Increased Body Fat Content Research Articles

EATING BEHAVIOUR OF VERY PRETERM BABIES AT DISCHARGE FROM NICU: AN OBSERVATIONAL STUDY UTILIZING THE BABY EATING BEHAVIOUR QUESTIONNAIRE

Background: Early nutritional learning, including the development of appetite and satiety behaviour, relates to the long-term risk of obesity. Premature infants have an increased body fat content at term-corrected and a long-term risk of cardiovascular disease. This may be attributed to suboptimal nutrition, however, specific feeding behaviour learned in the Neonatal Intensive Care Unit (NICU) environment may contribute. This study assesses eating behaviour, reported by parents, of very preterm infants at discharge and correlates these results to weight and age characteristics. Methods: Parents of infants with a gestational age (GA) of <29 weeks and/or <1250 grams completed the Baby Eating Behaviour Questionnaire (BEBQ) at discharge home. Anthropometric and clinical data were collected from bedside charts. Results: Thirty infants with a GA at birth of 27.4 ± 2.12 weeks (mean ± SD) were assessed at a GA of 40.7 ± 3.7 weeks. BEBQ values were (mean ± SD): enjoyment of food: 4.38 ± 0.54; food responsiveness: 2.13 ± 0.63; general appetite: 3.76 ± 1.02; slowness in eating: 2.92 ± 0.76; and satiety responsiveness: 2.54 ± 0.73. There was a negative correlation between general appetite scores and change in weight z-scores from birth to discharge. Conclusion: This is the first study to date that applies the BEBQ to preterm infants and in real time. Results are in line with previously published results. Correlation analysis shows higher general appetite scores in infants with slower weight gain. A longitudinal follow up of growth parameters and the BEBQ is planned at 2 years.

Crowding of Drosophila larvae affects lifespan and other life-history traits via reduced availability of dietary yeast.

Conditions experienced during development have often long-lasting effects persisting into adulthood. In Drosophila, it is well-documented that larval crowding influences fitness-related traits such as body size, starvation resistance and lifespan. However, the underlying mechanism of this phenomenon is not well understood. Here, we show that the effects of increased larval density on life-history traits can be explained by decreased yeast availability in the diet during development. Yeast-poor larval diet alters various life-history traits and mimics the effects of larval crowding. In particular, reduced amount of yeast in larval diet prolongs developmental time, reduces body size, increases body fat content and starvation resistance, and prolongs Drosophila lifespan. Conversely, the effects of larval crowding can be rescued by increasing the concentration of the dietary yeast in the diet during development. Altogether, our results show that the well-known effects of larval crowding on life-history traits are mainly caused by the reduced availability of dietary yeasts due to increased larval competition.

Risk of Obesity-Related Cardiometabolic Complications in Special Populations: A Crisis in Asians

The prospect of a significant increase in global health-related costs associated with high cardiometabolic complications of obesity in Asians has encouraged more attention to be focused on the problem of growing obesity prevalence in these populations. Although these studies have shown that cardiometabolic complications occur more frequently and at a lower body mass index (BMI) in Asians than in European populations, the mechanisms involved have yet to be discovered. Ethnic/racial differences in body composition and fat distribution have been studied extensively. Although these studies have shown that increasing BMI is associated with larger increases in body fat content in Asians, growing evidence points to factors other than body fat content and fat distribution indetermining a higher prevalence of cardiometabolic complications in these populations. Here, we provide support to our view that earlier onset of adipocyte maturation arrest/insulin resistance during weight gain could be a major factor in increasing the cardiometabolic risk of Asian populations at a lower BMI.

Differential Effects of Dietary Fat Content and Protein Source on Bone Phenotype and Fatty Acid Oxidation in Female C57Bl/6 Mice.

BackgroundGlycomacropeptide (GMP) is a 64-amino acid glycophosphopeptide released from κ-casein during cheesemaking that promotes satiety, reduces body fat, increases bone mass and infers prebiotic and anti-inflammatory effects. The impact of adiposity and gender on bone health is unclear.ObjectiveTo determine how feeding female mice diets providing 60% Fat Kcal (high-fat) or 13% Fat Kcal (control) with either GMP or casein as the protein source impacts: body composition, ex vivo fatty acid oxidation, bone (femoral) biomechanical performance, and the relationship between body composition and bone.MethodsWeanling female C57Bl/6 mice were fed high-fat (60% Fat Kcal) or control diets (13% Fat Kcal) with GMP or casein from 3 to 32 weeks of age with assessment of body weight and food intake. Body composition was assessed by dual-energy X-ray absorptiometry (DXA). Fatty acid oxidation was measured in liver, muscle, and fat tissues using 14C-palmitate. Plasma concentrations of hormones and cytokines were determined. Bone biomechanical performance was assessed by the 3-point bending test.ResultsFemale mice fed high-fat diets showed increased fatty acid oxidation capacity in both gastrocnemius muscle and brown adipose tissue compared to mice fed the control diets with a lower fat content. Despite increased fat mass in mice fed the high-fat diets, there was little evidence of glucose impairment or inflammation. Mice fed the high-fat diets had significantly greater total body bone mineral density (BMD), femoral BMD, and femoral cross-sectional area than mice fed the control diets. Femora of mice fed the high-fat diets had increased yield load and maximum load before fracture, consistent with greater bone strength, but reduced post-yield displacement or ductility, consistent with bone brittleness. Female mice fed a high-fat GMP diet displayed increased fat oxidation capacity in subcutaneous fat relative to mice fed the high-fat casein diet. Regardless of dietary fat content, GMP increased total body bone mineral content and femur length. The prebiotic properties of GMP may mediate the beneficial effects of GMP on bone.ConclusionsFemale mice adapt to high-fat feeding by increasing oxidative capacity in muscle tissue and to a lesser extent brown adipose tissue. High-fat feeding in female mice leads to development of a bone phenotype where femora show increased BMD and are stronger, yet more brittle. The increased brittleness of bone was associated with increased body fat content due to high-fat feeding. In summary, high-fat feeding in female mice increases mineralization of bone, but negatively impacts bone quality resulting in brittle bones.

The endocannabinoid anandamide during lactation increases body fat content and CB1 receptor levels in mice adipose tissue.

Type 1 cannabinoid receptors (CB1R) modulate energy balance; thus, their premature activation may result in altered physiology of tissues involved in such a function. Activation of CB1R mainly occurs after binding to the endocannabinoid Anandamide (AEA). The objective of this study was to evaluate the effects of AEA treatment during lactation on epididymal and body fat content, in addition to CB1R protein level at weaning. With this purpose, male mice pups were orally treated with AEA (20 μg g−1 body weight) or vehicle during lactation. Mice (21 days old) were killed and epididymal fat was extracted to evaluate its amount, adipocyte size and CB1R protein levels by western blot analysis. Total body fat percentage was also evaluated. Anandamide-treated mice showed an increased body fat content at 21 and 150 days of age. Moreover, epididymal adipose tissue amount, adipocyte size and CB1R protein levels were higher in the AEA-treated group. This in vivo study shows for the first time that a progressive increase in body fat accumulation can be programmed in early stages of life by oral treatment with the endocannabinoid AEA, a fact associated with an increased amount of epididymal fat pads and a higher expression of CB1R in this tissue.

Hepatic SirT1-Dependent Gain of Function of Stearoyl-CoA Desaturase-1 Conveys Dysmetabolic and Tumor Progression Functions.

Obesity is associated with higher incidence of cancer, but the predisposing mechanisms remain poorly understood. The NAD(+)-dependent deacetylase SirT1 orchestrates metabolism, cellular survival, and growth. However, there is no unifying mechanism to explain the metabolic and tumor-related effects of SirT1. In this work, we demonstrate that genetic ablation of the endogenous inhibitor of SirT1, Deleted-in-Breast-Cancer-1 (Dbc1), unexpectedly results in obesity and insulin resistance. Dbc1 deficiency promoted SirT1-dependent gain of function of stearoyl-coenzyme A desaturase 1 (Scd1), increasing plasma and tissue levels of unsaturated fatty acids. The metabolic abnormalities in Dbc1(-/-) mice were reversed by ablation of hepatic SirT1 or by inhibition of Scd1 activity. Furthermore, loss of Dbc1 impaired activation of the master tumor suppressor p53 and treatment with an Scd1 inhibitor extended survival of tumor-prone TP53(-/-) mice by decreasing tumor-related death. Together, our findings illustrate a shared mechanism of obesity and tumor progression mediated by hepatic SirT1 and resulting in the activation of a key lipid synthetic enzyme, with potential therapeutic implications.

Gender differences in the effect of cardiovascular drugs: a position document of the Working Group on Pharmacology and Drug Therapy of the ESC.

Cardiovascular (CV) disease is the leading cause of morbidity and mortality in both sexes in developed countries, but gender differences exists in its diagnosis and treatment. Figure 1 Gender differences in absorption and distribution and excretion of drugs responsible for gender differences in pharmacokinetic and pharmacodynamic actions. Since the number of women included in CV studies has often been low, most recommendations in women have often been inferred from effects observed in men.1 This position paper discusses the gaps in knowledge on the effects of gender on pharmacokinetics (PK) and pharmacodynamics (PD) of CV drugs. ### Differences in pharmacokinetics/pharmacodynamics Gender-related differences in PK may arise from differences in body composition, plasma protein binding, metabolizing enzymes and transporters, excretion activity, and/or physiological hormonal changes ( Figure 1 ).2,3 Oral drug absorption is influenced by gastric acid secretion and emptying time, gastrointestinal blood flow and surface area, gut and hepatic metabolism.2,3 Although gender differences in these mechanisms exist, they do not significantly affect drug absorption between the two sexes.2,3 Drug distribution depends on body composition, plasma volume, blood flow, and tissue and plasma protein binding. Women have higher per cent of body fat and lower body weight, plasma volume, and organ blood flow. Increased body fat content explains the faster onset and prolonged duration of action and higher volume of distribution (Vd) of lipophilic drugs, while the Vd of hydrophilic drugs is smaller, producing higher initial plasma levels and greater effects when compared with males.3–5 Plasma and tissue drug concentrations depend on the Vd and clearance (Cl). Exogenous sex hormones increase serum-binding globulins levels.2–5 This effect may be …

Effects of raw milk and starter feed on intake and body composition of Holstein × Gyr male calves up to 64 days of age

The objective was to evaluate the effect of supplying different levels of raw milk, alone or in combination, with access to a starter feed, on the intake, digestibility, daily gain, N balance, and body composition of Holstein × Gyr crossbred suckling calves until 64 d of age. Thirty-nine male calves aged 4 d with an average initial live weight of 36±1.0 kg were used. Five calves were defined as a reference group and slaughtered at 4 d of age to estimate the initial body composition of the animals. The other calves were distributed according to a completely randomized design in a 3×2 factorial arrangement consisting of 3 levels of milk (2, 4, or 8 L/d) and 2 levels of starter feed (presence or absence in diet). At 15 and 45 d of age, 4 animals from each treatment were subjected to digestibility trials with total collection of feces and urine and sampling of feeds. At 64 d of age, all animals were slaughtered and their body tissues were sampled for analyses. Total dry matter and nutrient intake increased linearly and starter intake decreased linearly in response to the supply of increasing amounts of milk. The digestibility coefficient of organic matter was not affected by the inclusion of starter feed and increased linearly as milk supply was elevated. Daily gain was greater at increased milk supply levels and also greater when starter was supplied, without any interaction between milk supply level and the presence or absence of starter. Fecal N excretion and N retention were higher in the animals fed starter feed. Fecal N excretion was not affected by milk levels, whereas N retention was affected. Body protein and ash contents decreased linearly according to increased milk allowance. In contrast, fat body content increased linearly according to milk supply. The presence of starter feed in the diet was responsible for the increased body fat content, but had no effect on protein or ash content. In conclusion, weight gain and N retention in calves up to 64 d of age increased with milk supply. Ad libitum access to starter further increased weight gain and N retention and no interaction with milk allowance level occurred. However, greater levels of milk are also associated with reduced starter feed intake, in addition to increased body fat content.

Gooey stuff, intra-activity, and differential obesities: Foregrounding agential adiposity within childhood obesity stories

In Canada, forces such as the media, medical discourse, and public policy work to position childhood obesity as increased body fat content or excess adiposity due to various personal, social, and economic factors. Drawing on Barad’s ‘agential realist ontology’, this article aims to inhabit-with obesity in an effort to disrupt dominant understandings of childhood obesity, as illustrated in images from three children’s picture books. By troubling the positivity inherent in dominant understandings of obesity, in which obesity is a knowable entity that refers to an anatomical body with excess adiposity, we might instead foreground the matterings of the human body at play amid the dynamic intra-actions of agential matter. This article will imagine how novel orientations toward childhood obesity might be made possible if we populate the adiposity of obese bodies such that we might engage with the intra-activity of agential adiposity.

Aerobic training prevents the impaired vascular reactivity of fructose‐treated rats (1106.22)

Fructose intake is associated with cardiometabolic disorders, but few studies investigated its role on vascular reactivity and the potential effects of exercise training. Thus, we assessed the effect of fructose intake on vascular reactivity in trained rats. Therefore male Wistar rats (n=7/group) received tap water (control group, C) or Fructose 10% (F group) ad libitum for two weeks. Then, rats underwent treadmill exercise for eight weeks (FT group). Caloric intake was higher in fructose groups compared with C group (P&lt;0.01), although we found no change in body weight and in lipid profile, except the higher HDL in FT group (P&lt;0.01). Training increased serum NO (C=296.5±42.8; F=325.8±51.6; FT=718.4±151.2; P&lt;0.01). Regarding body composition, F increased body fat content compared with C and FT groups (P=0.03), whereas the FT group showed higher protein content (P&lt;0.01). Finally, vascular vasoconstrictor reactivity was increased by fructose since F group required lower concentrations of phenylephrine to promote 50% of the maximum contractile effect when compared to C and FT groups (C=1.31‐6±2.4‐7; F=2.43‐7±6.5‐8; FT= 7.99‐7±1.5‐7 M; P&lt;0,01). Vasodilator response to acetylcholine was also impaired in F group and was preserved by exercise training (C= 3.13‐7±1.9‐7; F=3.64‐6±9.6‐7; FT=3.13‐7±1.9‐7M; P&lt;0.01). Thus, aerobic exercise prevented fructose‐impaired vascular reactivity in rats.Grant Funding Source: CNPq, FAPERJ, CAPES, FINEP

Interruption of ghrelin signaling in the PVN increases high-fat diet intake and body weight in stressed and non-stressed C57BL6J male mice

Chronic social stress has been associated with increased caloric intake and adiposity. These effects have been linked to stress induced changes in the secretion of ghrelin, a hormone that targets a number of brain regions to increase food intake and energy expenditure and promote increased body fat content. One of the brain sites targeted by ghrelin is the hypothalamic paraventricular nucleus (PVN), a region critical for both the regulation of the stress response and the regulation of energy balance. Given these data, we examined the contribution of ghrelin receptors in the PVN to the metabolic and behavioral changes that are seen during chronic social stress in mice. To do this, mice were implanted with cannulae attached to osmotic minipumps and delivering either vehicle or the ghrelin receptor (growth hormone secretagogue receptor) antagonist [D-Lys-3]-GHRP-6 (20 nmol/day/mouse). Following a week of recovery, half of the animals in each group were exposed to chronic social defeat stress for a period of 3 weeks whereas the other half were left undisturbed. During this time, all animals were given ad libitum access to standard laboratory chow and presented a high-fat diet for 4 h during the day. Results showed that the ghrelin receptor antagonism did not decrease stressed induced caloric intake, but paradoxically increased the intake of the high fat diet. This would suggest that ghrelin acts on the PVN to promote the intake of carbohydrate rich diets while decreasing fat intake and blockade of ghrelin receptors in the PVN leads to more consumption of foods that are high in fat.

Leptin-induced increase in body fat content of rats

We previously reported that peripheral leptin infusions in chronically decrebrate rats, in which the forebrain is neurally isolated from the hindbrain, increased body fat and decreased energy expenditure. Any central leptin response in decerebrate rats would depend upon the hindbrain. Here, we tested whether selective activation of hindbrain leptin receptors increased body fat. Fourth ventricle infusion of 0.6 μg leptin/day for 12 days increased body fat by 13% with no increase in food intake. Third ventricle leptin infusions decreased food intake, body fat, and lean tissue with a maximal response at 0.3 μg leptin/day. To test whether hindbrain receptors opposed activity of hypothalamic receptors, rats received peripheral infusions of 40 μg leptin/day and increasing 4th ventricle doses of the leptin receptor antagonist mutein protein. Mutein (3.0 μg/day) reduced body fat in PBS-infused rats to the same level as leptin-infused rats and reduced lean tissue in all rats. Leptin, but not mutein, inhibited food intake. By contrast, 3.0 μg/day mutein in the 3rd ventricle increased food intake and body fat in both PBS- and leptin-infused rats. In basal conditions, hindbrain leptin receptors may antagonize activity of forebrain receptors to protect lean and fat tissue, but there is no evidence for an anabolic role for hindbrain receptors when leptin is elevated. In a dietary study, rats increased energy intake when offered lard and 30% sucrose solution in addition to chow. Peripheral leptin infusion exaggerated the gain in body fat without altering energy intake confirming the potential for leptin to increase adiposity.

Male mice that lack the G-protein-coupled receptor GPR41 have low energy expenditure and increased body fat content

SCFA are produced in the gut by bacterial fermentation of undigested carbohydrates. Activation of the Gαi-protein-coupled receptor GPR41 by SCFA in β-cells and sympathetic ganglia inhibits insulin secretion and increases sympathetic outflow, respectively. A possible role in stimulating leptin secretion by adipocytes is disputed. In the present study, we investigated energy balance and glucose homoeostasis in GPR41 knockout mice fed on a standard low-fat or a high-fat diet. When fed on the low-fat diet, body fat mass was raised and glucose tolerance was impaired in male but not female knockout mice compared to wild-type mice. Soleus muscle and heart weights were reduced in the male mice, but total body lean mass was unchanged. When fed on the high-fat diet, body fat mass was raised in male but not female GPR41 knockout mice, but by no more in the males than when they were fed on the low-fat diet. Body lean mass and energy expenditure were reduced in male mice but not in female knockout mice. These results suggest that the absence of GPR41 increases body fat content in male mice. Gut-derived SCFA may raise energy expenditure and help to protect against obesity by activating GPR41.

Impact of the Gut Microbiota on the Development of Obesity: Current Concepts

Energy balance is an equilibrium between the amount of energy extracted from the diet and the amount expended. Selective pressures throughout evolution have programmed animals to protect energy stores through the accumulation of adipose tissue; as diets have changed and energy-dense foods have become readily available, obesity rather than malnutrition has become the primary concern in developed nations. Nevertheless, factors other than the types of food and their availability appear to be important. Recent evidence suggests that the gut microbiota play a role in energy harvest, storage, and expenditure. The preponderance of the evidence demonstrates that germ-free mice are protected against obesity and that the transfer of gut microbes from conventionally raised animals results in dramatic increases in body fat content and insulin resistance. Moreover, the composition of the gut microbiota has been shown to differ in lean and obese humans and animals and to change rapidly in response to dietary factors. The gut microbiota may also influence the development of conditions characterized by low-level inflammation, such as obesity and type 2 diabetes, through systemic exposure to bacterial lipopolysaccharide derived from the intestinal microbiota. Together, these data suggest that modification of the gut microbiota may be a relevant therapeutic avenue for obesity and other metabolic disorders.

Left Ventricular Function Impairment in Patients With Normal-Weight Obesity

Background— Obesity predisposes to left ventricular (LV) dysfunction and heart failure; however, the risk of these complications has not been assessed in patients with a normal body mass index (BMI) but increased body fat content (normal-weight obesity, NWO). We hypothesized that LV performance in NWO may be impaired and sought to investigate potential contributors to cardiac functional abnormalities. Methods and Results— One hundred sixty-eight subjects (age, 38±7 years) with BMI &lt;25kg/m 2 and no history of any disease affecting the myocardium were classified on the basis of body fat content into 2 groups: with NWO and without NWO. Echocardiographic indices of LV systolic and diastolic function, including myocardial velocities and deformation, serological fibrosis markers, indicators of proinflammatory activation, and metabolic control, were evaluated. Subjects with NWO demonstrated impaired LV systolic and diastolic function, increased fibrosis intensity (assessed by procollagen type I carboxy-terminal propeptide [PICP]), impaired insulin sensitivity, and increased proinflammatory activation as compared with individuals with normal body fat. The independent correlates of LV systolic and diastolic function variables were as follows: for strain, IL-18 (β=−0.17, P &lt;0.006), C-reactive protein (β=−0.20, P &lt;0.002) and abdominal fat deposit (β=−0.20, P &lt;0.003); for tissue S velocity, PICP (β=−0.21, P &lt;0.002) and abdominal fat deposit (β=−0.43, P &lt;0.0001); for tissue E velocity, abdominal fat deposit (β=−0.30, P &lt;0.0001), PICP (β=−0.31, P &lt;0.0001) and homeostasis model assessment of insulin resistance index (HOMA IR; β=−0.20, P &lt;0.002); and for E/e′-PICP, IL-18 (both β=0.18, P &lt;0.01) and HOMA IR (β=0.16, P &lt;0.04). Conclusions— In patients with NWO, subclinical disturbances of LV function are independently associated with the extent of abdominal fat deposit, profibrotic state (as reflected by circulating PICP), reduced insulin sensitivity, and proinflammatory activation.

Adipocyte Maturation Arrest: A Determinant of Systemic Insulin Resistance to Glucose Disposal

Adipocyte Maturation Arrest: A Determinant of Systemic Insulin Resistance to Glucose Disposal

Cystathionine Beta-Synthase Deficiency Causes Fat Loss in Mice

Cystathionine beta synthase (CBS) is the rate-limiting enzyme responsible for the de novo synthesis of cysteine. Patients with CBS deficiency have greatly elevated plasma total homocysteine (tHcy), decreased levels of plasma total cysteine (tCys), and often a marfanoid appearance characterized by thinness and low body-mass index (BMI). Here, we characterize the growth and body mass characteristics of CBS deficient TgI278T Cbs−/− mice and show that these animals have significantly decreased fat mass and tCys compared to heterozygous sibling mice. The decrease in fat mass is accompanied by a 34% decrease in liver glutathione (GSH) along with a significant decrease in liver mRNA and protein for the critical fat biosynthesizing enzyme Stearoyl CoA desaturase-1 (Scd-1). Because plasma tCys has been positively associated with fat mass in humans, we tested the hypothesis that decreased tCys in TgI278T Cbs−/− mice was the cause of the lean phenotype by placing the animals on water supplemented with N-acetyl cysteine (NAC) from birth to 240 days of age. Although NAC treatment in TgI278T Cbs−/− mice caused significant increase in serum tCys and liver GSH, there was no increase in body fat content or in liver Scd-1 levels. Our results show that lack of CBS activity causes loss of fat mass, and that this effect appears to be independent of low serum tCys.

Increased body fat content and waist circumference in healthy individuals with a family history of type 2 diabetes supports co-inheritance of susceptibilities to weight gain and type 2 diabetes

Increased body fat content and waist circumference in healthy individuals with a family history of type 2 diabetes supports co-inheritance of susceptibilities to weight gain and type 2 diabetes

Cats during gestation and lactation fed with canned food ad libitum: energy and protein intake, development of body weight and body composition

The NRC recommendations for cats for energy and protein supply during gestation and lactation are based on limited data. This study aimed to answer the question: Can the energy requirement be met with canned food or is the volume restrictive? Therefore, balance trials were conducted in 10 queens before mating, during the 4th and 7th week of gestation and during the 2nd and 6th week of lactation. The cats were fed with canned food ad libitum. Additionally, the body composition of the queens was measured by dual-energy X-ray absorptiometry (Dexa) before mating, after parturition and after weaning. Eight of 10 cats presented increased body fat content and lean body mass during gestation. The weight loss during lactation led to a loss of lean body mass, but only six cats lost body fat of widely differing amounts. It was evident that the queens' dry matter intake was consistent with that of queens fed ad libitum with dry food. The cats lost lean body mass during lactation and had negative protein balances in the 2nd week of lactation. This seems to be physiological in early lactation. Nevertheless, the protein recommendations for lactation seem to be too low.

MicroRNA links obesity and impaired glucose metabolism

MicroRNA links obesity and impaired glucose metabolism