Green satsuma mandarin orange (Citrus unshiu) extract reduces adiposity and induces uncoupling protein expression in skeletal muscle of obese mice

Abstract Uncoupling proteins (UCPs) are mitochondrial proteins that play a role in regulation of energy expenditure by uncoupling respiration from ATP synthesis. Lactation is a physiological condition characterized by negative energy balance due to the loss of energy sources to the production of milk. The objective of the current study was to investigate whether UCP mRNA and protein expressions were altered during lactation compared with those after 48 h of fasting. Lactation significantly reduced serum leptin levels, and removal of pups for 48 h increased serum leptin to higher levels than those observed in control rats. Compared with control rats, mRNA expression of UCP1 and UCP3 in brown adipose tissue (BAT) was dramatically reduced during lactation and fasting. The reduction in mRNAs was reflected by a lowered UCP1 protein level, and to some extent, UCP3 protein. Treatment of lactating rats with exogenous leptin (3 mg/kg) or removal of pups for 48 h completely reversed the down-regulation of UCP1 and UCP3 mRNA expression in BAT, and pup removal led to a recovery of protein expression. In contrast to BAT, UCP3 expression in skeletal muscle was increased in fasted rats and decreased during lactation. Similar changes were observed in serum free fatty acid levels. These changes are consistent with the idea that the utilization of free fatty acids as a fuel source is spared during lactation. As in BAT, leptin treatment and removal of pups were able to restore changes in mRNA expression of UCP3 in skeletal muscle during lactation. The present results suggest that the inhibition of leptin secretion during lactation is involved in the down-regulation of UCP expression in BAT and skeletal muscle, which, in turn, is responsible for the decrease in metabolic fuel oxidation and thermogenesis.

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Aroma Character Impact Compounds in Kinokuni Mandarin Orange (Citrus kinokuni) Compared with Satsuma Mandarin Orange (Citrus unshiu)

Bioscience Biotechnology and Biochemistry ◽

10.1271/bbb.90937 ◽

2010 ◽

Vol 74 (4) ◽

pp. 835-842 ◽

Cited By ~ 22

Author(s):

Norio MIYAZAWA ◽

Akira FUJITA ◽

Kikue KUBOTA

Keyword(s):

Citrus Unshiu ◽

Satsuma Mandarin ◽

Character Impact ◽

Mandarin Orange

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Performance of Satsuma Mandarin Protected from Freezing Temperatures by Microsprinkler Irrigation

HortTechnology ◽

10.21273/horttech.11.1.150a ◽

2001 ◽

Vol 11 (1) ◽

pp. 150a

Author(s):

Monte L. Nesbitt ◽

N.R. McDaniel ◽

Robert C. Ebel ◽

W.A. Dozier ◽

David G. Himelrick

Keyword(s):

Air Temperature ◽

Shoot Tip ◽

Citrus Unshiu ◽

The Third ◽

Satsuma Mandarin ◽

Freezing Temperatures ◽

Mandarin Orange

Several microsprinkler treatments were tested on 5-year-old satsuma mandarin orange (Citrus unshiu Marc.) trees to compare survivability of trunks and scaffold limbs in severe freezes. Three damaging freeze events occurred during winter, with two in 1995-96 and one in 1996-97. Air temperature dropped to -9.4, -5.6, and -6.7 °C, respectively. Almost 90% of the foliage was dead on the control plants after the first freezing event and 98% after the second. A single microsprinkler 1.6 m high in the canopy delivering 90.8 L·h-1 reduced injury; only 54% of the canopy was dead after the first freeze and 71% after the second. There was slightly more shoot-tip dieback on the plants in the microsprinkler treatments than on the control plants after the first two freezes. The amount of limb breakage by ice was minor. The third freeze killed 34% of the canopy in the control plants, but only 26% in the plants in the microsprinkler treatments. Use of microsprinklers increased yield in 1996, but yield for all treatments was very low. Yield for all treatments fully recovered in 1997, averaging 153 kg/tree. Although no death of scaffold limbs or trunks occurred, these results demonstrate that microsprinkler irrigation reduces damage to foliage and increases yield somewhat in severe freezes.

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Uncoupling protein expression in skeletal muscle and adipose tissue in response to in vivo porcine somatotropin treatment

Domestic Animal Endocrinology ◽

10.1016/j.domaniend.2007.12.001 ◽

2008 ◽

Vol 35 (2) ◽

pp. 130-141 ◽

Cited By ~ 3

Author(s):

T.G. Ramsay ◽

A.D. Mitchell ◽

M.P. Richards

Keyword(s):

Skeletal Muscle ◽

Adipose Tissue ◽

Protein Expression ◽

Uncoupling Protein ◽

Porcine Somatotropin

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Expression of uncoupling protein in skeletal muscle and white fat of obese mice treated with thermogenic beta 3-adrenergic agonist.

Journal of Clinical Investigation ◽

10.1172/jci118748 ◽

1996 ◽

Vol 97 (12) ◽

pp. 2898-2904 ◽

Cited By ~ 138

Author(s):

I Nagase ◽

T Yoshida ◽

K Kumamoto ◽

T Umekawa ◽

N Sakane ◽

...

Keyword(s):

Skeletal Muscle ◽

Uncoupling Protein ◽

Obese Mice ◽

Adrenergic Agonist ◽

White Fat

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Performance of Satsuma Mandarin Protected from Freezing Temperatures by Microsprinkler Irrigation

HortScience ◽

10.21273/hortsci.35.5.856 ◽

2000 ◽

Vol 35 (5) ◽

pp. 856-859

Author(s):

Monte L. Nesbitt ◽

N.R. McDaniel ◽

Robert C. Ebel ◽

W.A. Dozier ◽

David G. Himelrick

Keyword(s):

Air Temperature ◽

Shoot Tip ◽

Citrus Unshiu ◽

The Third ◽

Satsuma Mandarin ◽

Freezing Temperatures ◽

Mandarin Orange

Several microsprinkler treatments were tested on 5-year-old satsuma mandarin orange (Citrus unshiu Marc.) trees to compare survivability of trunks and scaffold limbs in severe freezes. Three damaging freeze events occurred during winter, with two in 1995–96 and one in 1996–97. Air temperature dropped to –9.4, –5.6, and –6.7 °C, respectively. Almost 90% of the foliage was dead on the control plants after the first freezing event and 98% after the second. A single microsprinkler 1.6 m high in the canopy delivering 90.8 L·h–1 reduced injury; only 54% of the canopy was dead after the first freeze and 71% after the second. There was slightly more shoot-tip dieback on the plants in the microsprinkler treatments than on the control plants after the first two freezes. The amount of limb breakage by ice was minor. The third freeze killed 34% of the canopy in the control plants, but only 26% in the plants in the microsprinkler treatments. Use of microsprinklers increased yield in 1996, but yield for all treatments was very low. Yield for all treatments fully recovered in 1997, averaging 153 kg/tree. Although no death of scaffold limbs or trunks occurred, these results demonstrate that microsprinkler irrigation reduces damage to foliage and increases yield somewhat in severe freezes.

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Chronic Blockade of Nitric Oxide Synthesis Reduces Adiposity and Improves Insulin Resistance in High Fat-Induced Obese Mice

Endocrinology ◽

10.1210/en.2006-1371 ◽

2007 ◽

Vol 148 (10) ◽

pp. 4548-4556 ◽

Cited By ~ 59

Author(s):

Kyoichiro Tsuchiya ◽

Haruna Sakai ◽

Noriko Suzuki ◽

Fumiko Iwashima ◽

Takanobu Yoshimoto ◽

...

Keyword(s):

Nitric Oxide ◽

Insulin Resistance ◽

Skeletal Muscle ◽

Adipose Tissue ◽

Uncoupling Protein ◽

Serine Phosphorylation ◽

Mrna Levels ◽

Obese Mice ◽

High Fat ◽

Brown Adipose

Genetic deletion of inducible nitric oxide synthase (NOS) in mice has been shown to improve high-fat diet (HFD)-induced insulin resistance. However, a pathophysiological role of endogenous nitric oxide (NO) in obesity-related insulin resistance remains controversial. To address this issue, we examined the metabolic phenotypes in HFD-induced obese mice with chronic blockade of NO synthesis by a NOS inhibitor, N(G)-nitro-l-arginine methyl ester (L-NAME). Six-week-old male C57BL/6j mice were provided free access to either a standard diet (SD) or a HFD and tap water with or without L-NAME (100 mg/kg·d) for 12 wk. L-NAME treatment significantly attenuated body weight gain of mice fed either SD or HFD without affecting calorie intake. L-NAME treatment in HFD-fed mice improved glucose tolerance and insulin sensitivity. HFD feeding induced inducible NOS mRNA expression, but not the other two NOS isoforms, in white adipose tissue (WAT) and skeletal muscle. L-NAME treatment up-regulated uncoupling protein-1 in brown adipose tissue of HFD-fed mice but down-regulated monocyte chemoattractant protein-1 and CD68 mRNAs levels in WAT. HFD feeding up-regulated leptin mRNA levels but conversely down-regulated adiponectin mRNA levels in WAT, but these effects were unaffected by L-NAME treatment. Moreover, L-NAME treatment also increased peroxisome proliferator-uncoupling protein-3 mRNA levels in skeletal muscles of HFD-fed mice. Increased urinary excretion of norepinephrine after HFD feeding was augmented in L-NAME-treated mice. Insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 and serine phosphorylation of Akt/Akt2 in soleus muscle was markedly impaired in HFD-fed mice but reversed by L-NAME treatment. In conclusion, chronic NOS blockade by L-NAME in mice ameliorates HFD-induced adiposity and glucose intolerance, accompanied by reduced adipose inflammation and improved insulin signaling in skeletal muscle, suggesting that endogenous NO plays a modulatory role in the development of obesity-related insulin resistance.

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Expression of uncoupling protein 3 is upregulated in skeletal muscle during sepsis

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00446.2002 ◽

2003 ◽

Vol 285 (3) ◽

pp. E512-E520 ◽

Cited By ~ 18

Author(s):

Xiaoyan Sun ◽

Curtis Wray ◽

Xintian Tian ◽

Per-Olof Hasselgren ◽

James Lu

Keyword(s):

Skeletal Muscle ◽

Protein Expression ◽

Ex Vivo ◽

Uncoupling Protein ◽

Cecal Ligation ◽

Skeletal Muscle Atrophy ◽

Protein Levels ◽

Mitochondrial Transporter ◽

Uncoupling Protein 3 ◽

Gene And Protein Expression

Uncoupling protein 3 (UCP3) is a member of the mitochondrial transporter superfamily that is expressed primarily in skeletal muscle. UCP3 is upregulated in various conditions characterized by skeletal muscle atrophy, including hyperthyroidism, fasting, denervation, diabetes, cancer, lipopolysaccharide (LPS), and treatment with glucocorticoids (GCs). The influence of sepsis, another condition characterized by muscle cachexia, on UCP3 expression and activity is not known. We examined UCP3 gene and protein expression in skeletal muscles from rats after cecal ligation and puncture and from sham-operated control rats. Sepsis resulted in a two- to threefold increase in both mRNA and protein levels of UCP3 in skeletal muscle. Treatment of rats with the glucocorticoid receptor antagonist RU-38486 prevented the sepsis-induced increase in gene and protein expression of UCP3. The UCP3 mRNA and protein levels were increased 2.4- to 3.6-fold when incubated muscles from normal rats were treated with dexamethasone (DEX) and/or free fatty acids (FFA ) ex vivo. In addition, UCP3 mRNA and protein levels were significantly increased in normal rat muscles in vivo with treatment of either DEX or FFA. The results suggest that sepsis upregulates the gene and protein expression of UCP3 in skeletal muscle, which may at least in part be mediated by GCs and FFA.

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Role of UCP3 in state 4 respiration during contractile activity-induced mitochondrial biogenesis

Journal of Applied Physiology ◽

10.1152/japplphysiol.00336.2004 ◽

2004 ◽

Vol 97 (3) ◽

pp. 976-983 ◽

Cited By ~ 35

Author(s):

Vladimir Ljubicic ◽

Peter J. Adhihetty ◽

David A. Hood

Keyword(s):

Skeletal Muscle ◽

Protein Expression ◽

Mitochondrial Biogenesis ◽

Contractile Activity ◽

Uncoupling Protein ◽

Uncoupling Protein 3 ◽

Chronic Electrical Stimulation ◽

The Relationship ◽

The Imf

In an effort to better characterize uncoupling protein-3 (UCP3) function in skeletal muscle, we assessed basal UCP3 protein content in rat intermyofibrillar (IMF) and subsarcolemmal (SS) mitochondrial subfractions in conjunction with measurements of state 4 respiration. UCP3 content was 1.3-fold ( P < 0.05) greater in IMF compared with SS mitochondria. State 4 respiration was 2.6-fold greater ( P < 0.05) in the IMF subfraction than in SS mitochondria. GDP attenuated state 4 respiration by ∼40% ( P < 0.05) in both subfractions. The UCP3 activator oleic acid (OA) significantly increased state 4 respiration in IMF mitochondria only. We used chronic electrical stimulation (3 h/day for 7 days) to investigate the relationship between changes in UCP3 protein expression and alterations in state 4 respiration during contractile activity-induced mitochondrial biogenesis. UCP3 content was increased by 1.9- and 2.3-fold in IMF and SS mitochondria, respectively, which exceeded the concurrent 40% ( P < 0.05) increase in cytochrome- c oxidase activity. Chronic contractile activity increased state 4 respiration by 1.4-fold ( P < 0.05) in IMF mitochondria, but no effect was observed in the SS subfraction. The uncoupling function of UCP3 accounted for 50–57% of the OA-induced increase in state 4 respiration in IMF mitochondria, which was independent of the induced twofold difference in UCP3 content due to chronic contractile activity. Thus modifications in UCP3 function are more important than changes in UCP3 expression in modifying state 4 respiration. This effect is evident in IMF but not SS mitochondria. We conclude that UCP3 at physiological concentrations accounts for a significant portion of state 4 respiration in both IMF and SS mitochondria, with the contribution being greater in the IMF subfraction. In addition, the contradiction between human and rat training studies with respect to UCP3 protein expression may partly be explained by the greater than twofold difference in mitochondrial UCP3 content between rat and human skeletal muscle.

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