scholarly journals The Influence of Genetic Increases in Body Weight on the Abdominal Fat Pad of Turkeys

1982 ◽  
Vol 61 (11) ◽  
pp. 2301-2304 ◽  
Author(s):  
KARL E. NESTOR
Keyword(s):  
Body Weight ◽  
Abdominal Fat ◽  
Fat Pad

scholarly journals The Influence of Genetic Increases in Body Weight and Shank Width on the Abdominal Fat Pad and Carcass Composition of Turkeys

1986 ◽  
Vol 65 (2) ◽  
pp. 391-397 ◽  
Author(s):  
WAYNE L. BACON ◽  
KARL E. NESTOR ◽  
PHILIP A. RENNER
Keyword(s):  
Body Weight ◽  
Abdominal Fat ◽  
Carcass Composition ◽  
Fat Pad

Massa adiposa ligamenti falciformis or anterior abdominal fat pad — Its dimension and relation to body weight

2018 ◽  
Vol 216 ◽  
pp. 100-102
Author(s):  
Friedemann Strobel ◽  
Eckart Schirg ◽  
Martin Schlaud ◽  
Thomas Tschernig
Keyword(s):  
Body Weight ◽  
Abdominal Fat ◽  
Fat Pad

scholarly journals Abdominal fat pad mass reduction by in ovo administration of anti-adipocyte monoclonal antibodies in chickens

2000 ◽  
Vol 79 (11) ◽  
pp. 1640-1644 ◽  
Author(s):  
Y.J. Wu ◽  
M. Valdez-Corcoran ◽  
J.T. Wright ◽  
AL Cartwright
Keyword(s):  
Monoclonal Antibodies ◽  
Abdominal Fat ◽  
Mass Reduction ◽  
Fat Pad ◽  
In Ovo

Defense of differfing body weight set points in diet-induced obese and resistant rats

1998 ◽  
Vol 274 (2) ◽  
pp. R412-R419 ◽  
Author(s):  
Barry E. Levin ◽  
Richard E. Keesey
Keyword(s):  
Body Weight ◽  
Diet Composition ◽  
Energy Homeostasis ◽  
Energy Content ◽  
Sprague Dawley ◽  
Fat Pad ◽  
Insulin Levels ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Plasma Leptin

Among outbred Sprague-Dawley rats, approximately one-half develop diet-induced obesity (DIO) and one-half are diet resistant (DR) on a diet relatively high in fat and energy content (HE diet). Here we examined the defense of body weight in these two phenotypes. After HE diet for 13 wk, followed by chow for 6 wk, DR rats gained weight comparably but their plasma leptin levels fell to 54% of chow-fed controls. When a palatable liquid diet (Ensure) was added for 13 wk, other DR rats became obese. But when switched to chow, their intakes fell by 60%, and body and retroperitoneal (RP) fat pad weights and plasma leptin and insulin levels all declined for 2 wk and then stabilized at control levels after 6 wk. In contrast, comparably obese DIO rats decreased their intake by only 20%, and their weights plateaued when they were switched to chow after 13 wk on HE diet. When a subgroup of these DIO rats was restricted to 60% of prior intake, their weights fell to chow-fed control levels over 2 wk. But their leptin and insulin levels both fell disproportionately to 30% of controls. When no longer restricted, their intake and feed efficiency rose immediately, and their body and RP pad weights and leptin and insulin levels rose to those of unrestricted DIO rats within 2 wk. Thus diet and genetic background interact to establish high (DIO) or low (DR) body weight set points, which are then defended against subsequent changes in diet composition and/or energy availability. If leptin affects energy homeostasis, it does so differentially in DIO vs. DR rats since comparably low and high levels were associated with differing patterns of weight change between the two phenotypes.

scholarly journals PHARMACOLOGICAL SCREENING OF ANTI-OBESITY POTENTIAL OF ACORUS CALAMUS LINN. IN HIGH FAT CAFETERIA DIET FED OBESE RATS

2017 ◽  
Vol 10 (4) ◽  
pp. 384 ◽  
Author(s):  
Athesh K ◽  
Joshi G
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Serum Glucose ◽  
In Vivo Studies ◽  
Acorus Calamus ◽  
Dependent Manner ◽  
Fat Pad ◽  
High Fat ◽  
Dose Levels ◽  
Dose Dependent

Objective: To study the anti-obesity potential of aqueous rhizome extract of Acoruscalamus Linn. (AREAC)in high fat diet fed obese rats.Methods: Adult strain male Wistar rats used in this study were fed with High Fat Diet (HFD) for 60 days. For the treatment groups,AREAC was administered in a dose levels of100, 200 and 300 mg/kgbw, orally once a day along with HFD. Rats fed with normal pellet chow were served as normal control. The effect of AREAC on physical parameterssuch as body weight, organ weight, fat pad weights and various biochemical parameterslike serum glucose, insulin, leptin,lipid profile, liver markers, kidney markers and oxidative stress markers were analysed.In-vitro pancreatic lipase inhibition assay of AREAC was also studied.Results: Data of in-vivo studies revealedsignificant (p<0.05) reduction in percentage body weight gain, organ weights, fat pad weights and levels of serum glucose, insulin and leptin after treatment with AREAC in a dose dependent manner. Also, administration of AREAC significantly inhibited the increases in the concentrations of triglycerides, total cholesterol, LDL-cholesterol, VLDL-cholesterol, free-fatty acid and phospholipids in a dose dependent manner whereas, the level of HDL-cholesterol was found to be elevated on treatment. Moreover, on treatment with test drug,the elevated levels of serum liver and kidney markerssuch as AST, ALT, ALP, urea, creatinine were also brought back to near normalcy. Antioxidant status was found to be enhanced in liver tissues after treatment.In-vitro studies showed significant inhibition in the activity of pancreatic lipaseby AREAC.Conclusion: The data of the results obtained clearly depicted that AREAC was found to have pronounced anti-obesity activity particularly at the dose levels of 300 mg/kg bw.Key Words: Obesity, High Fat Diet, Leptin, AcoruscalamusLinn., Orlistat.  

PP108-SUN WEIGHT CYCLING IS ASSOCIATED WITH BODY WEIGHT EXCESS AND ABDOMINAL FAT ACCUMULATION: A CROSS-SECTIONAL STUDY

2011 ◽  
Vol 6 (1) ◽  
pp. 65
Author(s):  
E. Cereda ◽  
A.E. Malavazos ◽  
R. Caccialanza ◽  
M. Rondanelli ◽  
G. Fatati ◽  
...  
Keyword(s):  
Body Weight ◽  
Cross Sectional Study ◽  
Abdominal Fat ◽  
Weight Cycling ◽  
Sectional Study ◽  
Cross Sectional ◽  
Fat Accumulation ◽  
Weight Excess

Modest weight gain is associated with sympathetic neural activation in nonobese humans

2007 ◽  
Vol 292 (5) ◽  
pp. R1834-R1838 ◽  
Author(s):  
Christopher L. Gentile ◽  
Jeb S. Orr ◽  
Brenda M. Davy ◽  
Kevin P. Davy
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Weight Gain ◽  
Body Fat ◽  
Muscle Sympathetic Nerve Activity ◽  
Fat Distribution ◽  
Abdominal Fat ◽  
Neural Activation ◽  
Burst Frequency ◽  
Weight Stability

We tested the hypothesis that modest, overfeeding-induced weight gain would increase sympathetic neural activity in nonobese humans. Twelve healthy males (23 ± 2 years; body mass index, 23.8 ± 0.7) were overfed ∼1,000 kcal/day until a 5-kg weight gain was achieved. Muscle sympathetic nerve activity (MSNA, microneurography), blood pressure, body composition (dual energy X-ray absorptiometry), and abdominal fat distribution (computed tomography) were measured at baseline and following 4 wk of weight stability at each individual's elevated body weight. Overfeeding increased body weight (73.5 ± 3.1 vs. 78.4 ± 3.2 kg, P < 0.001) and body fat (14.9 ± 1.2 vs. 18 ± 1.1 kg, P < 0.001) in 42 ± 8 days. Total abdominal fat increased (220 ± 22 vs. 266 ± 22 cm2, P < 0.001) with weight gain, due to increases in both subcutaneous (158 ± 15 vs. 187 ± 12 cm2, P < 0.001) and visceral fat (63 ± 8 vs. 79 ± 12 cm2, P = 0.004). As hypothesized, weight gain elicited increases in MSNA burst frequency (32 ± 2 vs. 38 ± 2 burst/min, P = 0.002) and burst incidence (52 ± 4 vs. 59 ± 3 bursts/100 heart beats, P = 0.026). Systolic, but not diastolic blood pressure increased significantly with weight gain. The change in MSNA burst frequency was correlated with the percent increase in body weight ( r = 0.59, P = 0.022), change in body fat ( r = 0.52, P = 0.043) and percent change in body fat ( r = 0.51, P = 0.045). The results of the current study indicate that modest diet-induced weight gain elicits sympathetic neural activation in nonobese males. These findings may have important implications for understanding the link between obesity and hypertension.

scholarly journals Effects of fructose and glucose on plasma leptin, insulin, and insulin resistance in lean and VMH-lesioned obese rats

2000 ◽  
Vol 278 (4) ◽  
pp. E677-E683 ◽  
Author(s):  
Asako Suga ◽  
Tsutomu Hirano ◽  
Haruaki Kageyama ◽  
Toshimasa Osaka ◽  
Yoshio Namba ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Body Weight Gain ◽  
Intravenous Glucose Tolerance Test ◽  
Fat Pad ◽  
Intravenous Glucose ◽  
Dietary Fructose ◽  
Obese Rats ◽  
Normal Chow ◽  
Plasma Leptin

To determine the influence of dietary fructose and glucose on circulating leptin levels in lean and obese rats, plasma leptin concentrations were measured in ventromedial hypothalamic (VMH)-lesioned obese and sham-operated lean rats fed either normal chow or fructose- or glucose-enriched diets (60% by calories) for 2 wk. Insulin resistance was evaluated by the steady-state plasma glucose method and intravenous glucose tolerance test. In lean rats, glucose-enriched diet significantly increased plasma leptin with enlarged parametrial fat pad, whereas neither leptin nor fat-pad weight was altered by fructose. Two weeks after the lesions, the rats fed normal chow had marked greater body weight gain, enlarged fat pads, and higher insulin and leptin compared with sham-operated rats. Despite a marked adiposity and hyperinsulinemia, insulin resistance was not increased in VMH-lesioned rats. Fructose brought about substantial insulin resistance and hyperinsulinemia in both lean and obese rats, whereas glucose led to rather enhanced insulin sensitivity. Leptin, body weight, and fat pad were not significantly altered by either fructose or glucose in the obese rats. These results suggest that dietary glucose stimulates leptin production by increasing adipose tissue or stimulating glucose metabolism in lean rats. Hyperleptinemia in VMH-lesioned rats is associated with both increased adiposity and hyperinsulinemia but not with insulin resistance. Dietary fructose does not alter leptin levels, although this sugar brings about hyperinsulinemia and insulin resistance, suggesting that hyperinsulinemia compensated for insulin resistance does not stimulate leptin production.

scholarly journals Inactivity induces increases in abdominal fat

2007 ◽  
Vol 102 (4) ◽  
pp. 1341-1347 ◽  
Author(s):  
Matthew J. Laye ◽  
John P. Thyfault ◽  
Craig S. Stump ◽  
Frank W. Booth
Keyword(s):  
Caloric Intake ◽  
Cell Number ◽  
Abdominal Fat ◽  
Cell Diameter ◽  
Fat Pad ◽  
Voluntary Running ◽  
Old Rats ◽  
Ad Libitum ◽  
Running Wheels ◽  
Omental Fat

Previously, inducing inactivity for 53 h after 21 days of voluntary running resulted in a 25 and 48% increase in epididymal and omental fat pad weights, respectively, while rats continued to eat more than a group that never had access to a running wheel ( J Physiol 565: 911–925, 2005). We wanted to test the hypothesis that inactivity, independent of excessive caloric intake, could induce an increase in fat pad mass. Twenty-one-day-old rats were given access to voluntary running wheels for 42–43 days so that they were running ∼9 km/day in the last week of running, after which wheels were locked for 5, 53, or 173 h (WL5, WL53, WL173) before the rats were killed. During the 53 and 173 h of inactivity, one group of animals was pair fed (PF) to match sedentary controls, whereas the other continued to eat ad libitum (AL). Epididymal and retroperitoneal fat masses were significantly increased in the WL173-PF vs. the WL5 group, whereas epididymal, perirenal, and retroperitoneal fat masses were all significantly increased in the WL173-AL group compared with the WL5 group. Additionally, hyperplasia, and not hypertrophy, of the epididymal fat mass was responsible for the increase at WL173-AL as demonstrated by a significant increase in cell number vs. WL5, with no change in cell diameter or volume. Thus two important findings have been elucidated: 1) increases in measured abdominal fat masses occur in both AL and PF groups at WL173, and 2) adipocyte expansion via hyperplasia occurred with an ad libitum diet following cessation of voluntary running.

Regional differences in fat pad responses to short days in Siberian hamsters

1989 ◽  
Vol 257 (6) ◽  
pp. R1533-R1540 ◽  
Author(s):  
T. J. Bartness ◽  
J. M. Hamilton ◽  
G. N. Wade ◽  
B. D. Goldman
Keyword(s):  
Body Weight ◽  
Body Fat ◽  
Subcutaneous Fat ◽  
Short Photoperiod ◽  
Fat Pad ◽  
Initial Exposure ◽  
Short Day ◽  
Siberian Hamsters ◽  
Long Day ◽  
Induced Changes

Siberian hamsters exhibit decreased body weight and fat after initial exposure to short photoperiods and increased body weight and fat after extended short photoperiod exposure. The purpose of the present experiments was to determine if uniform changes in white adipose tissue (WAT) pad weights and lipid metabolism correspond to these short photoperiod-induced changes in body fat. Carcass lipid content and testes and fat pad weights [retroperitoneal WAT (RWAT), epididymal WAT (EWAT), and inguinal and dorsal subcutaneous WAT, respectively] were decreased in male hamsters relative to their long day counterparts after 6 and 12 wk of short-day exposure. Moreover, EWAT and RWAT weight, EWAT specific lipoprotein lipase activity, and specific and total lipogenesis were disproportionately decreased relative to the subcutaneous fat pads. The changes in fat pad weight and metabolism were generally reversed coincident with the return to a long-day-like reproductive status after prolonged short-day exposure (24 and 30 wk). In a less detailed experiment, female Siberian hamsters had decreased body, fat pad, and uterine weights after 6 wk of short-day exposure; however, no fat pad-specific changes in weight were observed. The results of these experiments demonstrate that short-day-exposed male Siberian hamsters may be a useful model for examining mechanisms underlying fat pad-specific responses. In addition, gender appears to influence the pattern of short-day-induced lipid depletion in this species.

Sign in / Sign up

Export Citation Format

Share Document