Effects of diet and obesity on brown adipose metabolism

1984 ◽  
Vol 246 (5) ◽  
pp. E418-E425
Author(s):  
B. E. Levin ◽  
M. B. Finnegan ◽  
E. Marquet ◽  
J. Triscari ◽  
K. Comai ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Metabolic Activation ◽  
Mitochondrial Morphology ◽  
Sprague Dawley ◽  
High Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Obese Rats ◽  
And Control

The effect of diet-induced obesity on interscapular brown adipose tissue (IBAT) was assessed after feeding male Sprague-Dawley rats a high-fat diet for 3-5 mo beginning at 3 mo of age. IBAT pads in 6-mo-old obese rats were heavier (22%), had more lipid (71%), and larger unilocular cells (38%) than chow-fed controls. Mitochondrial morphology, beta-adrenergic receptor binding ([ 125I]iodocyanopindolol), and norepinephrine-stimulated lipolysis were similar in IBAT from obese and control rats. When 8-mo-old chow-fed rats were switched to the high-fat diet for 7-14 days, IBAT pads became hypercellular without cell hypertrophy and with a 70% increase in norepinephrine-induced lipolysis. However, when 8-mo-old obese rats that had been on the high-fat diet for 5 mo were switched to chow for 3 days, IBAT cellularity was unchanged, but norepinephrine-induced lipolysis was increased 70%. Therefore, in lean and obese 6- to 8-mo-old rats, short-term dietary manipulation led to metabolic activation, whereas chronic diet-induced obesity on a stable diet was associated with a return of IBAT metabolism to control levels.

Brown adipose and metabolic features of chronic diet-induced obesity

1985 ◽  
Vol 248 (6) ◽  
pp. R717-R723 ◽  
Author(s):  
B. E. Levin ◽  
M. Finnegan ◽  
J. Triscari ◽  
A. C. Sullivan
Keyword(s):  
Metabolic Efficiency ◽  
Sprague Dawley ◽  
High Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Plasma Insulin Levels

Half of the 3-mo male Sprague-Dawley rats fed a high-fat (DIO) diet for 5 mo became obese and had increased carcass lipid (106%) and plasma insulin levels (61%), despite 8% less total energy intake than chow-fed controls. Their interscapular brown adipose tissue (IBAT) was 52% heavier with 45% more lipid and larger uni- and multilocular cells. Norepinephrine turnover was normal in their hearts, pancreases, and aortas but undetectable in IBAT where in vitro lipolysis, but not O2 consumption (VO2), was enhanced. Half the rats fed the DIO diet ate 17% fewer calories, gained weight equally to controls, but still had 34% more carcass lipid. Their IBAT was heavier, contained 103% more protein, with no detectable norepinephrine turnover, whereas maximal lipolysis was 73% lower and maximal VO2 was the same or even lower than controls. IBAT VO2 was stimulated by switching 8-mo chow-fed controls to the DIO diet for 7 days (which caused a 480% greater weight gain) but not by switching 8-mo obese rats to chow for 3 days. Therefore metabolic efficiency was increased while BAT VO2 and norepinephrine turnover were unchanged or reduced compared with controls by either chronic obesity or a high-fat diet.

Altered sympathetic activity during development of diet-induced obesity in rat

1983 ◽  
Vol 244 (3) ◽  
pp. R347-R355 ◽  
Author(s):  
B. E. Levin ◽  
J. Triscari ◽  
A. C. Sullivan
Keyword(s):  
Adipose Tissue ◽  
Lipid Content ◽  
Sympathetic Activity ◽  
Turnover Rates ◽  
Sprague Dawley ◽  
Interscapular Brown Adipose Tissue ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Obese Rats ◽  
Relative Body Weight

Sprague-Dawley rats developed diet-induced obesity (DIO) after 3 mo on a high-fat, high-sucrose diet (DIO diet), with associated increases in total body and interscapular brown adipose tissue (IBAT) lipid content. After 7 days on the DIO diet, rats had increased levels of tyrosine hydroxylase (TH; 34%), norepinephrine (NE; 34%), and NE turnover (94%; estimated by alpha-methyl-p-tyrosine inhibition of TH) in their IBAT compared with chow-fed controls. After 3 mo on the DIO diet, NE levels and/or turnover were reduced by 27–50% in aortas, hearts, and pancreata in obese rats. While IBAT NE turnover was normal, TH inhibition failed to increase the lipid content of IBAT in obese rats as it did in controls, suggesting a postsynaptic defect in basal NE-stimulated lipolysis in this thermogenically active tissue. When obese rats were switched from the DIO diet to rat chow for 3 days, NE levels remained depressed in their hearts (25%) and aortas (14%) but were increased by 36–45% in IBAT, pancreata, and white adipose tissue. NE turnover rates and/or constants were increased by 37–110% in hearts, aortas, pancreata, and IBAT of these obese rats while there were increased IBAT TH (20%) and dopamine-beta-hydroxylase (87%) activities compared with chow-fed controls. Therefore, sympathetic activity varied markedly as a function of both dietary composition and relative body weight during the development of DIO.

scholarly journals Does a high-fat diet-induced obesity model brown adipose tissue thermogenesis? A systematic review

2019 ◽  
Author(s):  
Gabriela S. Perez ◽  
Gabriele D.S. Cordeiro ◽  
Lucimeire S. Santos ◽  
Djane D.A. Espírito-Santo ◽  
Gilson T. Boaventura ◽  
...  
Keyword(s):  
Systematic Review ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

scholarly journals Taurine Stimulates Thermoregulatory Genes in Brown Fat Tissue and Muscle without an Influence on Inguinal White Fat Tissue in a High-Fat Diet-Induced Obese Mouse Model

Foods ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 688 ◽  
Author(s):  
Kyoung Soo Kim ◽  
Hari Madhuri Doss ◽  
Hee-Jin Kim ◽  
Hyung-In Yang
Keyword(s):  
Adipose Tissue ◽  
Mouse Model ◽  
High Fat Diet ◽  
Fat Deposition ◽  
Chow Diet ◽  
Fat Tissue ◽  
High Fat ◽  
Taurine Supplementation ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose

This study was conducted to investigate if taurine supplementation stimulates the induction of thermogenic genes in fat tissues and muscles and decipher the mechanism by which taurine exerts its anti-obesity effect in a mildly obese ICR (CD-1®) mouse model. Three groups of ICR mice were fed a normal chow diet, a high-fat diet (HFD), or HFD supplemented with 2% taurine in drinking water for 28 weeks. The expression profiles of various genes were analyzed by real time PCR in interscapular brown adipose tissue (BAT), inguinal white adipose tissue (iWAT), and the quadriceps muscles of the experimental groups. Genes that are known to regulate thermogenesis like PGC-1α, UCP-1, Cox7a1, Cox8b, CIDE-A, and β1-, β2-, and β3-adrenergic receptors (β-ARs) were found to be differentially expressed in the three tissues. These genes were expressed at a very low level in iWAT as compared to BAT and muscle. Whereas, HFD increased the expression of these genes. Taurine supplementation stimulated the expression of UCP-1, Cox7a1, and Cox8b in BAT and only Cox7a1 in muscle, while there was a decrease in iWAT. In contrast, fat deposition-related genes, monoamine oxidases (MAO)-A, and -B, and lipin-1, were decreased by taurine supplementation only in iWAT and not in BAT or muscle. In conclusion, the potential anti-obesity effects of taurine may be partly due to upregulated thermogenesis in BAT, energy metabolism of muscle, and downregulated fat deposition in iWAT.

Diet, lighting, and food intake affect norepinephrine turnover in dietary obesity

1987 ◽  
Vol 252 (2) ◽  
pp. R402-R408 ◽  
Author(s):  
T. Yoshida ◽  
J. S. Fisler ◽  
M. Fukushima ◽  
G. A. Bray ◽  
R. A. Schemmel
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Brown Fat ◽  
Light Cycle ◽  
High Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Dietary Obesity

The effects of dietary fat content, lighting cycle, and feeding time on norepinephrine turnover in interscapular brown adipose tissue, heart, and pancreas, and on blood 3-hydroxybutyrate, serum glucose, insulin, and corticosterone have been studied in two strains of rats that differ in their susceptibility to dietary obesity. S 5B/Pl rats, which are resistant to dietary obesity, have a more rapid turnover of norepinephrine in interscapular brown adipose tissue and heart and a greater increase in the concentration of norepinephrine in brown fat when eating a high-fat diet than do Osborne-Mendel rats, which are sensitive to fat-induced obesity. Light cycle and feeding schedule are important modulators of sympathetic activity in heart and pancreas but not in brown fat. Rats of the resistant strain also have higher blood 3-hydroxybutyrate concentrations and lower insulin and corticosterone levels than do rats of the susceptible strain. A high-fat diet increases 3-hydroxybutyrate concentrations and reduces insulin levels in both strains. These studies show, in rats eating a high-fat diet, that differences in norepinephrine turnover, particularly in brown adipose tissue, may play an important role in whether dietary obesity develops and in the manifestations of resistance to this phenomenon observed in the S 5B/Pl rat.

Catecholamine turnover in S 5B/P1 and Osborne-Mendel rats: response to a high-fat diet

1984 ◽  
Vol 247 (2) ◽  
pp. R290-R295 ◽  
Author(s):  
J. S. Fisler ◽  
T. Yoshida ◽  
G. A. Bray
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
High Fat Diet ◽  
Turnover Rate ◽  
High Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Catecholamine Turnover ◽  
Norepinephrine Turnover ◽  
Brown Adipose

Catecholamine turnover in response to fasting, cold exposure, and a high-fat diet has been measured in the Osborne-Mendel rat, which readily develops obesity when fed a high-fat diet, and the S 5B/P1 rat, which does not. We have tested the hypothesis that this difference in response to diet might be associated with altered rates of norepinephrine or epinephrine turnover. The endogenous norepinephrine concentration in interscapular brown adipose tissue was significantly greater in fasted S 5B/P1 rats than in fasted Osborne-Mendel rats. The fractional norepinephrine turnover rate in interscapular brown adipose tissue of fasted animals was also greater in the S 5B/P1 rat than in the Osborne-Mendel rat. Cold exposure increased the fractional norepinephrine turnover rate in interscapular brown adipose tissue for both strains of rats but increased the fractional norepinephrine turnover rate in the pancreas in only the Osborne-Mendel rats. The turnover of epinephrine and the adrenal concentration of this hormone were not different between the two strains. Normal and high-fat diets were fed to both strains; the Osborne-Mendel rats were pair fed the high-fat diet to prevent excess weight gain. Endogenous concentrations of norepinephrine in interscapular brown adipose tissue was increased by the high-fat diet; the increase was greater in S 5B/P1 rats. The high-fat diet resulted in increased norepinephrine turnover in interscapular brown adipose tissue of the S 5B/P1 rat but not the Osborne-Mendel rat.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effects of Diet-Induced Obesity and Deficient in Vitamin D on Spermatozoa Function and DNA Integrity in Sprague-Dawley Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
O. Merino ◽  
R. Sánchez ◽  
B. M. Gregorio ◽  
F. J. Sampaio ◽  
J. Risopatrón
Keyword(s):  
Vitamin D ◽  
Dna Fragmentation ◽  
High Fat Diet ◽  
Control Diet ◽  
Sperm Function ◽  
Sprague Dawley ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
The Impact

Obesity has adverse effects on male fertility and usually is diagnosed with a prevalence of vitamin D deficiency (VD-). Discussion on the impact of obesity/VD- on sperm function has been limited. This study analyzed the effects of diet-induced obesity/VD- on viability and plasma membrane integrity (PMI), superoxide anion (O2-) level, and DNA fragmentation (DNAfrag) in sperm Sprague-Dawley rats. The males were randomized into four groups and fed for a period of 12 weeks: G1: control diet with vitamin D (C/VD+), G2: control diet without vitamin D (C/VD-), G3: high-fat diet with vitamin D (HF/VD+), and G4: high-fat diet without vitamin D (HF/VD-). Sperm function parameters were analyzed by flow cytometry. PMI percentages and O2- levels were not affected by any of the diets. DNA fragmentation was increasing significantly (p<0.05) in the spermatozoa of animals with diets vitamin D deficient (G2) and diet-induced obesity (G4). Our results allow us to point out that diet-induced obesity and VD- produce greater damage in DNA sperm of rats. The use of nutraceuticals containing vitamin D could be reducing the risk of fragmentation of DNA in spermatozoa.

Hypertension and sympathetic hyperactivity induced in rats by high-fat or glucose diets

1991 ◽  
Vol 260 (1) ◽  
pp. E95-E100 ◽  
Author(s):  
L. N. Kaufman ◽  
M. M. Peterson ◽  
S. M. Smith
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Control Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Hypertensive Rats ◽  
Diet Treatment ◽  
Sprague Dawley Rats ◽  
Sympathetic Nervous ◽  
And Control

Male Sprague-Dawley rats fed either a high-fat diet or a glucose-enriched diet developed higher blood pressure (BP) than rats fed a control diet. After 8 wk of diet treatment systolic BP was 11% higher (P less than 0.01) in fat-fed rats and 7% higher (P less than 0.05) in glucose-fed rats when compared with rats fed the control diet. Rats fed the high-fat diet developed hypertension only when they were allowed to overeat and become obese and hyperinsulinemic. But when their feeding was restricted to prevent obesity and hyperinsulinemia, they remained normotensive. In contrast, elevated BP developed in rats consuming the glucose diet in the absence of obesity or hyperinsulinemia. After 7 wk of diet treatment, urinary norepinephrine excretion was 1.9 +/- 0.1, 1.9 +/- 0.1, and 1.5 +/- 0.1 micrograms/day in rats fed the high-fat, glucose, and control diets, respectively (P less than 0.05 vs. control). Higher norepinephrine excretion in hypertensive rats suggests that increased sympathetic nervous system (SNS) activity might participate in mediating the effects of dietary fat or glucose on BP. In addition, insulin may contribute to raising BP in rats fed the high-fat diet, either directly or indirectly through its stimulatory effect on the SNS. We conclude that chronic feeding of diets high in fat or glucose increases BP and enhances SNS activity in rats.

scholarly journals Differential Effects of Combined Soluble Epoxide Hydrolase Inhibitor t-TUCB and n-3 Epoxides in Diet-Induced Obesity

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1260-1260
Author(s):  
Yang Yang ◽  
Xinyun Xu ◽  
Christophe Morisseau ◽  
Bruce Hammock ◽  
Ahmed Bettaieb ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Protein Expression ◽  
Cold Tolerance ◽  
High Fat Diet ◽  
Epoxide Hydrolase ◽  
Soluble Epoxide Hydrolase ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Brown Adipose

Abstract Objectives Brown adipose tissue (BAT) is a promising target for obesity prevention. N-3 epoxides are fatty acid epoxides produced from n-3 polyunsaturated fatty acids and shown to be beneficial for health. However, these epoxides are unstable and quickly metabolized by the cytosolic soluble epoxide hydrolase (sEH). Here, we investigated the effects of sEH inhibitor (t-TUCB) alone or combined with two different n-3 epoxides on BAT activation in the development of diet-induced obesity and associated metabolic disorders. Methods Male C57BL6/J mice were fed a high-fat diet and received either of the following treatment: the vehicle control, t-TUCB alone (T), or t-TUCB combined with 19,20-EDP (T + EDP) or 17,18-EEQ (T + EEQ) via osmotic minipump delivery near the interscapular BAT for 6 weeks. Mice were examined for changes in body weight, food intake, glucose, insulin, and cold tolerance tests, and indirect calorimetry. Blood and tissue biochemical analyses were also performed to assess changes in metabolic homeostasis. Results Although no differences in food intake were observed, there were small but significant increases in body weight in both T and T + EDP groups. Mice in the T + EDP and T + EEQ groups showed significant decreases in fasting glucose and serum TG levels, higher core body temperature, and better cold tolerance compared to the controls. However, heat production was significantly increased only in the T + EEQ group. Thermogenic UCP1 protein expression showed a moderate, but not significant, increase in the T + EEQ group. On the other hand, PGC1 α protein expression was significantly increased in the T, T + EDP, and T + EEQ groups compared to the controls. Perilipin protein expression and phosphorylation were also significantly increased in the three treated groups. In contrast, protein expression of FABP4 and HSL was only increased in the T and T + EDP groups, and CD36 protein expression was only increased in the T + EEQ group. Conclusions Our results suggest that sEH pharmacological inhibition by t-TUCB combined with n-3 epoxides may prevent high-fat diet-induced glucose and lipid disorders, in part through increased thermogenesis and upregulating of protein expression of thermogenic and lipid metabolic genes. Funding Sources The work was supported by NIH grants to L.Z., A.B., and B.D.H.

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