Genetic analysis of carcass traits of steers adjusted to age, weight, or fat thickness slaughter endpoints.
(1/902)
Carcass measurements from 1,664 steers from the Germ Plasm Utilization project at U.S. Meat Animal Research Center were used to estimate heritabilities (h(2)) of, and genetic correlations (r(g)) among, 14 carcass traits adjusted to different endpoints (age, carcass weight, and fat thickness): HCW (kg), dressing percent (DP), adjusted fat thickness (AFT, cm), LM area (LMA, cm(2)), KPH (%), marbling score (MS), yield grade (YG), predicted percentage of retail product (PRP), retail product weight (RPW, kg), fat weight (FW, kg), bone weight (BNW, kg), actual percentage retail product (RPP), fat percent (FP), and bone percent. Fixed effects in the model included breed group, feed energy level, dam age, birth year, significant (P < 0.05) interactions, covariate for days on feed, and the appropriate covariate for endpoint nested (except age) within breed group. Random effects in the model were additive genetic effect of animal and total maternal effect of dam. Parameters were estimated by REML. For some traits, estimates of h(2) and phenotypic variance changed with different endpoints. Estimates of h(2) for HCW, DP, RPW, and BNW at constant age, weight, or fat thickness were 0.27, -, and 0.41; 0.19, 0.26, and 0.18; 0.42, 0.32, and 0.50; and 0.43, 0.32, and 0.48, respectively. Magnitude and/or sign of r(g) also changed across endpoints for 54 of the 91 trait pairs. Estimates for HCW-LMA, AFT-RPW, LMA-YG, LMA-PRP, LMA-FW, LMA-RPP, and LMA-FP at constant age, weight, or fat thickness were 0.32, -, and 0.51; -0.26, -0.77, and -; -0.71, -0.89, and -0.66; 0.68, 0.85, and 0.63; -0.16, -0.51, and 0.22; 0.47, 0.57, and 0.27; and -0.44, -0.43, and -0.18, respectively. Fat thickness was highly correlated with YG (0.86 and 0.85 for common age and weight) and PRP (-0.85 and -0.82 for common age and weight), indicating that selection for decreased fat thickness would improve YG and PRP. Carcass quality, however, would be affected negatively because of moderate r(g) (0.34 and 0.35 for common age and weight) between MS and AFT. Estimates of h(2) and phenotypic variance indicate that enough genetic variation exists to change measures of carcass merit by direct selection. For some carcass traits, however, magnitude of change would depend on effect of endpoint on h(2) and phenotypic variance. Correlated responses to selection would differ depending on endpoint. (+info)
The "lipid accumulation product" performs better than the body mass index for recognizing cardiovascular risk: a population-based comparison.
(2/902)
BACKGROUND: Body mass index (BMI, kg/m2) may not be the best marker for estimating the risk of obesity-related disease. Consistent with physiologic observations, an alternative index uses waist circumference (WC) and fasting triglycerides (TG) concentration to describe lipid overaccumulation. METHODS: The WC (estimated population minimum 65 cm for men and 58 cm for women) and TG concentration from the third National Health and Nutrition Examination Survey (N = 9,180, statistically weighted to represent 100.05 million US adults) were used to compute a "lipid accumulation product" [LAP = (WC-65) x TG for men and (WC-58) x TG for women] and to describe the population distribution of LAP. LAP and BMI were compared as categorical variables and as log-transformed continuous variables for their ability to identify adverse levels of 11 cardiovascular risk factors. RESULTS: Nearly half of the represented population was discordant for their quartile assignments to LAP and BMI. When 23.54 million with ordinal LAP quartile > BMI quartile were compared with 25.36 million with ordinal BMI quartile > LAP quartile (regression models adjusted for race-ethnicity and sex) the former had more adverse risk levels than the latter (p < 0.002) for seven lipid variables, uric acid concentration, heart rate, systolic and diastolic blood pressure. Further adjustment for age did not materially alter these comparisons except for blood pressures (p > 0.1). As continuous variables, LAP provided a consistently more adverse beta coefficient (slope) than BMI for nine cardiovascular risk variables (p < 0.01), but not for blood pressures (p > 0.2). CONCLUSION: LAP (describing lipid overaccumulation) performed better than BMI (describing weight overaccumulation) for identifying US adults at cardiovascular risk. Compared to BMI, LAP might better predict the incidence of cardiovascular disease, but this hypothesis needs prospective testing. (+info)
A technique for the measurement of visceral fat by ultrasonography: comparison of measurements by ultrasonography and computed tomography.
(3/902)
OBJECTIVE: This study aims to create a method of calculating intra-abdominal visceral fat volume by using ultrasound (US). The visceral fat volume measured by US was evaluated by comparison with the volume measured by computed tomography (CT). METHODS: Eighty-seven patients (52 males and 35 females) were enrolled in this study. Both US and CT were performed, and the visceral fat volume was measured. Both the distance and thickness of the parameters in US were measured as follows: 1) the distance between the internal surface of the abdominal muscle and the splenic vein, 2) the distance between the internal surface of the abdominal muscle and the posterior wall of aorta on the umbilicus, and 3) the thickness of the fat layer of the posterior right renal wall. RESULTS: The equation was calculated as follows: [visceral fat volume]=-9.008+1.191x[distance between the internal surface of the abdominal muscle and the splenic vein (mm)]+0.987x[distance between the internal surface of the abdominal muscle and the posterior wall of the aorta on the umbilicus (mm)]+3.644x[thickness of the fat layer of the posterior right renal wall (mm)]. There was a good correlation between the visceral fat volume calculated by the above equation and the volume by CT described (r=0.860, p<0.0001). CONCLUSION: The measurement of the visceral fat volume using US provided results as effectively as CT, and it was proven to be a useful method. (+info)
Dietary coconut oil increases conjugated linoleic acid-induced body fat loss in mice independent of essential fatty acid deficiency.
(4/902)
Conjugated linoleic acid (CLA) induces a body fat loss that is enhanced in mice fed coconut oil (CO), which lacks essential fatty acids (EFA). Our objective was to determine if CO enhancement of CLA-induced body fat loss is due to the lack of EFA. The CLA-EFA interaction was tested by feeding CO and fat free (FF) diets for varying times with and without replenishment of individual EFA. Mice fed CO during only the 2-week CLA-feeding period did not differ from control mice in their adipose EFA content but still tended (P=0.06) to be leaner than mice fed soy oil (SO). Mice raised on CO or FF diets and fed CLA were leaner than the SO+CLA-fed mice (P<0.01). Mice raised on CO and then replenished with linoleic, linolenic, or arachidonic acid were leaner when fed CLA than mice raised on SO (P<0.001). Body fat of CO+CLA-fed mice was not affected by EFA addition. In summary, CO-fed mice not lacking in tissue EFA responded more to CLA than SO-fed mice. Also, EFA addition to CO diets did not alter the enhanced response to CLA. Therefore, the increased response to CLA in mice raised on CO or FF diets appears to be independent of a dietary EFA deficiency. (+info)
Mitogen-activated protein kinases regulate platelet-activating factor-induced hyperpermeability.
(5/902)
OBJECTIVE: The authors tested the hypothesis that p42/44- (ERK-1/2) and/or p38-mitogen-activated protein kinases (MAPK) are in vivo regulatory elements in the platelet-activating factor (PAF) activated signaling cascade that stimulates microvascular hyperpermeability. METHODS: FITC-dextran 70 was used as the macromolecular tracer for microvascular permeability in the mouse mesenteric fat tissue. Interstitial integrated optical intensity (IOI) was used as an index of permeability. RESULTS: An application of 10(-7) M PAF increased IOI from 23.1 +/- 3.6 to 70.8 +/- 7.4 (mean +/- SEM). Inhibition of ERK-1/2 with 3 microM and 30 microM AG126 reduced IOI to 32.3 +/- 2.5. Similarly, inhibition of p38-MAPK with 6 nM, 60 nM and 600 nM SB203580 lowered IOI to 29.1 +/- 2.4. CONCLUSIONS: The results demonstrate that ERK-1/2 and p38MAPK participate in the signaling cascade that regulates PAF-induced microvascular hyperpermeability in vivo. (+info)
All obese individuals are not created equal: insulin resistance is the major determinant of cardiovascular disease in overweight/obese individuals.
(6/902)
The ability of insulin to mediate glucose disposal varies more than six-fold in an apparently healthy population, and approximately one third of the most insulin-resistant of these individuals are at increased risk to develop cardiovascular disease. Differences in degree of adiposity account for approximately 25% of this variability, and another 25% varies as a function of level of physical fitness. The more overweight/obese the person, the more likely they are to be insulin-resistant and at increased risk of cardiovascular disease, but substantial numbers of overweight/obese individuals remain insulin-sensitive, and not all insulin-resistant persons are obese. Of greater clinical relevance is evidence that the metabolic benefit and decrease in risk of cardiovascular disease following weight loss occurs primarily in those overweight/obese individuals that are also insulin-resistant. The relationship between insulin resistance and overall obesity, as assessed by measurement of body mass index, is essentially the same as the relationship between insulin action and abdominal obesity as quantified by determining waist circumference. Finally, there appears to be a comparable relationship between insulin-mediated glucose disposal and amount of visceral fat, subcutaneous fat, and total fat as quantified by various imaging techniques, and the magnitude of these relationships is no greater than that between insulin action and simple measure of body mass index. (+info)
Effect of voluntary exercise on peripheral tissue glucocorticoid receptor content and the expression and activity of 11beta-HSD1 in the Syrian hamster.
(7/902)
Recent findings indicate that elevated levels of glucocorticoids (GC), governed by the expression of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) and GC receptors (GR), in visceral adipose tissue and skeletal muscle lead to increased insulin resistance and the metabolic syndrome. Paradoxically, evidence indicates that aerobic exercise attenuates the development of the metabolic syndrome even though it stimulates acute increases in circulating GC levels. To investigate the hypothesis that training alters peripheral GC action to maintain insulin sensitivity, young male hamsters were randomly divided into sedentary (S) and trained (T) groups (n = 8 in each). The T group had 24-h access to running wheels over 4 wk of study. In muscle, T hamsters had lower 11beta-HSD1 protein expression (19.2 +/- 1.40 vs. 22.2 +/- 0.96 optical density, P < 0.05), similar 11beta-HSD1 enzyme activity (0.9 +/- 0.27% vs. 1.1 +/- 0.26), and lower GR protein expression (9.7 +/- 1.86 vs. 15.1 +/- 1.78 optical density, P < 0.01) than S hamsters. In liver, 11beta-HSD1 protein expression tended to be lower in T compared with S (19.2 +/- 0.56 vs. 21.4 +/- 1.05, P = 0.07), whereas both enzyme activity and GR protein expression were similar. In contrast, visceral adipose tissue contained approximately 2.7-fold higher 11beta-HSD1 enzyme activity in T compared with S (12.9 +/- 3.3 vs. 4.8 +/- 1.5% conversion, P < 0.05) but was considerably smaller in mass (0.24 +/- 0.02 vs. 0.71 +/- 0.06 g). Thus the intracellular adaptation of GC regulators to exercise is tissue specific, resulting in decreases in GC action in skeletal muscle and increases in GC action in visceral fat. These adaptations may have important implications in explaining the protective effects of aerobic exercise on insulin resistance and other symptoms of the metabolic syndrome. (+info)
Exercise-induced reversal of insulin resistance in obese elderly is associated with reduced visceral fat.
(8/902)
Exercise improves glucose metabolism and delays the onset and/or reverses insulin resistance in the elderly by an unknown mechanism. In the present study, we examined the effects of exercise training on glucose metabolism, abdominal adiposity, and adipocytokines in obese elderly. Sixteen obese men and women (age = 63 +/- 1 yr, body mass index = 33.2 +/- 1.4 kg/m2) participated in a 12-wk supervised exercise program (5 days/wk, 60 min/day, treadmill/cycle ergometry at 85% of heart rate maximum). Visceral fat (VF), subcutaneous fat, and total abdominal fat were measured by computed tomography. Fat mass and fat-free mass were assessed by hydrostatic weighing. An oral glucose tolerance test was used to determine changes in insulin resistance. Exercise training increased maximal oxygen consumption (21.3 +/- 0.8 vs. 24.3 +/- 1.0 ml.kg(-1).min(-1), P < 0.0001), decreased body weight (P < 0.0001) and fat mass (P < 0.001), while fat-free mass was not altered (P > 0.05). VF (176 +/- 20 vs. 136 +/- 17 cm2, P < 0.0001), subcutaneous fat (351 +/- 34 vs. 305 +/- 28 cm2, P < 0.03), and total abdominal fat (525 +/- 40 vs. 443 +/- 34 cm2, P < 0.003) were reduced through training. Circulating leptin was lower (P < 0.003) after training, but total adiponectin and tumor necrosis factor-alpha remained unchanged. Insulin resistance was reversed by exercise (40.1 +/- 7.7 vs. 27.6 +/- 5.6 units, P < 0.01) and correlated with changes in VF (r = 0.66, P < 0.01) and maximal oxygen consumption (r = -0.48, P < 0.05) but not adipocytokines. VF loss after aerobic exercise training improves glucose metabolism and is associated with the reversal of insulin resistance in older obese men and women. (+info)