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Ablation of AMP-Activated Protein Kinase \(\alpha\)2 Activity Exacerbates Insulin Resistance Induced by High-Fat Feeding of Mice

Ablation of AMP-Activated Protein Kinase \(\alpha\)2 Activity Exacerbates Insulin Resistance Induced by High-Fat Feeding of Mice

Expression of insulin signaling molecules. Because ␣ 2i TG mice showed decreased insulin sensitivity for glucose transport, we also determined the effects of diet and genotype on protein expression of key insulin signal- ing molecules. Since use of the entire soleus muscle was necessary to measure glucose transport, we used gastroc- nemius muscles for these analyses. The decrease in insu- lin-stimulated glucose transport in the ␣ 2i TG mice fed the high-fat diet was accompanied by reductions in insulin receptor- ␤ subunit, IRS-1, and Akt compared with wild- type mice fed the high-fat diet (Fig. 4). Expression of these molecules was not significantly different between ␣ 2i TG and wild-type mice fed the control diet. Therefore, lack of AMPK ␣ 2 activity itself does not seem to be a trigger for the downregulation of insulin signaling molecules. Instead, there may be synergic effects of high-fat feeding and a lack of AMPK ␣ 2 activity on the expression of these proteins. Interestingly, GLUT4 expression was not different among the four groups (Fig. 4). Although it has been reported that activation of AMPK by 5-aminoimidazole-4-carboxamide- 1- ␤ -4-ribofuranoside (AICAR) increases GLUT4 expres- sion in skeletal muscle (21,22), our results show that ablation of AMPK activity does not affect GLUT4 protein expression.

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PPARγ ablation sensitizes proopiomelanocortin neurons to leptin during high fat feeding

PPARγ ablation sensitizes proopiomelanocortin neurons to leptin during high fat feeding

The results of this study unmasked a crucial role for PPARγ in POMC neurons to bring about cellular bio- logical adaptations of these cells to the changing metabolic environment. We showed that the arcuate nucleus POMC neurons are important sites of action of PPARγ during high-fat feeding. We showed that dele- tion of PPARγ in POMC neurons attenuates hyperpha- gia, increases EE, and protects the mice from DIO and the development of leptin resistance. The cellular mechanisms responsible for these effects involve proliferation of peroxisomes, changes in ROS levels, and mitochondrial ER interactions. Abla- tion of PPARγ in POMC neurons prevented the increase of perox- isome density and increased ROS levels and mitochondrial ER in association with higher activity of POMC neurons. Considering that PPARγ is widely expressed within the central nervous system, our work also highlights PPARγ as a potential general metabolic switch of neurons.

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Distinct contributions of hyperglycemia and high-fat feeding in metabolic syndrome-induced neuroinflammation

Distinct contributions of hyperglycemia and high-fat feeding in metabolic syndrome-induced neuroinflammation

Having established the presence of systemic inflamma- tion in HFD-fed mice, we characterised whether this was associated with the presence of adherent leukocytes to the cerebral vasculature. The extravasation of leukocytes from the peripheral vasculature into the brain parenchyma is a critical component in both acute and chronic neuroin- flammatory disorders. This phenomenon has been pre- dominantly explored in rodent models of multiple sclerosis (MS) and ischaemic stroke in vivo [38, 39], yet the influences by which this occurs are not fully under- stood. Here, we observed adherent GR1 + granulocytes (neutrophils/monocytes) in the surface cerebrovasculature of STZ + CON mice after 18, but not 9 weeks. Interest- ingly, this adherence was not associated with any increases of IL-6 or other cytokines measured, suggesting that the recruitment of these cells is independent of systemic in- flammation and high-fat feeding. Hyperglycemic condi- tions have been shown to induce endothelial cell dysfunction and promote low-grade inflammation [40]. Indeed, previous in vitro studies of human brain endothe- lial cell cultures reveal a high degree of apoptosis under hyperglycemic conditions [41]. To our knowledge, this is the first study of its kind to demonstrate in vivo granulo- cyte trafficking along the cerebrovasculature of hypergly- cemic mice. Moreover, immunofluorescence of the cortex of STZ + CON mice after 18 weeks demonstrated an in- crease in the presence of CD45 + blood-derived leukocytes. Given the lack of changes in inflammatory cells and markers measured using flow cytometry at the level of hemispheric tissue, it is possible that the GR1 + granulo- cytes detected with intravital microscopy eventually trans- migrated into the brain parenchyma and presented as this CD45 + population.

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CCR2 modulates inflammatory and metabolic effects of high fat feeding

CCR2 modulates inflammatory and metabolic effects of high fat feeding

obese following 20 weeks of high-fat diet feeding. There were no significant genotype-dependent differences in fast- ing glucose or insulin concentrations in lean animals. How- ever, fasting glucose and insulin concentrations were lower in obese Ccr2 –/– compared with obese Ccr2 +/+ mice despite

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Obesity does not promote tumorigenesis of localized patient- derived prostate cancer xenografts

Obesity does not promote tumorigenesis of localized patient- derived prostate cancer xenografts

There are established epidemiological links between obesity and the severity of prostate cancer. We directly tested this relationship by assessing tumorigenicity of patient-derived xenografts (PDXs) of moderate-grade localized prostate cancer in lean and obese severe combined immunodeficiency (SCID) mice. Mice were rendered obese and insulin resistant by high-fat feeding for 6 weeks prior to transplantation, and PDXs were assessed 10 weeks thereafter. Histological analysis of PDX grafts showed no differences in tumor pathology, prostate-specific antigen, androgen receptor and homeobox protein Nkx-3.1 expression, or proliferation index in lean versus obese mice. Whilst systemic obesity per se did not promote prostate tumorigenicity, we next asked whether the peri-prostatic adipose tissue (PPAT), which covers the prostate anteriorly, plays a role in prostate tumorigenesis. In vitro studies in a cellularized co- culture model of stromal and epithelial cells demonstrated that factors secreted from human PPAT are pro-tumorigenic. Accordingly, we recapitulated the prostate-PPAT spatial relationship by co-grafting human PPAT with prostate cancer in PDX grafts. PDX tissues were harvested 10 weeks after grafting, and histological analysis revealed no evidence of enhanced tumorigenesis with PPAT compared to prostate cancer grafts alone. Altogether, these data demonstrate that prostate cancer tumorigenicity is not accelerated in the setting of diet-induced obesity or in the presence of human PPAT, prompting the need for further work to define the at-risk populations of obesity-driven tumorigenesis and the biological factors linking obesity, adipose tissue and prostate cancer pathogenesis.

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Serum alkaline phosphatase in hypophosphatasia

Serum alkaline phosphatase in hypophosphatasia

It is recognized that serum alkaline phosphatase may reflect enzyme contributions from bone, liver, and intestine. We have investigated serum alkaline phosphatases in two siblings with hypophosphatasia. After administration of long-chain triglycerides, the major alkaline phosphatase component of their sera was shown to be of intestinal origin on the basis of inhibition by l-phenylalanine. Starch block electrophoresis suggested that there were other regions of l-phenylalanine-sensitive alkaline phosphatase in addition to the major slow-moving intestinal band. Medium-chain triglycerides which are absorbed by the portal route did not cause a similar augmentation of intestinal alkaline phosphatase activity. These studies indicate that serum levels of intestinal alkaline phosphatase are increased normally after long-chain fat feeding in hypophosphatasia and may be the major component of total serum alkaline phosphatase activity.

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High fat diet-induced non alcoholic fatty liver disease in rats is associated with hyperhomocysteinemia caused by down regulation of the transsulphuration pathway

High fat diet-induced non alcoholic fatty liver disease in rats is associated with hyperhomocysteinemia caused by down regulation of the transsulphuration pathway

The results of our experiments show that plasma Hcy is significantly increased in high fat diet-induced NAFLD in rats, and that this change is accompanied by a decrease in plasma Cys (Figure 2A,B), suggesting that the transsulphuration pathway is affected. Determination of the activities of the two enzymes of the pathway showed that both are significantly down-regulated in high fat diet-induced NAFLD (Figure 2C,D). We found no evidence, however, for changes in the expression of other key enzymes in the hepatic methionine cycle, including MAT1A, the gene which encodes the catalytic subunit of the isoenzymes MATI and MATIII which are expressed in adult liver [29], and the methyltransferases GNMT and PEMT (Table 3). Since these enzymes are methyltransferases while CBS and CGL are lyases, it is likely that they are regulated by different mechanisms. In addition, we have only measured mRNA expression for these enzymes, thus we cannot rule out the possibi- lity that there may be post transcriptional changes which modulate their activity in response to high fat feeding. In contrast to our results, Kwon et al. [30] have reported that CBS activity was unchanged in rats in which NAFLD was induced by feeding a diet containing 71% of the energy as fat, while CGL activity was increased by about 35%. In this study, however, the con- trol diet contained 35% of energy from fat, which is con- siderably higher than the 10% of energy from fat in our control diet. Thus, our findings indicate that high fat diet-induced NAFLD is associated with HHcy, and that this is caused by reduced conversion to Cys via the transsulphuration pathway, while the expression of methyltransferases involved in liver methionine metabo- lism is not changed. As it has been estimated that as much as 50% of the Cys required for GSH synthesis is formed from Hcy via this route, and the availability of Cys is a limiting factor for GSH production [12,31], in the long term this may lead to a decrease in body levels of this antioxidant.

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The role of dietary fatty acids in predicting myocardial structure in fat-fed rats

The role of dietary fatty acids in predicting myocardial structure in fat-fed rats

When possible, the above discussion has focused on models of OC without concomitant genetic anomalies or induced pathology (i.e. aortic banding, spontaneous hypertension). Within these studies, the data collectively suggest that there may be strain differences and variabil- ity in whole animal vs. ex vivo outcomes. Regarding strain, Wistar and SD rats have distinct lipid metabo- lism,[85] and Wistars may develop myocardial pathology with shorter dietary interventions[56,86]. Additional strain differences in metabolic and myocardial responses to high-fat feeding have been demonstrated[87,88]. Regarding model type, evidence suggests that ex vivo studies of OC reveal more profound pathology than observed in vivo, and this has been partly attributed to endogenous protective mechanisms[21]. While contrac- tile dysfunction may have been present in isolated mus- cles or cells from the rats in this study, overall gross systolic and diastolic function was seemingly intact. As noted, there may be distinct signaling pathways that are specific to predominant dietary fatty acids but result in overtly similar outcomes. For this reason, it will be important to subsequently characterize genotype and major hypertrophic pathways to investigate potential dif- ferences at the cellular level.

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Non-alcoholic fatty liver disease and its associations among adolescents in an urban, Sri Lankan community

Non-alcoholic fatty liver disease and its associations among adolescents in an urban, Sri Lankan community

final measure. Total body fat (TBF) and visceral fat percentage (VFP) were measured using a body com- position monitor using the proven bioelectrical im- pedance method according to the instruction manual (Omron HBF-362 body composition monitor, Omron Healthcare Co LTD Kyoto, Japan). All subjects under- went ultrasonography of the liver with a 5-MHz 50 mm convex probe (MindrayDP-10 Ultrasound Diagnostic Systems, Mindray Medical International Limited, Shenzhen, China). Ultrasonographic examin- ation was carried out by five doctors who had been specially trained in liver ultrasonography. A 10 mL sample of venous blood was obtained from each sub- ject. This was used to determine fasting serum tri- glycerides (TG), high density lipoproteins cholesterol (HDL), low density lipoprotein cholesterol (LDL), very low density lipoprotein cholesterol (VLDL), serum ala- nine aminotransferase activity (ALT), fasting plasma glucose levels and serum insulin.

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Serial Changes in Norepinephrine Kinetics Associated With Feeding Dogs a High Fat Diet

Serial Changes in Norepinephrine Kinetics Associated With Feeding Dogs a High Fat Diet

Unlike insulin resistance, the increase in BP that occurs with the high-fat diet did not correlate to the increase in sympathetic activity until the ani- mals had received 6 weeks of the diet (Figure 2). This observation is also consistent with our knowl- edge of BP regulation in this animal model of obes- ity. We and others have demonstrated that the hypertension associated with feeding dogs a high- fat diet is due to chronic sodium retention. 26,30 We also know that the SNS is involved in the hyperten- sion based on both pharmacologic studies 32,33 as

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Stimulation of Adipose Tissue Lipoprotein Lipase Activity Improves Glucose Metabolism and Increases High Density Lipoprotein Cholesterol in the Spontaneously Hypertensive Stroke-Prone Rat

Stimulation of Adipose Tissue Lipoprotein Lipase Activity Improves Glucose Metabolism and Increases High Density Lipoprotein Cholesterol in the Spontaneously Hypertensive Stroke-Prone Rat

Insulin resistance syndrome (IRS), high blood pressure, elevated blood glucose and triacylglycerol-rich lipoproteins (TG-RL), as well as low levels of high-density lipoprotein (HDL-C) are disorders that combine to define metabolic syndrome (MetS). Metabolic syndrome is on the rise in the United States and is believed to be a powerful predictor of risk for diabetes and coronary events. Modulation of the activity of lipoprotein lipase (LPL) in MetS affects lipolysis of TG-RL, which has a direct correlation with the levels of plasma HDL-C. This study examined if increasing LPL activity by dietary means in a model for MetS leads to reduced IRS and increase in plasma HDL-C concentration. Ninety day-old Spontaneously Hypertensive Stroke-Prone male rats were originally fed lab chow diet for seven days. This was followed by feeding a fatty acid diet for 7 days containing one of the following: triolein (TO), trans fatty acids-rich (TFA, margarine) and 0 fatty acids (Control) with /without an LPL-rising drug (NO-1866) by gavages (5 mg or 25 mg/kg b. wt.). The results show that blood glucose and triacylglycerol levels were decreased with NO-1886. HDL-C levels increased with NO-1866 in the control and triolein group but not in the TFA group. Animals in the triolein group had higher levels of phospholipids and lower levels of insulin. Inclusion of NO-1866 lowered HOMA- IR by almost 40% in the control and the TFA group, but no further reduction was observed in the TO group. The control TFA groups had up to 45% higher HOMA-IR than the TO group. Overall the data suggest that raising the activity of lipoprotein lipase by dietary means, including the feeding of monounsaturated fat may increase HDL-C, reduce plasma triacylglycerol and other indices of MetS risk, and thus may decrease the incidence of vascular complications through the normalization of lipid metabolism in subjects with MetS.

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Effect of Melatonin and Time Restricted Feeding In The Diabetic Rats

Effect of Melatonin and Time Restricted Feeding In The Diabetic Rats

In this review we focus on two particular approaches to resetting glucose level rhythm city in the context of restricted feeding (TRF; access to food is restricted for specific time intervals during the day without calorie restrictions) and melatonin, it’s a hormone produced predominantly in the pineal gland. Its release is triggered by the loss of light exposure to the retina. Hence, melatonin indicates the time of day, or ambient light, to various organs and tissues in the bodyit is hereby a ‘‘Zeitgeber,’’ entraining circadian rhythm. Indeed, control of circadian rhythm at several levels, including the pancreatic β cellexplore the possibility of pursuing circadian realignment via nutritionally inspired interventions Therefore understanding the health-promoting roles of regulating (i.e., restoring) circadian rhythms, thus suppressing harmful effects of circadian deregulations, would likely improve treatment. This review study the effects of time restricted feeding and how it affects the secretion of melatonin, which in turn improves the secretion of insulin in diabetic mice in high- fat diets, with studying many aspects and their effect on the production of melatonin such as light, dark, temperature and interference with met form in and time restriction feeding it has been argued that studies are warranted to determine whether there is any use in restoring circadian rhythms in diabetic patients, what therapeutic goals should be targeted, and how these could be achieved.

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Effect of Melatonin and Time Restricted Feeding in the Diabetic Rats

Effect of Melatonin and Time Restricted Feeding in the Diabetic Rats

Restricted feeding (TRF) is essentially imposing rhythms on nutrient availability. Entrainment by TRF has generated significant interest due to the possibility of synchronizing peripheral clocks without clear influences on (or from) the central pacemaker (SCN) .It has been speculated that restricted feeding (RF) entrains rhythms in peripheral tissues (liver and lung) 48 is likely independent of the SCN. These works challenge the basic hierarchical paradigm that light entrains the SCN which subsequently entrains the peripheral clocks and emphasized the role of RF as an entraining signal. The hypothesis of independently entrained peripheral clocks has been further reinforced by the observation that even lesions in brain nuclei do not eliminate food anticipatory activity, thus pointing to likelihood of a distributed system maintaining and regulating food-anticipatory activities 49,50 . One of the main justifications is that when food accessibility adopts specific rhythmic characteristics so will the physiology and behavior to match nutritional resource availability. It has been shown that feeding mice during the day completely reverses the phase of circadian oscillators (specifically, four clock components, Per1, Per2, Per3, Cry1 ; and the two circadian transcription factors DBP and Rev- erb α) in multiple peripheral cells (liver, kidney, heart and pancreas), but has little if any effect on the

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Egg quality, fatty acid composition and immunoglobulin Y content in eggs from laying hens fed full fat camelina or flax seed

Egg quality, fatty acid composition and immunoglobulin Y content in eggs from laying hens fed full fat camelina or flax seed

Camelina sativa or “false flax” or “wild flax” is an oilseed crop of the Brassica (Cruciferae) family that contains high levels of n-3 fatty acids [10, 11]. Although camelina has been cultivated since the Bronze Age, there is renewed interest in camelina as a feedstock for bio-fuel production. Investigations on the nutritional value in poultry feeding such as metabolizable energy [12, 13], di- gestibility [13, 14], egg and meat n-3 enriching [14–16] and antioxidant properties [17] of camelina coproducts (e.g. meal, cake) have been documented. However, no in- formation is available on n-3 fatty acid enriching and immune-related effects of feeding full fat seeds of came- lina in poultry. Considering the high demand of flax for human health-food uses, finding alternate sources of n-3 fatty acid-rich feeds will reduce production costs and will provide n-3 PUFA-enriched foods for human con- sumption. In this context, the objectives of the current study were to investigate the effect of feeding full fat camelina seeds to laying hens on egg quality, lipid and fatty acid composition, and egg production, during a 4 mo period of feeding trial. It was hypothesized that feeding camelina seeds will enhance n-3 fatty acid in- corporation in eggs without affecting egg quality or hen production aspects. In addition, egg immunoglobulin Y (IgY) content was also determined, as our previous stud- ies have shown that feeding linseed or fish oil rich in n-3 fatty acids led to significant increase in egg yolk IgY [18]. Chicken egg has been extensively studied as an im- portant source of commercial antibodies and investiga- tions on hen diet modulation to produce IgY may provide novel value-added nutraceuticals from eggs.

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The NuGO proof of principle study package: a collaborative research effort of the European Nutrigenomics Organisation

The NuGO proof of principle study package: a collaborative research effort of the European Nutrigenomics Organisation

also amino acid metabolism (5) are insulin-dependent and change during a decline of tissue insulin sensitivity, another aim of PPS3 is to assess whether changes in plasma amino acid levels or patterns can serve as biomarkers of insulin resistance. LC-MS/MS will be applied to quantify 45 amino acids and derivatives in plasma samples collected every second week from animals fed the 10 or the 45% energy from fat diets over the 12-week period. Another study arm embedded into PPS3 is comprised of a leptin challenge (coordinated by B.deR. and L.M.W.). In this study we perform transcriptomic analysis of the hypothalamus, pro- teomic analysis histochemical analysis of hepatic cells in mice fed 10 or 45% energy from fat for 1 or 4 weeks, with or without an acute leptin challenge. This will allow us to assess, at the tissue level, changes in leptin sensitivity and alterations that are central to satiety and metabolic control [1, 5]. Such changes will be related to plasma leptin and glucose levels.

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A Brief Overview of Resting Energy Expenditure and It’s Predictive Equations

A Brief Overview of Resting Energy Expenditure and It’s Predictive Equations

The REE is the energy necessary to run the basic process of the body such as the energy to maintain electrochemical gradients, generate heat and synthesize proteins required by body cell to maintain post absorptive homeostatic functions in resting subjects. REE is also used routinely by clinicians for estimation of energy requirements in patients care as well as by governmental agencies and health organizations in defining population energy requirement and it accounts for approximately 60% to 70% of the TEE [4,5,7]. A minor change in REE could lead to a significant energy imbalance and a huge change of body weight over a long period and REE decreases with muscle wasting, not losing fat alone [8]. For an average adult, the REE is fairly close to 1 kcal/kg body weight/hr or about 1,680 kcal/day for an individual weighing 70kg(5). Weight-controlling can be supported by

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Effect of fish oil intake on glucose levels in rat prefrontal cortex, as measured by microdialysis

Effect of fish oil intake on glucose levels in rat prefrontal cortex, as measured by microdialysis

Unlike the prefrontal cortex, the hypothalamus has been largely studied with respect to the mechanisms of glucose interaction with neurons. In this region, glucose-inhibited and glucose-excited neurons have been characterized, both types displaying abnormal response to glucose varia- tions in obese rats. Particularly in the medial hypothal- amus, increment of glucose levels has been shown to decrease firing rate of NPY-expressing glucose-inhibited neurons while increasing that of POMC-expressing neu- rons, thus leading to feeding inhibition [13,50-52]. Thus, failure of i.c.v. glucose to consistently inhibit feeding in the fish-oil group could rely on impaired glucose action on these neurons. This notion is compatible with the demonstration that glucose transporter 2 null mice be- came hyperphagic, had disrupted hypothalamic neuropep- tides expression, and failed to respond with hypophagia to either i.c.v. or intraperitoneal glucose [53].

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Exploring the fat mass and fat free mass of term and moderate to late preterm infants : an observational study : a thesis presented in partial fulfilment of the requirements for the degree of Master of Science in Nutrition and Dietetics at Massey Universi

Exploring the fat mass and fat free mass of term and moderate to late preterm infants : an observational study : a thesis presented in partial fulfilment of the requirements for the degree of Master of Science in Nutrition and Dietetics at Massey University, Albany, New Zealand

Table 2.1: Studies that have Used ADP to Determine % FM of Full Term Infants at Birth...........22 Table 2.2: Studies that have Used ADP to Determine % FM of Preterm Infants at Birth and/or During the Period until Term-Corrected Age (TCA)......................................................................28 Table 4.1: Characteristics of Infants............................................................................................45 Table 4.2: Anthropometric Outcomes of Male and Female Term Infants...................................46 Table 4.3: Characteristics at Birth of Preterm Infants Measured For the First Time within the First and Second Weeks after Birth.............................................................................................47 Table 4.4: Anthropometric Outcomes of Preterm Infants Measured for the First Time within the First and Second Weeks after Birth.............................................................................................48 Table 4.5: Characteristics at Birth of Preterm Infants Measured at ≥ 36 weeks’ Postmenstrual Age and Term Infants..................................................................................................................49 Table 4.6: Anthropometric Outcomes of Preterm Infants at ≥ 36 weeks’ Postmenstrual Age Compared to Term Infants after Birth.........................................................................................50 Table 4.7: Change in Anthropometric Parameters between First and Second Measurements...51 Table 4.8: Description of Preterm Infants at Birth According to Feeding Group.........................52 Table 4.9: Anthropometric Measurements of Preterm Infants at the First Measurement

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Input rich Writing Tasks and Student Writing on an English Language Proficiency Test

Input rich Writing Tasks and Student Writing on an English Language Proficiency Test

weight and other proxies of adiposity do not accurately capture body fat content. 23 To better understand how nutrition modulates early patterns of adipose tissue deposition, numerous studies and meta-analyses have also investigated body composition differences among breastfed and formula-fed infants over the first year of life with methods ranging from anthropometry to a wide variety of in-vivo measurement techniques. 10,20,50-53 These studies have also employed a variety of outcome measures, the majority of which have been total body fat or percentage body fat. While these studies have not assessed the direct effect of diet on adipose tissue cellularity, a reported positive association between cell size, cell number, and percent body fat 31 provides insight into how these studies may translate at the cellular level. These studies do not, however, describe how feeding practices affect the distribution of adipose tissue deposition. As it is critical to assess both the amount and distribution of adipose tissue, literature describing site-specific differences in adiposity is more limited.

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The Influence of Feeding Regimen on the Composition of the Fat Pads  in the Bovine Digital Cushion

The Influence of Feeding Regimen on the Composition of the Fat Pads in the Bovine Digital Cushion

The aim of the present study was to investigate the influence of 2 different feeding regimens on lipids of the fat pads of the digital cushion in beef cattle and to compare the results with the effects on subcutaneous fat. Moreover, it is known that the pressure distribution under the claw strongly varies and that certain areas of the claw are more prone to lesions [13]. The trial therefore should also clarify if feeding regimen influences lipid composition in the various locations within the claw and/or the front and hind claws differently. The results should be compared with findings of digital pads and subcutaneous fat of dairy cows.

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