scholarly journals In uteroand postnatal exposure to a high-protein or high-carbohydrate diet leads to differences in adipose tissue mRNA expression and blood metabolites in kittens

2009 ◽  
Vol 102 (8) ◽  
pp. 1136-1144 ◽  
Author(s):  
Brittany M. Vester ◽  
Kari J. Liu ◽  
Tonya L. Keel ◽  
Thomas K. Graves ◽  
Kelly S. Swanson

The objective of the present study was to measure the differences in body composition, adipose tissue gene expression, blood metabolite and hormone concentrations, and insulin sensitivity in kittens exposed to high-protein (HP) or high-carbohydrate (HC) nutritionin uteroand through the growth period. Eight dams were randomised onto two test diets, and fed the diets throughout gestation and lactation. Male offspring were evaluated for 9 months. Kittens were weaned at 2 months of age onto the same treatment diet as the dam and were allowed to consume dietsad libitum. The HC diet contained 34·3 % crude protein (CP), 19·2 % fat and 30·8 % digestible carbohydrate, while the HP diet contained 52·9 % CP, 23·5 % fat and 10·8 % digestible carbohydrate. Blood samples were collected at 6 months after birth. Body composition was determined at 2 and 8 months of age and an intravenous glucose tolerance test, neutering and adipose tissue biopsy conducted at 8 months of age. Physical activity was quantified at 6 and 9 months. Energy intake, DM intake and body weight were not different between groups. At 2 months, blood TAG were greater (P < 0·05) in kittens fed the HP diet. At 8 months, blood leptin was higher (P < 0·05) in kittens fed the HC diet, while chemokine receptor 5, hormone-sensitive lipase, uncoupling protein 2, leptin and insulin receptor mRNA were greater (P < 0·05) in kittens fed the HP diet. The present results demonstrate some of the changes in blood metabolites and hormones, physical activity and mRNA abundance that occur with feeding high protein levels to kittens.

2015 ◽  
Vol 53 (3) ◽  
pp. 237-247
Author(s):  
C. Popescu ◽  
Violeta Bojincă ◽  
Daniela Opriş ◽  
Ruxandra Ionescu

Abstract Aim. Rheumatoid arthritis (RA) may influence not only abdominal fat, but also whole body adiposity, since it is associated with chronic inflammation and disability. The study aims to evaluate the whole body adiposity of RA patients and to assess potential influences of disease specific measures. Methods. The study was designed to include Caucasian postmenopausal female RA patients and age-matched postmenopausal female controls. Each subject underwent on the same day clinical examination, laboratory tests, whole body dual X-ray absorptiometry (DXA) composition and physical activity estimation using a self-administered questionnaire. Results. A total of 107 RA women and 104 matched controls were included. Compared to controls, the RA group had less physical activity and a higher prevalence of normal weight obesity. Overfat RA women had a significantly higher toll of inflammation, disease activity, glucocorticoid treatment and sedentary behavior. RA women with inflammation, glucocorticoid treatment and higher disease activity class had higher whole body and trunk adipose tissue indices and higher prevalence of overfat status. Glucocorticoid treatment, inflammation, disease duration and severity correlated with whole body adipose tissue and significantly predicted high adiposity content and overfat phenotypes. Conclusions. RA disease duration and severity are associated with higher whole body and regional adiposity. Low-dose glucocorticoid treatment seems to contribute to adiposity gain and redistribution. Clinicians may need to assess body composition and physical activity in RA patients in order to fully manage cardiovascular outcomes and quality of life.


Molecules ◽  
2020 ◽  
Vol 25 (24) ◽  
pp. 5954
Author(s):  
Kyeong Jo Kim ◽  
Eui-Seon Jeong ◽  
Ki Hoon Lee ◽  
Ju-Ryun Na ◽  
Soyi Park ◽  
...  

Previously, we demonstrated that a 5% ethanol extract of unripe Rubus coreanus (5-uRCK) and ellagic acid has hypocholesterolemic and antiobesity activity, at least partially mediated by the downregulation of adipogenic and lipogenic gene expression in high-fat diet (HFD)-fed animals. The present study investigated the thermogenic and lipolytic antiobesity effects of 5-uRCK and ellagic acid in HFD-induced obese C57BL/6 mice and explored its mechanism of action. Mice fed an HFD received 5-uRCK or ellagic acid as a post-treatment or pretreatment. Both post-treated and pretreated mice showed significant reductions in body weight and adipose tissue mass compared to the HFD-fed mice. The protein levels of lipolysis-associated proteins, such as adipose triglyceride lipase (ATGL), phosphorylated hormone-sensitive lipase (p-HSL), and perilipin1 (PLIN1), were significantly increased in both the 5-uRCK- and ellagic acid-treated mouse epididymal white adipose tissue (eWAT). Additionally, thermogenesis-associated proteins, such as peroxisome proliferator-activated receptor α (PPARα), carnitine palmitoyl transferase-1 (CPT1), uncoupling protein 1 (UCP1), and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α), in inguinal white adipose tissue (ingWAT) were clearly increased in both the 5-uRCK- and ellagic acid-treated mice compared to HFD-fed mice. These results suggest that 5-uRCK and ellagic acid are effective for suppressing body weight gain and enhancing the lipid profile.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Xiaomin Zhang ◽  
Qibin Qi ◽  
Frank Hu ◽  
Frank Sacks ◽  
Lu Qi

OBJECTIVE The fat mass and obesity-associated gene (FTO) variant has shown the strongest association with obesity. Recent studies suggest that dietary intake may modify the genetic effects of FTO. We tested the effect of FTO variant on long-term weight loss and change in body composition in a 2-year randomized intervention trial. RESEARCH DESIGN AND METHODS FTO SNP rs1558902 was genotyped in 742 overweight or obese adults who were randomly assigned to one of four diets differing in the percentages of energy derived from fat, protein and carbohydrate (20, 15, and 65%; 20, 25, and 55%; 40, 15, and 45%; and 40, 25, and 35%) in the Pounds Lost Trial for 2 years. Body composition and fat distribution were measured in 424 and 195 participants by Dual-energy X-ray absorptiometry (DXA) and computed tomography (CT), respectively. RESULTS We found significant modification effects for diet intervention varying in protein (low vs high), but not in fat, on 2-year changes in total fat, fat free mass (FFM), fat mass% (FM%), trunk fat%, total adipose tissue mass (TAT), visceral adipose tissue mass (VAT) and superficial adipose tissue mass (SAT) (P for interactions=0.045, 0.036, 0.033, 0.048, 0.001, 0.008 and 0.002, respectively). Carriers of the risk allele (A allele) had a greater loss of weight and regional fat in response to high protein diet, while an opposite genetic effect was observed on changes in TAT and SAT in response to low protein diet at 2 years. Significant gene by diet interventions (low vs high protein) were also observed at 6 months of intervention, when the maximum of weight-loss was achieved, for changes in FFM, TAT, VAT and SAT (P for interactions=0.007, 0.019, 0.036 and 0.041, respectively). Patterns of change in body composition and fat distribution by diet intervention were similar at 6 month and 2 year. CONCLUSIONS Our data suggest that a high-protein diet may be beneficial for weight loss in individuals with the risk allele of the FTO variant rs1558902.


2009 ◽  
Vol 29 (4) ◽  
pp. 237-243 ◽  
Author(s):  
María del Mar Romero ◽  
José A. Fernández-López ◽  
Montserrat Esteve ◽  
Marià Alemany

In the present study we intended to determine how BAT (brown adipose tissue) maintained thermogenesis under treatment with OE (oleoyl-oestrone), a powerful slimming hormone that sheds off body lipid but maintains the metabolic rate. Overweight male rats were subjected to daily gavages of 10 nmol/g of OE or vehicle (control) for 10 days. A PF (pair-fed) vehicle-receiving group was used to discount the effects attributable to energy availability limitation. Interscapular BAT mass, lipid, DNA, mRNA and the RT-PCR (real-time PCR) expression of lipid and energy metabolism genes for enzymes and regulatory proteins were measured. BAT mass and lipid were decreased in OE and PF, with the latter showing a marked reduction in tissue mRNA. Maintenance of perilipin gene expression in PF and OE rats despite the loss of lipid suggests the preservation of the vacuolar interactive surface, a critical factor for thermogenic responsiveness. OE and, to a lesser extent, PF maintained the expression of genes controlling lipolysis and fatty acid oxidation, but markedly decreased the expression of those genes involved in lipogenic and acyl-glycerol synthesis. OE did not affect UCP1 (uncoupling protein 1) (decreased in PF), β3 adrenergic receptors or hormone-sensitive lipase gene mRNAs, which may translate in maintaining a full thermogenic system potential. OE rats were able to maintain a less energetically stressed BAT (probably through glucose utilization) than PF rats. These changes were not paralleled in PF rats, in which lower thermogenesis and glucose preservation resulted in a heavier toll on internal fat stores. Thus the mechanism of action of OE is more complex and tissue-specific than previously assumed.


2018 ◽  
Vol 108 (1) ◽  
pp. 62-76 ◽  
Author(s):  
Simon Bissonnette ◽  
Nathalie Saint -Pierre ◽  
Valerie Lamantia ◽  
Catherine Leroux ◽  
Viviane Provost ◽  
...  

ABSTRACT Background To optimize the prevention of type 2 diabetes (T2D), high-risk obese subjects with the best metabolic recovery after a hypocaloric diet should be targeted. Apolipoprotein B lipoproteins (apoB lipoproteins) induce white adipose tissue (WAT) dysfunction, which in turn promotes postprandial hypertriglyceridemia, insulin resistance (IR), and hyperinsulinemia. Objective The aim of this study was to explore whether high plasma apoB, or number of plasma apoB lipoproteins, identifies subjects who best ameliorate WAT dysfunction and related risk factors after a hypocaloric diet. Design Fifty-nine men and postmenopausal women [mean ± SD age: 58 ± 6 y; body mass index (kg/m2): 32.6 ± 4.6] completed a prospective study with a 6-mo hypocaloric diet (−500 kcal/d). Glucose-induced insulin secretion (GIIS) and insulin sensitivity (IS) were measured by 1-h intravenous glucose-tolerance test (IVGTT) followed by a 3-h hyperinsulinemic-euglycemic clamp, respectively. Ex vivo gynoid WAT function (i.e., hydrolysis and storage of 3H-triolein–labeled triglyceride-rich lipoproteins) and 6-h postprandial plasma clearance of a 13C-triolein–labeled high-fat meal were measured in a subsample (n = 25). Results Postintervention first-phase GIISIVGTT and total C-peptide secretion decreased in both sexes, whereas second-phase and total GIISIVGTT and clamp IS were ameliorated in men (P < 0.05). Baseline plasma apoB was associated with a postintervention increase in WAT function (r = 0.61) and IS (glucose infusion rate divided by steady state insulin (M/Iclamp) r = 0.30) and a decrease in first-phase, second-phase, and total GIISIVGTT (r = −0.30 to −0.35) without sex differences. The association with postintervention amelioration in WAT function and GIISIVGTT was independent of plasma cholesterol (total, LDL, and HDL), sex, and changes in body composition. Subjects with high baseline plasma apoB (1.2 ± 0.2 g/L) showed a significant increase in WAT function (+105%; P = 0.012) and a decrease in total GIISIVGTT (−34%; P ≤ 0.001), whereas sex-matched subjects with low plasma apoB (0.7 ± 0.1 g/L) did not, despite equivalent changes in body composition and energy intake and expenditure. Conclusions High plasma apoB identifies obese subjects who best ameliorate WAT dysfunction and glucose-induced hyperinsulinemia, independent of changes in adiposity after consumption of a hypocaloric diet. We propose that subjects with high plasma apoB represent an optimal target group for the primary prevention of T2D by hypocaloric diets. This trial was registered at BioMed Central as ISRCTN14476404.


2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Shengjie Tang ◽  
Fang Wu ◽  
Xihua Lin ◽  
Weiwei Gui ◽  
Fenping Zheng ◽  
...  

Purpose. Peroxisome proliferator-activated receptor α (PPARα) plays a crucial role in the control of lipid homeostasis. Here, we investigated the effects of CP775146, a new selective PPARα agonist, on lipid metabolism in diet-induced obese mice and its possible mechanism. Methods. C57BL/6 mice were fed a high-fat diet (HFD) for 12 weeks to induce obesity and then received CP775146 via intraperitoneal injection for 3 days. The content/morphology of the liver, serum lipid, and liver function was measured. The expression of genes related to lipolysis and synthesis in liver was detected by quantitative real-time PCR (qRT-PCR). Results. The safe dose of CP775146 was <0.3 mg/kg. CP775146 reduced the serum levels of liver enzymes, such as alanine aminotransferase (ALT) and glutamic-oxaloacetic transaminase (AST) and lipid metabolism-related biomarkers, including triglycerides (TGs) and low-density lipoprotein cholesterol (LDL-c), non-high-density lipoprotein cholesterol (non-HDL-c), and hepatic TG content, at a dosage of 0.1 mg/kg. HFD-induced pathological liver changes improved after CP775146 treatment. The expression of genes involved in liver fatty acid oxidation (acyl-coenzyme A dehydrogenase, long chain (Acadl), acyl-CoA oxidase 1 (Acox-1), carnitine palmitoyltransferase-1 (CPT-1), and enoyl-CoA, hydratase/3-hydroxyacyl CoA dehydrogenase (Ehhadh)) was upregulated in CP775146-treated mice. Furthermore, CP775146 induced the expression of thermogenesis genes (cell death-inducing DFFA-like effector a (Cidea), uncoupling protein 1 (Ucp1)) and lipolysis genes (hormone-sensitive lipase (Hsl), adipose tissue triglyceride lipase (Atgl)) in epididymal white adipose tissue (eWAT), activating browning and thermogenesis. Conclusion. CP775146 efficiently alleviates obesity-induced liver damage, prevents lipid accumulation by activating the liver fatty acid β-oxidation pathway, and regulates the expression of genes that control brown fat-like pathway in eWAT.


2014 ◽  
Vol 41 (10) ◽  
pp. 1974-1979 ◽  
Author(s):  
Hiba AbouAssi ◽  
K. Noelle Tune ◽  
Brian Gilmore ◽  
Lori A. Bateman ◽  
Gary McDaniel ◽  
...  

Objective.In prior reports, individuals with rheumatoid arthritis (RA) exhibited increased insulin resistance. However, those studies were limited by either suboptimal assessment methods for insulin sensitivity or a failure to account for important determinants such as adiposity and lack of physical activity. Our objectives were to carefully assess, compare, and determine predictors of skeletal muscle insulin sensitivity in RA, accounting for adiposity and physical activity.Methods.Thirty-nine individuals with established (seropositive or erosions) and treated RA and 39 controls matched for age, sex, race, body mass index, and physical activity underwent a frequently sampled intravenous glucose tolerance test to determine insulin sensitivity. Inflammation, body composition, and physical activity were assessed with systemic cytokine measurements, computed tomography scans, and accelerometry, respectively. Exclusions were diabetes, cardiovascular disease, medication changes within 3 months, and prednisone use over 5 mg/day. This investigation was powered to detect a clinically significant, moderate effect size for insulin sensitivity difference.Results.Despite elevated systemic inflammation [interleukin (IL)-6, IL-18, tumor necrosis factor-α; p < 0.05 for all], persons with RA were not less insulin sensitive [SIgeometric mean (SD): RA 4.0 (2.4) vs control 4.9 (2.1)*10−5min−1/(pmol/l); p = 0.39]. Except for visceral adiposity being slightly greater in controls (p = 0.03), there were no differences in body composition or physical activity. Lower insulin sensitivity was independently associated with increased abdominal and thigh adiposity, but not with cytokines, disease activity, duration, disability, or disease-modifying medication use.Conclusion.In established and treated RA, traditional risk factors, specifically excess adiposity, play more of a role in predicting skeletal muscle insulin sensitivity than do systemic inflammation or other disease-related factors.


Obesity ◽  
2015 ◽  
Vol 23 (8) ◽  
pp. 1633-1642 ◽  
Author(s):  
J. Patrizia Stohn ◽  
Qiaozeng Wang ◽  
Matthew E. Siviski ◽  
Kevin Kennedy ◽  
Yong-Ri Jin ◽  
...  

2020 ◽  
Vol 52 (7S) ◽  
pp. 984-984
Author(s):  
Hannah K. Schulte ◽  
Sarah E. Neil-Sztramko ◽  
Nagarajan Kannan ◽  
Gift Nyamundanda ◽  
Anguraj Sadanandam ◽  
...  

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