Osmotically inactive skin Na+ storage in rats

2003 ◽  
Vol 285 (6) ◽  
pp. F1108-F1117 ◽  
Author(s):  
Jens Titze ◽  
Rainer Lang ◽  
Christoph Ilies ◽  
Karl H. Schwind ◽  
Karl A. Kirsch ◽  
...  
Keyword(s):  
Dry Weight ◽  
The Body ◽  
Sprague Dawley ◽  
Connective Tissues ◽  
Salt Diet ◽  
Sd Rats ◽  
Ovx Rats ◽  
Dry Ashing ◽  
Total Body ◽  
Salt Sensitive Hypertension

Compared with age-matched men, women are resistant to the hypertensive effects of dietary NaCl; however, after menopause, the incidence of salt-sensitive hypertension is similar in women and men. We recently suggested that osmotically inactive Na+ storage contributes to the development of salt-sensitive hypertension. The connective tissues, including those immediately below the skin that may serve as a reservoir for osmotically inactive Na+ storage, are affected by menopause. We tested the hypothesis that ovariectomy (OVX) might reduce osmotically inactive Na+ storage capacity in the body, particularly in the skin. Male, female-fertile, and female OVX Sprague-Dawley (SD) rats were fed a high (8%)- or low (0.1%)-NaCl diet. The groups received the diet for 4 or 8 wk. At the end of the experiment, subgroups received 0.9% saline infusion and urinary Na+ and K+ excretion was measured. Wet and dry weight (DW), water content in the body and skin, total body Na+ (rTBNa+) and skin Na+ (rSKNa+) content were measured relative to DW by desiccation and dry ashing. There were no gender differences in osmotically inactive Na+ storage in SD rats. All SD rats accumulated Na+ if fed 8% NaCl, but rTBNa+ was lower in OVX rats than in fertile rats on a low ( P < 0.001)- and a high ( P < 0.05)-salt diet. OVX decreased rSKNa+ ( P < 0.01) in the rats. A high-salt diet led to Na+ accumulation (ΔSKNa+) in the skin in all SD rats. Osmotically inactive skin Na+ accumulation was ∼66% of ΔSKNa+ in female and 82% in male-fertile rats, but there was no osmotically inactive Na+ accumulation in OVX rats fed 8% NaCl. We conclude that skin is an osmotically inactive Na+ reservoir that accumulates Na+ when dietary NaCl is excessive. OVX leads to an acquired reduction of osmotically inactive Na+ storage in SD rats that predisposes the rats to volume excess despite a reduced Na+ content relative to body weight.

Reduced osmotically inactive Na storage capacity and hypertension in the Dahl model

2002 ◽  
Vol 283 (1) ◽  
pp. F134-F141 ◽  
Author(s):  
Jens Titze ◽  
Holger Krause ◽  
Hermann Hecht ◽  
Peter Dietsch ◽  
Jörn Rittweger ◽  
...  
Keyword(s):  
Water Retention ◽  
Storage Capacity ◽  
Sprague Dawley ◽  
Fluid Accumulation ◽  
Rat Strains ◽  
Sd Rats ◽  
Inactive Form ◽  
Dry Ashing ◽  
Total Body

Recent evidence suggested that Na can be stored in an osmotically inactive form. We investigated whether osmotically inactive Na storage is reduced in a rat model of salt-sensitive (SS) hypertension. SS and salt-resistant (SR) Dahl-Rapp rats as well as Sprague-Dawley (SD) rats were fed a high (8%)- or low (0.1%)-NaCl diet for 4 wk ( n = 10/group). Mean arterial pressure (MAP) was measured at the end of the experiment. Wet and dry weights, water content, total body Na (TBS), and bone Na content were measured by dessication and dry ashing. MAP was higher in both Dahl strains than in SD rats. In SS rats, 8% NaCl led to Na accumulation, water retention, and hypertension due to impaired renal Na excretion. There was no dietary-induced Na retention in SR and SD rats. TBS was variable; nevertheless, TBS was significantly correlated with body water and MAP in all strains. However, the extent of Na-associated volume and MAP increases was strain specific. Osmotically inactive Na in SD rats was threefold higher than in SS and SR rats. Both SS and SR Dahl rat strains displayed reduced osmotically inactive Na storage capacity compared with SD controls. A predisposition to fluid accumulation and high blood pressure results from this alteration. Additional factors, including impaired renal Na excretion, probably contribute to hypertension in SS rats. Our results draw attention to the role of osmotically inactive Na storage.

Abstract P327: Increased Brain iNOS Contributes to Hypertension in Dahl Salt Sensitive Rats

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Michael J Huber ◽  
Fengli Zhu ◽  
Robert A Larson ◽  
Qing-Hui Chen ◽  
Zhiying Shan
Keyword(s):  
Hypertonic Saline ◽  
Neural Mechanism ◽  
Neuronal Cultures ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Inos Activity ◽  
Arterial Blood ◽  
Sd Rats ◽  
Inos Inhibitor ◽  
Salt Sensitive Hypertension

The hypothalamic paraventricular nucleus (PVN) is one of the key central nuclei to play an important role in regulating arterial blood pressure (ABP) of salt-sensitive hypertension (SSH). However, the detailed molecular mechanism(s) whereby the PVN increases ABP are not well understood. Here, we tested the hypothesis that high salt (HS) loading increases expression of iNOS in the PVN which contributes to SSH. Six-week-old male Dahl salt sensitive (Dahl S) rats and age matched Sprague Dawley (SD) rats were fed either a HS (4% NaCI) or a normal salt (NS, 0.4% NaCl) diet (n=4~7/group). Mean arterial pressure (MAP) was measured via tail cuff method. Five weeks following diet treatment, HS diet induced hypertension in Dahl S rats (HS: 153±9; vs. NS: 122±2 mmHg, P<0.05), but not in SD rats (HS: 107±3; vs. NS: 107±2 mmHg). Rats were then euthanized and PVN tissues were punched out for real time PCR. The HS diet induced dramatic increases in mRNA levels of iNOS (25-fold), and Fra1 (3.6-fold), a chronic neuronal activation marker, in Dahl S rat but not in SD rats. Next, we investigated the effect of intracerebroventricular (ICV) administration of hypertonic saline on PVN iNOS and Fra1 expression in SD rats. Anesthetized adult male SD rats received ICV infusion of isotonic NaCI (0.15 M, 2μl, as control) or hypertonic NaCI (2M, 2μl) (n=7~8/group). Three hours following ICV infusion, rats were euthanized and PVN mRNA levels of iNOS and Fra1 were assayed. ICV hypertonic saline increased mRNA levels of iNOS (9.5-fold) and Fra1 (4.1-fold). We further tested whether these increases in iNOS and Fra1 expression occurred in neurons. Incubation of hypertonic saline (10 mM NaCI) for 3 hours increased iNOS (6-fold) and Fra1 (2.8-fold) mRNA levels in neuronal cultures from the hypothalamus containing the PVN. Finally, we tested whether increased iNOS activity contributes to ABP elevation in Dahl SSH. In anaesthetized Dahl S rats, bilateral PVN microinjection of the iNOS inhibitor, aminoguanidine (250 pmol) significantly decreased MAP in HS treated animals compared to rats with a NS diet (HS: -13±3; vs. NS: -2±2 mmHg, P<0.05) (n=5/group). These observations suggest that HS intake increases iNOS expression in PVN neurons, which may contribute to the central neural mechanism of Dahl SSH.

Mobilization of osmotically inactive Na+ by growth and by dietary salt restriction in rats

2007 ◽  
Vol 292 (5) ◽  
pp. F1490-F1500 ◽  
Author(s):  
Markus Schafflhuber ◽  
Nicola Volpi ◽  
Anke Dahlmann ◽  
Karl F. Hilgers ◽  
Francesca Maccari ◽  
...  
Keyword(s):  
Binding Capacity ◽  
Dry Weight ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Salt Restriction ◽  
Sprague Dawley Rats ◽  
Low Salt ◽  
Total Body ◽  
Dietary Salt Restriction

The idea that an osmotically inactive Na+ storage pool exists that can be varied to accommodate states of Na+ retention and/or Na+ loss is controversial. We speculated that considerable amounts of osmotically inactive Na+ are lost with growth and that additional dietary salt excess or salt deficit alters the polyanionic character of extracellular glycosaminoglycans in osmotically inactive Na+ reservoirs. Six-week-old Sprague-Dawley rats were fed low-salt (0.1%; LS) or high-salt (8%; HS) diets for 1 or 4 wk. At their death, we separated the tissues and determined their Na+, K+, and water content. Three weeks of growth reduced the total body Na+ content relative to dry weight (rTBNa+) by 23%. This “growth-programmed” Na+ loss originated from the bone and the completely skinned and bone-removed carcasses. The Na+ loss was osmotically inactive (45–50%) or osmotically active (50–55%). In rats aged 10 wk, compared with HS, 4 wk of LS reduced rTBNa+ by 9%. This dietary-induced Na+ loss was osmotically inactive (≈50%) and originated largely from the skin, while ≈50% was osmotically active. LS for 1 wk did not reduce skin Na+ content. The mobilization of osmotically inactive skin Na+ with long-term salt deprivation was associated with decreased negatively charged skin glycosaminoglycan content and thereby a decreased water-free Na+ binding capacity in the extracellular matrix. Our data not only serve to explain discrepant results in salt balance studies but also show that glycosaminoglycans may provide an actively regulated interstitial cation exchange mechanism that participates in volume and blood pressure homeostasis.

Abstract 296: Norepinephrine Evoked Salt-Sensitive Hypertension Results in Impaired NCC Function, but Not Expression

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Kathryn Walsh ◽  
Sarah Mahne ◽  
Jill T Kuwabara ◽  
Richard D Wainford
Keyword(s):  
Salt Intake ◽  
Pcr Analysis ◽  
Kidney Cortex ◽  
Sprague Dawley ◽  
Sodium Homeostasis ◽  
Sd Rats ◽  
High Salt Intake ◽  
Induced Hypertension ◽  
Salt Sensitive Hypertension ◽  
The Impact

Aim: Recent controversial studies have proposed that excess norepinephrine (NE) evokes impaired NCC regulation to drive salt-sensitive hypertension. The following studies examine the impact of excess NE on salt-sensitivity and sodium homeostasis in conscious Sprague-Dawley (SD) rats. Methods: Naïve male SD rats, rats receiving a s.c. vehicle infusion (DMSO/Saline, 50:50), or rats receiving a s.c. NE infusion (600ng/min) were fed a 0.4% (NS) or 8% NaCl (HS) diet for 14 days. Additional rats received s.c. hydrochlorothiazide (HCTZ, 4mg/kg/d) in combination with NE (600ng/min) for 14 days on HS. On day 14, MAP, FENa, MAP response to i.v. hexamethonium (30mg/kg), and peak natriuresis to i.v. HCTZ (2mg/kg) infusion were assessed (N=4/gp). A PCR array examining NCC associated genes was performed on kidney cortex samples from each group. Results: NE increased MAP, FENa and vascular sympathetic tone (MAP [mmHg] NS 127±2, NE+NS 151±3, p<0.05). We observed no difference between the naïve and vehicle rats. A HS diet exacerbated NE induced hypertension (MAP [mmHg] HS 129±2, NE+HS 172±4, p<0.05), reduced FENa and prevented a salt stimulated reduction in HCTZ evoked natriuresis. Co-infusion of HCTZ with NE abolished the salt-sensitive component of NE-induced hypertension (MAP [mmHg] NE+HCTZ+HS: 152±3, p<0.05). PCR analysis revealed a significant increase in serine/threonine kinase 39 (0.83-fold increase vs. Naïve SD on NS) mRNA in NE+HS rats. We did not see NE or HS evoked changes in OSR-1, WNK4 or NCC mRNA in any group. Conclusion: The results support previous studies in mice and highlight an opposing interaction between excess NE and high salt intake on sodium homeostasis which exacerbated NE-induced hypertension via a mechanism independent of NE-mediated vascular constriction. Physiologically, our results show impaired NCC function, supporting previous data. In contrast, we failed to detect elevated NCC or WNK4 mRNA in response to NE infusion contradicting data generated in mice and suggesting a key role of altered NCC phosphorylation versus expression in NE treated rats.

scholarly journals Failure to upregulate the adenosine2A receptor-epoxyeicosatrienoic acid pathway contributes to the development of hypertension in Dahl salt-sensitive rats

2008 ◽  
Vol 295 (6) ◽  
pp. F1696-F1704 ◽  
Author(s):  
Elvira L. Liclican ◽  
John C. McGiff ◽  
John R. Falck ◽  
Mairéad A. Carroll
Keyword(s):  
Renal Perfusion ◽  
Epoxyeicosatrienoic Acid ◽  
Sprague Dawley ◽  
Salt Loading ◽  
Vasodilator Response ◽  
Sd Rats ◽  
Acid Pathway ◽  
Salt Sensitive Hypertension ◽  
Dose Dependent

Adenosine-activated renovascular dilatation in Sprague-Dawley (SD) rats is mediated by stimulating adenosine2A receptors (A2AR), which is linked to epoxyeicosatrienoic acid (EET) synthesis. The A2AR-EET pathway is upregulated by high salt (HS) intake in normotensive SD rats. Because this pathway is antipressor, we examined the role of the A2AR-EET pathway in Dahl salt-sensitive (SS) rats. Male Dahl salt-resistant (SR) and SS rats were fed either HS (8.0% NaCl) or normal salt (NS; 0.4% NaCl) diet for 7 days. On day 8, isolated kidneys were perfused with Krebs-Henseleit buffer containing indomethacin and NG-nitro-l-arginine methyl ester and preconstricted with phenylephrine. Bolus injections of the stable adenosine analog 2-chloroadenosine (2-CA; 0.1–20 μg) elicited dose-dependent dilation in both Dahl SR and SS rats. Dahl SR rats fed a HS diet demonstrated a greater renal vasodilator response to 10 μg of 2-CA, as measured by the reduction in renal perfusion pressure, than that of Dahl SR rats fed a NS diet (−104 ± 6 vs. −77 ± 7 mmHg, respectively; P < 0.05). In contrast, Dahl SS rats did not exhibit a difference in the vasodilator response to 2-CA whether fed NS or HS diet (96 ± 6 vs. 104 ± 13 mmHg in NS- and HS-fed rats, respectively). In Dahl SR but not Dahl SS rats, HS intake significantly increased purine flux, augmented the protein expression of A2AR and the cytochrome P-450 2C23 and 2C11 epoxygenases, and elevated the renal efflux of EETs. Thus the Dahl SR rat is able to respond to HS intake by recruiting EET formation, whereas the Dahl SS rat appears to have exhausted its ability to increase EET synthesis above the levels observed on NS intake, and this inability of Dahl SS rats to upregulate the A2AR-EET pathway in response to salt loading may contribute to the development of salt-sensitive hypertension.

scholarly journals Increased activity of the orexin system in the paraventricular nucleus contributes to salt-sensitive hypertension

2017 ◽  
Vol 313 (6) ◽  
pp. H1075-H1086 ◽  
Author(s):  
Michael J. Huber ◽  
Yuanyuan Fan ◽  
Enshe Jiang ◽  
Fengli Zhu ◽  
Robert A. Larson ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Paraventricular Nucleus ◽  
Mrna Levels ◽  
Nacl Solution ◽  
Sprague Dawley ◽  
Orexin A ◽  
Intracerebroventricular Infusion ◽  
Sd Rats ◽  
Salt Sensitive Hypertension ◽  
Increased Activity

The orexin system is involved in arginine vasopressin (AVP) regulation, and its overactivation has been implicated in hypertension. However, its role in salt-sensitive hypertension (SSHTN) is unknown. Here, we tested the hypothesis that hyperactivity of the orexin system in the paraventricular nucleus (PVN) contributes to SSHTN via enhancing AVP signaling. Eight-week-old male Dahl salt-sensitive (Dahl S) and age- and sex-matched Sprague-Dawley (SD) rats were placed on a high-salt (HS; 8% NaCl) or normal-salt (NS; 0.4% NaCl) diet for 4 wk. HS intake did not alter mean arterial pressure (MAP), PVN mRNA levels of orexin receptor 1 (OX1R), or OX2R but slightly increased PVN AVP mRNA expression in SD rats. HS diet induced significant increases in MAP and PVN mRNA levels of OX1R, OX2R, and AVP in Dahl S rats. Intracerebroventricular infusion of orexin A (0.2 nmol) dramatically increased AVP mRNA levels and immunoreactivity in the PVN of SD rats. Incubation of cultured hypothalamus neurons from newborn SD rats with orexin A increased AVP mRNA expression, which was attenuated by OX1R blockade. In addition, increased cerebrospinal fluid Na+ concentration through intracerebroventricular infusion of NaCl solution (4 µmol) increased PVN OX1R and AVP mRNA levels and immunoreactivity in SD rats. Furthermore, bilateral PVN microinjection of the OX1R antagonist SB-408124 resulted in a greater reduction in MAP in HS intake (−16 ± 5 mmHg) compared with NS-fed (−4 ± 4 mmHg) anesthetized Dahl S rats. These results suggest that elevated PVN OX1R activation may contribute to SSHTN by enhancing AVP signaling. NEW & NOTEWORTHY To our best knowledge, this study is the first to investigate the involvement of the orexin system in salt-sensitive hypertension. Our results suggest that the orexin system may contribute to the Dahl model of salt-sensitive hypertension by enhancing vasopressin signaling in the hypothalamic paraventricular nucleus.

Abstract P334: Sympathetically Mediated Alpha-1 Adrenoceptor Regulation of the NCC During High Salt Intake: A New Therapeutic Target for Resistant Hypertension

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Richard D Wainford ◽  
Kathryn R Walsh
Keyword(s):  
Salt Intake ◽  
Dietary Sodium ◽  
Primary Role ◽  
Sprague Dawley ◽  
Sd Rats ◽  
High Salt Intake ◽  
Adrenoceptor Regulation ◽  
Salt Sensitive Hypertension ◽  
Expression And Activity

Aim: We hypothesize that excess norepinephrine (NE) modulates NCC activity via an α1 adrenoceptor pathway to drive the development of salt-sensitive hypertension (HTN). Methods: Male Sprague-Dawley (SD) rats receiving a continuous s.c. saline or NE (600ng/min) infusion and naïve Dahl Salt-Sensitive (DSS) rats were fed a 0.6% (NS) or 8% NaCl (HS) diet for 14 or 21 days respectively (N=4/gp). On day 14 (SD) or 21 (DSS) MAP and NCC activity (peak natriuresis to iv hydrochlorothiazide (HCTZ; 2mg/kg) infusion) and expression (via immunoblotting) was assessed. Additional groups of NE infused SD and DSS rats received a propranolol (9.9mg/kg/day; s.c.) or prazosin (2.5mg/kg/day; oral) and a NS or HS diet for 14 or 21 days. Results: SD rats exhibit HS evoked suppression of NCC expression and activity. In contrast, NE infused SD rats and DSS rats exhibit HTN and fail to suppress NCC expression and activity during HS-intake. β-adrenoceptor antagonism (confirmed pharmacologically) reduced MAP in NE infused SD and DSS rats, but failed to decrease NCC activity or expression. In contrast α1-adreoceptor antagonism (confirmed pharmacologically) abolished the salt-sensitive component of HTN and restored dietary sodium evoked suppression of NCC activity and expression in NE infused SD rats and DSS rats. Conclusion: Our data suggests NE activates α, but not β, adrenoceptors to prevent dietary sodium evoked suppression of NCC activity and the development of salt-sensitive hypertension. The PATHWAY-2 Trial reported a primary role of sodium retention in resistant HTN suggesting α1-adreoceptor antagonism represents a new therapeutic approach for resistant and sympathetically mediated HTN.

Regulatory Effect of Angelica sinensis Polysaccharide on Bcl-2/Bax/Caspase-3 Signal Pathway in Spleen of Rats with Radiation Injury

2020 ◽  
Vol 14 (4) ◽  
pp. 579-583
Author(s):  
Tian-Li Chen ◽  
Tong-Tong Song ◽  
Xu Sun ◽  
Yi-Wen Gu ◽  
Wen-Jing Du ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Signal Pathway ◽  
The Body ◽  
Normal Group ◽  
Angelica Sinensis ◽  
High Dose ◽  
Model Group ◽  
Sprague Dawley ◽  
Expression Levels ◽  
Sd Rats

To investigate the protective effect of Angelica sinensis polysaccharide (ASP) on spleen injury and its influence of Bcl-2/Bax/Caspase-3 signal pathway in radiation rats, 60 Sprague Dawley (SD) rats were divided into 5 groups randomly: the normal group, the model group, low-, middle- and high- dose of ASP groups. On the 15th day after the appropriate medication, all the rats except the normal group received the 60Co γ-ray irradiation once with a total dose of 4.0Gy. The levels of NF-kBp65 and IKKa in serum, the contents of MDA, GSH and SOD in spleen of each group were detected with ELISA after 24 h of irradiation, and the protein expression levels of Bcl-2, Bax, Caspase-3, HSPBP1 and TIMM8B in spleen of each group were detected by western blotting. The results showed that compared with the model group, NF-kBp65, IKKa and MDA contents were decreased while GSH and SOD contents were increased in the middle and high dose groups. The level of Bcl-2 and TIMM8B were increased while Bax, caspase-3 and HSPBP1 were decreased in all groups. In conclusion, Angelica sinensis polysaccharide can reduce the expression levels of Bax and caspase-3, while increase the level of Bcl-2 in spleen of rats induced by radiation and antagonize the body injury caused by radiation by regulating Bcl 2/Bax/Caspase 3 signaling pathway.

VARIATIONS IN THE VOLUME AND CONCENTRATION OF THE BLOOD OF THE SNAIL, HELIX POMATIA L., IN RELATION TO THE WATER CONTENT OF THE BODY

1964 ◽  
Vol 42 (6) ◽  
pp. 1085-1097 ◽  
Author(s):  
R. F. Burton
Keyword(s):  
Water Content ◽  
Blood Volume ◽  
Total Body Water ◽  
Helix Pomatia ◽  
Dry Weight ◽  
Sodium Concentration ◽  
The Body ◽  
Albumen Gland ◽  
Snail Helix Pomatia ◽  
Total Body

A convenient measure of the "size" of a snail is its dry weight, exclusive of shell and albumen gland, and, where calculable, its blood solutes. The specimens of Helix pomatia studied contained between 3.8 and 10.2 g of Water per gram dry weight and between 51 and 456 mg of copper per kilogram dry weight. When "copper space" was defined as the weight of blood water that would contain the amount of copper present in the body, copper spaces varied between 1.1 and 4.4 g of water per gram dry weight. Variations in copper space (approximately equal to blood volume) accounted for the greater part of the variation in total body water, though the amount of water in the tissues was also variable. The concentration of sodium in the blood varied naturally over the range 46–129 mmole/kg of water, varying proportionately with chloride. Variations in sodium concentration are largely due to variations in the volume of blood in which the sodium is dissolved, but a given change in blood volume is, in general, associated with a proportionately smaller change in sodium concentration.

scholarly journals Effect of Acupuncture on Simple Obesity and Serum Levels of Prostaglandin E and Leptin in Sprague-Dawley Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Xiaomin Li ◽  
Zijian Wu ◽  
Yenong Chen ◽  
Ronglin Cai ◽  
Zhizhen Wang
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Serum Levels ◽  
Normal Diet ◽  
The Body ◽  
Liver Fat ◽  
Prostaglandin E ◽  
Sprague Dawley ◽  
Sd Rats ◽  
Simple Obesity

Aim. The study is aimed at investigating the curative effect of acupuncture on simple obesity and its influence on serum levels of prostaglandin E and leptin in Sprague-Dawley (SD) rats. Methods. In the study, there are 50 male SD rats. We took 10 as healthy controls and fed 40 with a diet of high fat for 8 weeks. After the 40 rat model was established successfully, we fed 10 rats in the model group with a normal diet and treated 10 rats in the acupuncture group by acupuncture. During the experiment, the body fat and body length of rats were measured weekly, and Lee’s index was calculated. After the treatment, the levels of leptin, prostaglandin E, C-reactive protein (CRP), triacylglycerol (TG), cholesterol (CHO), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) were detected, and the liver fat morphology was observed by electron microscope. Results. Acupuncture significantly downregulated the serum levels of CRP, TG, CHO, LDL, leptin, and prostaglandin E and upregulated the serum levels of HDL in rats with simple obesity. Conclusion. On basis of these results, it was found that acupuncture could boost fat metabolism and weight loss by inhibiting the production of leptin and prostaglandin E.

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