Adult Female Rats Defend “Appropriate” Energy Intake after Adaptation to Dietary Energy

Objective: To determine if adult female rats adapt to lower and higher dietary energy density. Research Methods and Procedures: Study 1 compared high‐fat (56%), high‐energy density (HD) (21.6 kJ/g) and high‐fat (56%), low‐energy density (LD) (16.0 kJ/g) diets before surgery (two groups, 2 weeks, n = 16) and after surgery [ovariectomy (O) Sham (S); 2 × 2 factorial, n = 8; 6 weeks]. The second study (no surgery) compared high‐fat (60.0%), high‐energy (22.0 kJ/g) and low‐fat (10.0%), low‐energy (15.1 kJ/g) diets (n = 8). Results: In study 1, food intake was similar for the first 2 weeks, but rats on the LD diet consumed less energy, gained less weight, and had lower nonfasted serum leptin (all p < 0.0001) than rats on the HD diet. After surgery, rats on the LD and HD diets had similar weight gain, but rats on the LD diet consumed more food (p < 0.0001) and less energy (p < 0.009). O rats consumed more food and gained more weight (p < 0.0001) than S rats. Results from study 2 were similar to those from study 1. Discussion: The results demonstrated that O and S surgery rats and rats with no surgery adjust their food intake to defend a level of energy intake. This defense only occurred after a 2‐week adaptation period. The major differences in final body weights and abdominal fat resulted from the initial 2 weeks before adaptation to energy density. Rats fed higher‐energy diets seemed to “settle” at a higher level of adiposity, and rats fed lower‐energy diets consumed more food to increase energy consumption.     

Plasma Enterostatin: Identification and Release in Rats in Response to a Meal

Objective: To discover a possible absorption and/or secretion of enterostatin into the circulating blood, as well as to compare the levels of circulating enterostatin after high‐fat feeding and low‐fat feeding. Research Methods and Procedures: Using a specific enzyme‐linked immunosorbent assay, plasma enterostatin levels were determined after feeding a high‐fat, a high‐fat/‐sucrose, or a low‐fat meal to Sprague‐Dawley rats deprived of food overnight. Results: The enterostatin levels were increased by all diets; the response to the high‐fat and the high‐fat/‐sucrose meals was greater in magnitude and duration than that to the low‐fat meal. In addition, enterostatin levels correlated with the intake of dietary fat. Plasma enterostatin levels after high‐fat feeding were found to be similar to those after intravenous administration of exogenous enterostatin known to inhibit high‐fat food intake. Gel chromatography of pooled postprandial plasma extracts followed by high‐performance liquid chromatography analysis showed that plasma enterostatin was identical to synthetic enterostatin. Affinity cross‐linking of plasma proteins with ¹²⁵I‐enterostatin on sodium dodecyl sulfate‐polyacrylamide gel electrophoresis, followed by autoradiography, revealed a single band with a molecular weight of about 66 kDa, indicating the presence of a potential enterostatin‐binding protein in plasma. Discussion: The measurements of plasma enterostatin may be a sensitive indicator for the measurement of fat intake.     

Altered Hypothalamic Signaling and Responses to Food Deprivation in Rats Fed a Low‐Carbohydrate Diet

Objective: To model how consuming a low‐carbohydrate (LC) diet influences food intake and body weight. Research Methods and Procedures: Food intake and body weight were monitored in rats with access to chow (CH), LC‐high‐fat (HF), or HF diets. After 8 weeks, rats received intracerebroventricular injections of a melanocortin agonist (melanotan‐II) and antagonist (SHU9119), and feeding responses were measured. At sacrifice, plasma hormones and hypothalamic expression of mRNA for proopiomelanocortin (POMC), melanocortin‐4 receptor, neuropeptide Y (NPY), and agouti related protein (AgRP) were assessed. A second set of rats had access to diet (chow or LC‐HF) for 4 weeks followed by 24 h food deprivation on two occasions, after which food intake and hypothalamic POMC, NPY, and AgRP mRNA expression were measured. Results: HF rats consumed more food and gained more weight than rats on CH or LC‐HF diets. Despite similar intakes and weight gains, LC‐HF rats had increased adiposity relative to CH rats. LC‐HF rats were more sensitive to melanotan‐II and less sensitive to SHU9119. LC‐HF rats had increased plasma leptin and ghrelin levels and decreased insulin levels, and patterns of NPY and POMC mRNA expression were consistent with those of food‐deprived rats. LC‐HF rats did not show rebound hyperphagia after food deprivation, and levels NPY, POMC, and AgRP mRNA expression were not affected by deprivation. Discussion: Our results demonstrate that an LC diet influences multiple systems involved in the controls of food intake and body weight. These data also suggest that maintenance on an LC‐HF diet affects food intake by reducing compensatory responses to food deprivation.     

Oligofructose Promotes Satiety in Rats Fed a High‐Fat Diet: Involvement of Glucagon‐Like Peptide‐1

Objective: To analyze the putative interest of oligofructose (OFS) in the modulation of food intake after high‐fat diet in rats and to question the relevance of the expression and secretion of intestinal peptides in that context. Research Methods and Procedures: Male Wistar rats were pretreated with standard diet or OFS‐enriched (10%) standard diet for 35 days followed by 15 days of high‐fat diet enriched or not with OFS (10%) treatment. Body weight, food intake, triglycerides, and plasma ghrelin levels were monitored during the treatment. On day 50, rats were food‐deprived 8 hours and anesthetized for blood and intestinal tissue sampling for further proglucagon mRNA, glucagon‐like peptide (GLP)‐1, and GLP‐2 quantification. Results: The addition of OFS in the diet protects against the promotion of energy intake, body weight gain, fat mass development, and serum triglyceride accumulation induced by a high‐fat diet. OFS fermentation leads to an increase in proglucagon mRNA in the cecum and the colon and in GLP‐1 and GLP‐2 contents in the proximal colon, with consequences on the portal concentration of GLP‐1 (increase). A lower ghrelin level is observed only when OFS is added to the standard diet of rats. Discussion: In rats exposed to high‐fat diet, OFS is, thus, able to modulate endogenous production of gut peptides involved in appetite and body weight regulation. Because several approaches are currently used to treat type 2 diabetes and obesity with limited effectiveness, dietary fibers such as OFS, which promote the endogenous production of gut peptides like GLP‐1, could be proposed as interesting nutrients to consider in the management of fat intake and associated metabolic disorders.     

Leptin Expression in Hypothalamic PVN Reverses Dietary Obesity and Hyperinsulinemia but Stimulates Ghrelin*

Objective: In order to circumvent the multiple peripheral effects of hyperleptinemia and leptin resistance, the efficacy of leptin transgene expression in the hypothalamic paraventricular nucleus (PVN) to reinstate the central energy homeostasis in obesity was examined. Research Methods and Procedures: A recombinant adeno‐associated viral vector encoding either leptin (rAAV‐lep) or green fluorescent protein (rAAV‐GFP) was microinjected into the PVN of obesity‐prone rats consuming a high‐fat diet (HFD). Results: rAAV‐lep, and not rAAV‐GFP, microinjection significantly reduced energy intake and enhanced energy expenditure, thereby resulting in normalization of weight and blood levels of leptin, insulin, free fatty acids, and glucose concomitant with enhanced ghrelin secretion during the extended period of observation. Discussion: Thus, we show, for the first time, that amelioration of leptin insufficiency with enhanced localized leptin availability in the PVN alone can reverse dietary obesity and the attendant hyperinsulinemia and concurrently block the central stimulatory effects of elevated endogenous ghrelin on food intake and adiposity.     

A novel kinase regulates dietary restriction‐mediated longevity in Caenorhabditis elegans

Although dietary restriction (DR) is known to extend lifespan across species, from yeast to mammals, the signalling events downstream of food/nutrient perception are not well understood. In Caenorhabditis elegans, DR is typically attained either by using the eat‐2 mutants that have reduced pharyngeal pumping leading to lower food intake or by feeding diluted bacterial food to the worms. In this study, we show that knocking down a mammalian MEKK3‐like kinase gene, mekk‐3 in C. elegans, initiates a process similar to DR without compromising food intake. This DR‐like state results in upregulation of beta‐oxidation genes through the nuclear hormone receptor NHR‐49, a HNF‐4 homolog, resulting in depletion of stored fat. This metabolic shift leads to low levels of reactive oxygen species (ROS), potent oxidizing agents that damage macromolecules. Increased beta‐oxidation, in turn, induces the phase I and II xenobiotic detoxification genes, through PHA‐4/FOXA, NHR‐8 and aryl hydrocarbon receptor AHR‐1, possibly to purge lipophilic endotoxins generated during fatty acid catabolism. The coupling of a metabolic shift with endotoxin detoxification results in extreme longevity following mekk‐3 knock‐down. Thus, MEKK‐3 may function as an important nutrient sensor and signalling component within the organism that controls metabolism. Knocking down mekk‐3 may signal an imminent nutrient crisis that results in initiation of a DR‐like state, even when food is plentiful.     

Skeletal muscle adiposity is associated with serum lipid and lipoprotein levels in Afro‐Caribbean men

Objective: When compared with other ethnic groups, African ancestry individuals have lower triglycerides and higher High‐density lipoprotein cholesterol (HDL‐C) levels, although the mechanisms for these differences remain unclear. A comprehensive array of factors potentially related to fasting serum lipid and lipoprotein levels in African ancestry men was evaluated. Design and Methods: Men (1,821) underwent dual‐energy X‐ray absorptiometry measures of total body fat and quantitative computed tomography assessments of calf skeletal muscle adiposity [subcutaneous and intermuscular adipose tissue (AT), and muscle density as a measure of intra‐muscular AT]. Results: Multivariable linear regression analysis identified age (?), total body fat (+), subcutaneous AT (?), fasting glucose (+), fasting insulin (+), diastolic blood pressure (+), and non‐African ancestry (+) as independent correlates of triglycerides (all P < 0.05). Total body fat (+), intra‐muscular AT (?), and diastolic blood pressure (+) were independent correlates of Low‐density lipoprotein cholesterol (LDL‐C) (all P < 0.001). Age (+), waist circumference (?), fasting insulin (?), physical activity (+), and alcohol intake (+) were independent correlates of HDL‐C (all P < 0.05). Conclusions: A novel relationship between skeletal muscle adiposity and serum lipid and lipoprotein levels in African ancestry men, independent of total and central adiposity was illuminated. In African ancestry populations, genetic factors are likely a significant determinant of triglycerides levels.     

Fat Intake Affects Adiposity,Comorbidity Factors,and Energy Metabolism of Sprague‐Dawley Rats

Objective: Childhood obesity is an emerging health problem. This study assesses the effects of three levels of dietary fat (10%, 32%, and 45% measured by kilocalories) on weight gain, body composition, energy metabolism, and comorbidity factors in rats from weaning through maturation. Research Methods and Procedures: The role of dietary fat on the susceptibility to obesity was assessed by feeding diets containing three levels of dietary fat to rats from weaning through 7 months of age. Body composition was analyzed by DXA after 6 and 12 weeks of dietary treatment. Energy metabolism was measured by indirect calorimetry. Results: Energy intake, weight gain, fat mass, and plasma glucose, cholesterol, triglyceride, free fatty acid, leptin, and insulin levels increased dose‐dependently with increased dietary fat. No difference in absolute lean mass among the three groups was observed. Therefore, the differences in weight gain are accounted for primarily by increased fat accretion. Compared with rats that were relatively resistant to obesity when on a 45% fat diet, diet‐induced obesity‐prone rats were in positive energy balance and had an elevated respiratory quotient, indicating a switch in energy substrate use from fat to carbohydrate, which promotes body‐fat accretion. Discussion: Our data support the hypothesis that administration of increasing amount of dietary fat to very young rats enhances susceptibility to diet‐induced obesity and its comorbidities.     

Is Dietary Fat Intake Related to Liking or Household Availability of High‐ and Low‐Fat Foods?

Objectives : Despite the increasing availability of low‐ and reduced‐fat foods, Americans continue to consume more fat than recommended, which may be a contributing factor to the obesity epidemic. This investigation examined relationships between liking and household availability of high‐ and low‐fat foods and their association with dietary fat intake. Research Methods and Procedures : A food frequency questionnaire assessed percent calories from fat consumed over the past year in 85 men and 80 women. Participants reported their degree of liking 22 “high‐fat foods” (>45% calories from fat) and 22 “low‐fat foods” (<18% calories from fat), and the number and percentage (number of high‐ or low‐fat foods/total number of foods × 100) of these high‐ and low‐fat foods in their homes. Results : Hierarchical regression analyses examined the ability of liking and household availability of low‐ and high‐fat foods to predict percent dietary fat intake. After controlling for age, sex, and BMI, liking ratings for high‐ and low‐fat foods and the interaction of liking for low‐fat foods by the percentage of low‐fat foods in the household were significant predictors of percent dietary fat consumed. Greater liking of high‐fat foods and lower liking of low‐fat foods, both alone and combined with a lower percentage of low‐fat foods in the home, were predictive of higher dietary fat intake. Discussion : Interventions designed to reduce dietary fat intake should target both decreasing liking for high‐fat foods and increasing liking for low‐fat foods, along with increasing the proportion of low‐fat foods in the household.     

Effect of meta-chlorophenylpiperazine and cholecystokinin on food intake of Osborne-Mendel and S5B/P1 rats

Objective: To investigate whether there is a difference in sensitivity to a serotonin agonist, meta‐chlorophenylpiperazine (mCPP), or cholecystokinin (CCK‐8), an intestinal hormone that inhibits food intake, between the Osborne‐Mendel (OM) rat, which becomes obese eating a high‐fat diet, and the S5B/Pl (S5B) rat, which is resistant to dietary‐induced obesity. Research Methods and Procedures: OM and S5B rats were adapted to either a high‐saturated‐fat diet (56% energy as fat) or a low‐fat diet (10% energy as fat) or to both for 14 days and then treated with several doses of mCPP or CCK‐8. Results: Treatment with mCPP reduced food intake in both strains of rats. The dose‐response curve showed that the OM rats had an increased sensitivity to the serotonergic agonist. Animals eating the high‐fat diet had less response to mCPP; and in the S5B rats, the response was significantly reduced. After treatment with CCK‐8, there was a similar dose‐related suppression of food intake in both the OM and S5B rats. Discussion: These data are consistent with the hypothesis that the serotonin system in the S5B rat has a greater activity that could act to inhibit fat intake. The response to CCK was not significantly affected by strain or diet.     

Metabolic Implications of Dietary Trans‐fatty Acids

Dietary trans‐fatty acids are associated with increased risk of cardiovascular disease and have been implicated in the incidence of obesity and type 2 diabetes mellitus (T2DM). It is established that high‐fat saturated diets, relative to low‐fat diets, induce adiposity and whole‐body insulin resistance. Here, we test the hypothesis that markers of an obese, prediabetic state (fatty liver, visceral fat accumulation, insulin resistance) are also worsened with provision of a low‐fat diet containing elaidic acid (18:1t), the predominant trans‐fatty acid isomer found in the human food supply. Male 8‐week‐old Sprague–Dawley rats were fed a 10% trans‐fatty acid enriched (LF‐trans) diet for 8 weeks. At baseline, 3 and 6 weeks, in vivo magnetic resonance spectroscopy (¹H‐MR) assessed intramyocellular lipid (IMCL) and intrahepatic lipid (IHL) content. Euglycemic–hyperinsulinemic clamps (week 8) determined whole‐body and tissue‐specific insulin sensitivity followed by high‐resolution ex vivo ¹H‐NMR to assess tissue biochemistry. Rats fed the LF‐trans diet were in positive energy balance, largely explained by increased energy intake, and showed significantly increased visceral fat and liver lipid accumulation relative to the low‐fat control diet. Net glycogen synthesis was also increased in the LF‐trans group. A reduction in glucose disposal, independent of IMCL accumulation was observed in rats fed the LF‐trans diet, whereas in rats fed a 45% saturated fat (HF‐sat) diet, impaired glucose disposal corresponded to increased IMCL_TA. Neither diet induced an increase in IMCL_soleus. These findings imply that trans‐fatty acids may alter nutrient handling in liver, adipose tissue, and skeletal muscle and that the mechanism by which trans‐fatty acids induce insulin resistance differs from diets enriched with saturated fats.     

Chronic dietary vitamin A supplementation regulates obesity in an obese mutant WNIN/Ob rat model

Objective: To understand the possible role of chronic dietary high vitamin A supplementation in body weight regulation and obesity using a novel WNIN/Ob obese rat model developed at the National Centre for Laboratory Animal Sciences of National Institute of Nutrition, India. Research Methods and Procedures: Thirty‐six 7‐month‐old male rats of lean, carrier, and obese phenotypes were broadly divided into two groups; each group was subdivided into three subgroups consisting of six lean, six carrier, and six obese rats and received diets containing either 2.6 or 129 mg vitamin A/kg of diet for 2 months. Body weight gain, food intake, and weights of various organs were recorded. Adiposity index and BMI were calculated. Serum and liver retinol and brown adipose tissue (BAT)‐uncoupling protein1 (UCP1) mRNA expression levels were quantified. Results: Chronic feeding of high but non‐toxic doses of vitamin A through diet significantly reduced (P ≤ 0.05) body weight gain, adiposity index, and retroperitoneal white adipose tissue mass (without affecting food intake) in obese rats compared with their lean and carrier counterparts. In general, vitamin A treatment significantly improved hepatic retinol stores (P ≤ 0.05) in all phenotypes without affecting serum free retinol levels. However, augmented BAT‐UCP1 expression was observed only in carrier and obese rats (whose basal expression was low). Discussion: Our data suggest that chronic dietary vitamin A supplementation at high doses effectively regulates obesity in obese phenotype of the WNIN/Ob strain, possibly through up‐regulation of the BAT‐UCP1 gene and associated adipose tissue loss. However, in vitamin A‐supplemented lean and carrier rats, changes in adiposity could not be related to BAT‐UCP1 expression levels.     

Daily Oral Oleoyl‐Estrone Gavage Induces a Dose‐Dependent Loss of Fat in Wistar Rats

Objective: To establish whether single daily oral doses of oleoyl‐estrone result in dose‐dependent slimming effects on normal weight rats, and to determine the changes in energy parameters induced by this treatment. Research Methods and Procedures: The effects of a daily oral gavage of oleoyl‐estrone (0, 0.2, 0.5, 1, 2, 5, 10, and 20 μmol/kg per day) in 0.2 ml of sunflower oil given over a 10‐day period were studied in groups, each of which contained six adult female Wistar rats initially weighing 190 to 230 g. A group of intact control rats receiving no gavage was included for comparison. Body weight and food intake were measured daily. Rats were killed on day 10 of treatment, and body composition (protein nitrogen, lipids, and water), liver lipids, and plasma parameters (glucose, triacylglycerols, total cholesterol, free fatty acids, 3‐hydroxybutyrate, urea, aspartate, alanine transaminases, insulin, leptin, and free and acyl‐estrone) were measured. Results: The administration of oleoyl‐estrone resulted in a dose‐dependent loss of body fat, because of a partly maintained energy expenditure combined with decreased food intake. The differences in the energy budget were met by internal fat pools. The changes recorded did not affect the levels of the main plasma energy homeostasis indicators: unaltered glucose, triacylglycerols, free fatty acids, 3hydroxybutyrate, and urea. Protein was accrued even under conditions of severe lipid store drainage. There were no changes in transaminases. No lipid accumulation was recorded in the liver. Plasma insulin and leptin levels decreased with increased oleoyl‐estrone doses, whereas the levels of free and esterified estrone increased with treatment, although not in proportion to the dose received. Discussion: Oral treatment with oleoyl‐estrone resulted in the specific dose‐related loss of fat reserves with little change to other metabolic parameters. These results agree with the postulated role of oleoyl‐estrone as a ponderostat signal.     

Dietary Calcium Intake Is Associated With Less Gain in Intra‐Abdominal Adipose Tissue Over 1 Year

Calcium intake is reported to enhance weight loss with a preferential loss in trunk fat. Discrepant findings exist as to the effects of calcium intake on longitudinal changes in total fat mass and central fat deposition. Therefore, the purpose of this study was to determine associations between dietary calcium intake and 1‐year change in body composition and fat distribution, specifically intra‐abdominal adipose tissue (IAAT). A total of 119 healthy, premenopausal women were evaluated at baseline and 1 year later. Average dietary calcium was determined via 4‐day food records. Total fat was determined by dual‐energy X‐ray absorptiometry (DXA) and subcutaneous abdominal adipose tissue (SAAT) and IAAT by computed tomography. Over the study period, participants' reported daily calcium and energy intakes were 610.0 ± 229.9 mg and 1,623.1 ± 348.5 kcal, respectively. The mean change in weight, total fat, IAAT, and SAAT was 4.9 ± 4.4 kg, 5.3 ± 4.0 kg, 7.7 ± 19.5 cm², and 49.3 ± 81.1 cm², respectively. Average calcium intake was significantly, inversely associated with 1‐year change in IAAT (standardized β: ?0.23, P < 0.05) after adjusting for confounding variables. For every 100 mg/day of calcium consumed, gain in IAAT was reduced by 2.7 cm². No significant associations were observed for average calcium intake with change in weight, total fat, or SAAT. In conclusion, dietary calcium intake was significantly associated with less gain in IAAT over 1 year in premenopausal women. Further investigation is needed to verify these findings and determine the calcium intake needed to exert beneficial effects on fat distribution.     

Increased Carbohydrate Induced Ghrelin Secretion in Obese vs. Normal‐weight Adolescent Girls

Orexigenic and anorexigenic pathways mediate food intake and may be affected by meal composition. Our objective was to determine whether changes in levels of active ghrelin and peptide YY (PYY) differ in obese vs. normal‐weight adolescent girls following specific macronutrient intake and predict hunger and subsequent food intake. We enrolled 26 subjects: 13 obese and 13 normal‐weight girls, 12–18 years old, matched for maturity (as assessed by bone age) and race. Subjects were assigned a high‐carbohydrate, high‐protein, and high‐fat breakfast in random order. Active ghrelin and PYY were assessed for 4 h after breakfast and 1 h after intake of a standardized lunch. Hunger was assessed using a standardized visual analog scale (VAS). No suppression in active ghrelin levels was noted following macronutrient intake in obese or normal‐weight girls. Contrary to expectations, active ghrelin increased in obese girls following the high‐carbohydrate breakfast, and the percent increase was higher than in controls (P = 0.046). Subsequent food intake at lunch was also higher (P = 0.03). Following the high‐fat breakfast, but not other breakfasts, percent increase in PYY was lower (P = 0.01) and subsequent lunch intake higher (P = 0.005) in obese compared with normal‐weight girls. In obese adolescents, specific intake of high‐carbohydrate and high‐fat breakfasts is associated with greater increases in ghrelin, lesser increases in PYY, and higher intake at a subsequent meal than in controls. Changes in anorexigenic and orexigenic hormones in obese vs. normal‐weight adolescents following high‐carbohydrate and high‐fat meals may influence hunger and satiety signals and subsequent food intake.     

Association of eating frequency with body fatness in pre- and postmenopausal women

Objective: To examine associations between eating frequency (EF) and body fatness in pre‐ and postmenopausal women, after excluding potential low‐energy reporters. Research Methods and Procedures: In this cross‐sectional study of 220 free‐living women, 64 pre‐ and 50 postmenopausal non‐low‐energy‐reporting women were further analyzed (age, 24 to 74 years; BMI, 18.5 to 38.6 kg/m²). Anthropometric and body composition measurements (DXA) were performed in all study participants. EF, energy, and macronutrient intake were assessed by 3‐day food record. Physical activity level and energy expenditure were assessed by self‐reported questionnaire. Results: No association between EF and adiposity indices was detected in premenopausal women. In contrast, EF was positively correlated with percentage body fat in postmenopausal women (r = 0.30, p = 0.03). EF was positively correlated with total energy intake in both groups and with total energy expenditure in premenopausal women only (r = 0.34, p = 0.02). Multivariate analysis revealed that, in postmenopausal women, EF was a significant predictor of body fatness (standardized β = 0.41, p = 0.01). Discussion: Frequent eating was not found to be related to adiposity in premenopausal women, but it was associated with increased body fat in postmenopausal women. Possible explanations could be that the frequent eating is not associated with a physically active lifestyle in postmenopausal women or that frequent eating predisposes women after menopause to a higher energy intake by increasing food stimuli and rendering it more difficult for them to control energy balance.     

Visceral adiposity is associated with serum retinol binding protein-4 levels in healthy women

Objective: Retinol binding protein‐4 (RBP4) has been reported to impair insulin sensitivity throughout the body. We investigated the relationship between serum RBP4 levels and adiposity indices as well as metabolic risk variables. Research Methods and Procedure: We recruited a total of 102 healthy women 21 to 67 years old. We assessed body composition by computed tomography and divided the study population into four groups based on body weight and visceral fat area (non‐obese without visceral adiposity, non‐obese with visceral adiposity, obese without visceral adiposity, and obese with visceral adiposity). Serum RBP4 levels were measured by radioimmunoassay. Results: Despite similar levels of total body fat, non‐obese women had lower systolic blood pressure, total cholesterol, triglyceride (TG), low‐density lipoprotein (LDL)‐cholesterol levels, insulin resistance indices, and RBP4 levels than non‐obese women with visceral adiposity and had higher high‐density lipoprotein‐cholesterol levels. Similarly, obese women without visceral adiposity had lower blood pressure, total cholesterol, TG levels, insulin resistance indices, and RBP4 levels than obese women with visceral adiposity. In addition, despite having increased body fat, obese women without visceral adiposity had lower TGs, insulin resistance indices, and serum RBP4 levels than non‐obese women with visceral adiposity. By step‐wise multiple regression analysis, visceral fat areas and LDL‐cholesterol levels independently affected RBP4 levels. Discussion: We determined that serum RBP4 levels are independently associated with visceral fat and LDL‐cholesterol levels. These results suggest that, irrespective of body weight, visceral obesity is an independent predictor of serum RBP4 levels, and RBP4 may represent a link between visceral obesity and cardiovascular disease.     

Physical,Behavioral, and Body Image Characteristics in a Tri‐Racial Group of Adolescent Girls

Objectives: The purpose of this study was to evaluate physical characteristics, nutrient intake, physical activity level, and body image in white (CC), African‐American (AA), and Hispanic‐American (HA) female adolescents. Research Methods and Procedures: High school volunteers were solicited for this study. Self‐reported information was used to determine subject characteristics, family income, physical activity, body image, and nutrient intake. Physical evaluations were used to determine body mass index, percent body fat, fat distribution, resting heart rate, and blood pressure (BP). Results: Results showed that AA girls displayed significantly higher diastolic BP than HA girls (p = 0.029). CC adolescents showed greater physical activity (p = 0.010) and lower adiposity than HA adolescents (p = 0.048), as well as lower subscapular skinfold than AA adolescents (p = 0.018). AA adolescents selected a higher ideal body size than CC girls (p = 0.038). There was also a significant difference in percentage carbohydrates (p < 0.034) and cholesterol consumed (p < 0.016) among groups, with CC girls showing the highest values for carbohydrates and lowest values for cholesterol intake among groups. Discussion: Given our findings of higher adiposity and lower physical activity levels in HA adolescents and greater diastolic BP levels and subscapular skinfold in AA adolescents, more interventions should be targeted toward improving health‐related variables among minority populations.     

Intake compensates for resting metabolic rate variation in female C57BL/6J mice fed high-fat diets

Objective: The literature is divided over whether variation in resting metabolic rate (RMR) is related to subsequent obesity. We set out to see whether the effect of RMR on weight gain in mice could be revealed with high‐fat feeding. Research Methods and Procedures: Female C57BL/6J mice received a low‐ (10 kcal%fat n = 47), medium‐ (45 kcal%fat n = 50), or high‐fat diet (60 kcal%fat n = 50) for 12 weeks. Pre‐treatment RMR was measured by indirect calorimetry. Body composition was estimated using DXA before and after treatment. Results: Mice on the high‐fat diet gained 39% of body mass, whereas control animals gained 3.5%. There was no interaction between RMR and dietary type on weight gain, and there was no association between weight gain and RMR for any of the treatments. RMR accounted for 2.4% of the variation in pre‐treatment food intake corrected for initial body mass; however, the gradient of this relationship indicated that variations in RMR were, on average, compensated for by adjustments in food intake. Discussion: Individual variations in RMR did not predispose mice to weight gain independent of the dietary treatment. Deviations from the relationship between RMR and food intake were not associated with weight gain. This suggests that variations in energy expenditure, caused by RMR and physical activity, are closely linked to dietary intake, and, therefore, well compensated. Individual variations in the strength of this association may underpin individual variability in the responses to diet.     

Calcium and dairy product modulation of lipid utilization and energy expenditure

Objective: The purpose of this study was to investigate the impact of dietary calcium or dairy product intake on total energy expenditure (TEE), fat oxidation, and thermic effect of a meal (TEM) during a weight loss trial. Methods and Procedures: The intervention included a prescribed 500‐kcal deficit diet in a randomized placebo‐controlled calcium or dairy product intervention employing twenty‐four 18 to 31‐year‐old (22.2 ± 3.1 years, mean ± s.d.) overweight women (75.5 ± 9.6 kg). TEM and fat oxidation were measured using respiratory gas exchange after a meal challenge, and TEE was measured by doubly labeled water. Fat mass (FM) and lean mass (fat‐free mass (FFM)) were measured by dual‐energy X‐ray absorptiometry. Subjects were randomized into one of these three intervention groups: (i) placebo (<800 mg/day calcium intake); (ii) 900 mg/day calcium supplement; (iii) three servings of dairy products/day to achieve an additional 900 mg/day. Results: There were no group effects observed in change in TEE; however, a group effect was observed for fat oxidation after adjusting for FFM (P = 0.02). The treatment effect was due to an increase in fat oxidation in the calcium‐supplemented group of 1.5 ± 0.6 g/h, P = 0.02. Baseline 25‐hydroxyvitamin D (25OHD) was positively correlated with TEM (R = 0.31, P = 0.004), and trended toward a correlation with fat oxidation (P = 0.06), independent of group assignment. Finally, the change in log parathyroid hormone (PTH) was positively correlated with the change in trunk FM (R = 0.27, P = 0.03). Discussion: These results support that calcium intake increases fat oxidation, but does not change TEE and that adequate vitamin D status may enhance TEM and fat oxidation.