritis," the subsequent recognition of the more common association of obesity with diabetes, hypertension, and heart disease altered the listings and questioned its being a risk factor for kidney disease. An enlarging body of evidence, accrued over the past decade, now indicates a direct association of obesity with chronic kidney disease and its outcomes.

The Neurobiology of Obesity

Obesity is an energy balance regulation dysfunction thatleads to an excessive fat deposition, which increases the riskfor cardiovascular, respiratory, and metabolic diseases, inparticular when such deposition occurs within the abdomi-nal cavity. The high prevalence of obesity and its costlyco-morbidities has significantly contributed to intensify ef-forts to understand obesity, which is currently at the fore-front of biochemical, biomolecular, and neurobiological re-search. We now confront the tremendous challenge ofpreventing obesity and developing effective treatments.In the last 15 years, research has generated many impor-tant discoveries, including those of adipose tissue-derivedhormones such as leptin and adiponectin, those of the gas-trointestinal tract hormones such as ghrelin, and the deter-mination of numerous central and peripheral circuitries in-volved in energy balance regulation. The neurobiology ofobesity represents a rapidly growing research field that hasprovedtobeessentialintheunderstandingoftheetiologyofobesity. The brain plays a major role in energy balanceregulation as it exerts controls on both food intake andenergy expenditure (Figure 1). Three brain entities are par-ticularly important in these controls, namely the hypothal-amus, the dorsal vagal complex, and the reward system,which are inter-related structures capable of controllingenergy intake as well as thermogenesis. Brain systems con-trolling energy intake and energy expenditure have beendivided into anabolic and catabolic systems, each systemcomprising different types of neurons capable of controllingenergy intake as well as energy expenditure. These neuronsrelease various molecules that include neuropeptide Y, ag-outi-related peptide, melanin-concentrating hormone, theendocannabinoids, -melanocyte-stimulating hormone, co-caine- and amphetamine-regulated transcript, corticotropin-releasing factor, thyrotropin-releasing hormone, and seroto-nin. These neurosystems are modulated by short- and long-termsignalsthatreportonthestatusoftheenergystoresandenergy fluxes. Whereas leptin and insulin are recognized asthe main long-term signals, the gastrointestinal hormonesghrelin, peptide tyrosine-tyrosine, cholecystokinin, and glu-cagon-like peptide 1 are known as short-term signals thatinform about the nutritional status. The way an organismregulates energy balance is in large part a function of itsgenes and the environment. One energy expenditure com-ponent, which is perhaps not so important in human ener-getics but which is undoubtedly relevant in laboratory ro-dents used by most neurobiologists of obesity, is brownadipose tissue thermogenesis, the activity of which dependson factors activating the sympathetic nervous system. Theextraordinary thermogenic power of brown adipose tissue isattributable to uncoupling protein 1, a mitochondrial proteinuniquely found in brown adipose tissue.It is within the mission of the Merck Frosst/CIHR Re-search Chair in Obesity to provide continuing educationabout the best possible knowledge on obesity to scientists,physicians, health professionals, as well as to the public atlarge, regarding the causes, complications, treatment, andprevention of obesity. In this regard, the purpose of theannual symposium is to summarize evidence regarding im-portant topics related to obesity and to propose novel obe-sity research directions. Since its creation in 1997, theMerck Frosst/CIHR Research Chair in Obesity has held sixinternational symposia devoted entirely to obesity research.The first symposium of the series, entitled “The UncouplingProteins and Obesity,” was held in 1998 (1). The secondsymposium, which was organized the following year, wasoriented toward “The New Biology of Adipose Tissue” (2).In 2000, the third symposium was entitled “The Pon-derostat: From Behavior to Neural Substrates” (3) and fo-cused on the mechanisms whereby energy balance is regu-lated. The fourth symposium, organized in November 2002and entitled “Complications of Obesity: The InflammatoryLink,” summarized the latest most important findings on themechanisms underlying the link between obesity and itscomplications such as diabetes and cardiovascular diseases(4). In 2003, the fifth symposium brought a comprehensiveview on the “Role of Gene Regulation in Obesity and itsComplications” (5) and, specifically, on the regulation ofperoxisome proliferator-activated receptors, prostaglandin

Increasing Mangrof Leaves Meal Allowance in Layers Diets Through Enhancing its Nutritive Value

The objective of this study was to improve the nutritive value of mangrof leaves meal in order to increase its allowance in layer diets. The meal was subjected to boiling in an attempt to improve its nutritive value. The study also included testing the effect of supplementing the experimental diets containing the mangrove meal ( boiled or raw) with Natugrain or a mixture of spices on laying performance and biological responses associated with egg production. Four hundred and fifty 30- week old Hy-line laying hens were randomly distributed to 15 groups each contained 5 replicates of 6 hens under the same environmental conditions throughout the period of 20 wks. Dietary treatments included 3 levels of either raw or boile d mangrof leaves meal (0, 5 and 10% ) for 30 minutes. Each group was received one of these diets and with or without Natugrain and/or spices mixture. Diets were formulated to be isocaloric and iso-nitrogenous. Laying performance, quality of fresh and stored eggs (stored for one month in the refrigerators), intestinal characteristics, chemical composition of eggs and cholesterol contents of yolk as well as some blood plasma constituents were determined. Results obtained showed that mangrof leaves meal contains reasonable amount of the essential nutrients which play an important role in layers nutrition. Boiling process had an enhanced effect on the nutritive value by converting the deleterious materials to less toxic form. Mangrof leaves meal at level of 5% had no adverse effect on body weight gains of Hy-line hens during the laying period. However, increasing dietary Mangrof leaves to 10% adversely reduced weight gain by 19.7% compared to control group. Irrespective of Mangrof meal and feed additives, boiling treatment had no effect on weight gain of laying hens during 30-49 wk of age. Also, regardless of mangrove meal and boiling treatment, only Natugrain® increased weight gain by 24 and 9.6% compared to the negative control and spices supplemented group, respectively. Increasing inclusion level of mangrof leaves meal up to 10% significantly decreased laying rate percentage and egg mass during most of the experimental periods. Also, boiling or adding the feed additives did not stop this reduction. Irrespective of boiling treatment and feed additives, Mangrof leaves meal had no significant impact on egg weight during 30- 49 wk of age. Neither inclusion levels of the tested material nor boiling process nor Natugrain and spices supplementation had an enhancing effect on feed intake. Consequently, feed conversion was the worst as feeding diets containing un-boiled or boiled mangrof meal at level 10%. The impairment in FCR amount to 10.7% compared to control group. The opposite was true with feed additives supplementation which showed an enhanced effect. Increasing dietary mangrof leaves meal up to 10% significantly improved Haugh unit score, yolk color and shell thickness of fresh eggs and those stored for 30 days in the refrigerator, whilst there is different trend with yolk index. Boiling treatment and feed additives supplementation had no significant effect on egg quality traits. Also, mangrof meal levels, boiling process and feed additives had no adverse effect on chemica l composition of egg components and plasma constituents. There were no significant interactions between Mangrof meal and boiling treatment and / or feed additives on rate of laying, egg weight, egg mass, feed intake and feed conversion. However, there is a trend for rate of laying, egg mass and feed conversion to improve when Natugrain® or mixture of different spices were added to diet containing 10% of boiled Mangrof leaves. Also, similar finding was observed with the parameters of fresh egg quality of 41 or 49 wk-old hens and those stored in the refrigerators as well as those of intestinal characteristics and reproductive organs. 7-There was a significant effect as feeding boiled Mangrof leave meal-containing diet on plasma albumin, total lipids and yolk protein. Yolk lipid showed an opposite trend to that shown in yolk protein. In general, it may be recommended to incorporate mangrof leaves meal at level 5% as a non-traditiona l ingredient in laying hen diets without adverse effect on their performance in order to get higher economic return as well as to control excessive body fat deposition and to improve productive and reproductive performance.

Does overfeeding affect tench Tinca tinca (L.) juveniles?

Duplicate groups of tench (Tinca tinca) juveniles (mean weight 0.69 g) were fed at 28 °C for 70 days either a commercial formulated diet, Futura, or frozen Chironomidae larvae at four levels: below satiation, at about satiation, above satiation and well above satiation. These are represented by the feeding groups F1–F4 and C1–C4, respectively. No mortality was observed throughout the experiment. In groups F2–F4 a considerable incidence of uneaten food (>40% observations), deformities of the caudal penduncle, retarded growth, elevated condition coefficient (>1.2), reduced amounts of minerals in the tissue ( 5) and high caloric value of the tissue (>28 J mg−1 dry matter) (the latter two suggesting excessive fat deposits), were found. The combination of these indices was indicative of overfeeding in fish fed the Futura diet at the daily doses ≥2.7% fish biomass. First symptoms of overfeeding: a considerable incidence of uneaten food, retarded growth, and elevated C/N ratio were observed in the group fed Chironomidae larvae at the highest level, (C4, wet Chironomidae 20.7% of the fish biomass daily, that is, 3.9% of dry chironomids per fish biomass and day). Thus, restricted daily doses of formulated diet not exceeding 2.5% fish biomass are recommended for tench juveniles aged 130–200 days post hatch. Safe daily doses of frozen Chironomidae (in terms of larvae dry weight) remain below 3.5% of fish biomass.

High-fat feeding period affects gene expression in rat white adipose tissue

The expression of 76 sequences, previously isolated as differentially expressed in visceral white adipose tissue (WAT) of female rats, fed with a high-fat diet for 11 days (Lopez et al., Biochem Biophys Res Comm 318: 234-239, 2004), was analyzed in epidydimal WAT of male rats after a feeding period of 65 days with the same diet, using microarray technology. After Northern blot validation of the results, only three genes appeared upregulated (caveolin-2, the alpha-1 chain of haemoglobin and rat mammary tumor-7) and two downregulated (adiponectin and dystroglycan). We have also analyzed caveolin-1 gene expression and found that follows the opposite pattern of caveolin-2, indicating that they are inversely regulated. Our results suggest that if feeding with a high-fat diet is prolonged, many of the initial changes in gene expression, probably aimed to consume the energy surplus and prevent excessive fat deposition, are not maintained, and adaptation to an increased lipid storage is developed.

Comparison of characteristics of lambs fed concentrate or grazed on ryegrass to traditional or heavy slaughter weights. I. Production, carcass, and organoleptic characteristics1

The objectives of this study were to determine the effects of finishing lambs on concentrate (C) or by grazing ryegrass forage (F) to slaughter end weights of 52 (N) or 77 kg (H) on carcass characteristics and organoleptic properties. This experiment included 64 Targhee x Hampshire lambs (average BW = 24 +/- 1 kg) in a 2 x 2 x 2 factorial arrangement of treatments to compare wethers vs. ewes, C vs. F, and N vs. H slaughter weights. No interactions (P > 0.10) were observed between gender and other main effects. Hot carcass weight and dressing percent were greater (P < 0.001) for C- than for F-fed lambs. Backfat thickness also was greater (P < 0.001) for lambs fed C than for those fed F. Moreover, USDA lean quality score and USDA yield grades were higher (P < 0.001) for C- than for F-fed lambs, as well as for lambs slaughtered at H vs. N market weights. There was a higher (P < 0.005) incidence of off odors and off flavors in cooked muscle from F- vs. C-fed lambs, and also from H vs. N slaughter-weight lambs. The heavy C-fed lambs had juicier (P < 0.001) meat than other treatment combinations. Cooked meat from C-fed lambs received higher (P < 0.001) overall acceptability scores. Concentrate-finished lambs produced fatter carcasses and more palatable meat than forage-finished lambs; however, forage finishing allowed for slaughter at heavier weights without excessive fat deposition.