Chronic mild stress induces variations in locomotive behavior and metabolic rates in high fat fed...

Correspondence to J. A. Martínez (Tel. +34 948 425 600; Fax. +34 948 425 649; e-mail: [email protected]).

Chronic mild stress induces variations in locomotivebehavior and metabolic rates in high fat fed rats

D. F. García-Díaz1, J. Campion1, F. I. Milagro1, A. Lomba1, F. Marzo2

and J. A. Martínez1

1Department of Nutrition, Food Science, Physiology and Toxicology, University ofNavarra, 2Laboratory of Animal Physiology and Nutrition, School of Agronomy, Pub-

lic University of Navarra, Pamplona, Spain

(Received on November, 2007)

D. F. García-Díaz, J. Campion, F. I. Milagro, A. Lomba, F. Marzo and J. A.Martínez. Chronic mild stress induces variations in locomotive behaviour and meta-bolic rates in high fat fed rats. J. Physiol. Biochem., 63 (4), 337-346, 2007.

Chronic mild stress (CMS) has been often associated to the pathogenesis of manydiseases including obesity. Indeed, visceral obesity has been linked to the develop-ment of metabolic syndrome features and constitutes a serious risk factor for cardio-vascular diseases and diabetes. In order to study possible mechanistic relationshipsbetween stress and the onset of obesity, we developed during 11 weeks a model ofhigh-fat dietary intake (cafeteria diet) together with a CMS regimen in male Wistarrats. During the experimental period, basal metabolism by indirect calorimetry, rec-tal temperature, food intake, and locomotive markers were specifically analyzed.After 77 days, animals were sacrificed and body, adiposity and plasma biochemicalprofiles were also examined. As expected, cafeteria diet in unstressed animals induceda significative increase in body weight, adiposity, and insulin resistance markers.Locomotive variables, specifically distance, rearing and meander, were significantlyincreased by CMS on the first weeks of stress. Moreover, this model of CMS in Wis-tar rats increased significantly energy expenditure, and apparently interplayed withthe dietary treatment on the muscle weight/fat weight ratio. In summary, this chron-ic stress model did not affected weight gain in control and high fat fed animals, butinduced an interaction concerning the metabolic muscle/fat repartitioning.

Key-words: Obesity, Stress, Cafeteria diet, Locomotive activity, Calorimetry.

J. Physiol. Biochem., 63 (4), 337-346, 2007

A number of epidemiological and clin-ical studies performed in human beingshave documented that abdominal obesitymay be associated with stress-related oradverse life events (5, 9, 35). Furthermore,there are several studies linking metabolicsyndrome and type 2 diabetes with psy-chosocial factors (6, 34). In this context,the combination of chronic stress andhigh fat intake in developed Westerncountries could be related to the increaseof metabolic and cardiovascular diseasesin the adult population in some circum-stances (16, 30). Furthermore, a high-fatdiet may act as a background form ofchronic stress, elevating basal corticos-terone levels and enhancing the HPAresponse to stress (40).

Although it has been extensivelyreported that stress reduces body weight(19, 21, 22), some investigators claim thatsocial and not social stressors couldincrease body and lipid mass leading tometabolic disorders and obesity (36, 39).Furthermore, experimental studies com-bining a high fat diet consumption andstress present contradictory results. Thus,while stress combined with high-energydiets could lead to obesity (15, 24), nochanges (18) or reductions in body weightand adiposity (4, 14) were also observed.These contrasting outcomes may dependon the stress paradigms used, but also onthe species and strains of the rodent, typeand quality of the diet (31, 38). Addition-ally, it is known that stress may influencemacronutrient selection and palatablefood intake (11).

Although there is much evidence thatstress and obesity are related to the hypo-thalamic control of food intake andmetabolism (41), little is known about theperipheral processes by which stressaffects adiposity and insulin resistance.Thus, the participation in stress-inducedobesity of beta-adrenergic pathways,

parasympathetic activity or glucocorti-coids and the HPA axis have to be inves-tigated (10, 15). In this context, cafeteriadiet is a recognized model of obesityinduced by high-fat diet that shares com-mon Western diet features and drives tometabolic syndrome conditions (13, 32),which may involve inflammation (27, 28).glucocorticoids (8, 25) and catecholaminesIn addition, chronic mild stress (CMS) is adocumented model of anhedonia in ani-mals (3). Thus, the repeated administra-tion of a series of unpredictable mildstressors attempts to mimic the dailystress associated with the onset of clinicaldepression in humans that might cause theHPA axis hyperactivity (29).

In this work, it was sought to assesspossible interactions between stress andhigh fat intake on the development ofobesity, analyzing how a model of chron-ic unpredictable mild stress could affectthe nutrient partitioning in diet-inducedoverweight rats by measuring body com-position (e.g. fat/muscle ratio) and bio-chemical markers, as well as changes inenergy expenditure and locomotive vari-ables.

Material and Methods

Animals, diets and experimentaldesign.– Eight-weeks-old male Wistarrats, supplied by the Applied Pharmaco-biology Center (CIFA, Pamplona, Spain),were housed at 21-23 ºC at a five per cagedensity with a 12 hours light cycle (8 a.m.to 8 p.m.) and assigned into differentdietary groups. A group of animals (Con-trol group, n=20) were fed on standardpelleted diet (2014 Tekland Global 14%Protein Rodent Maintenance Diet, HarlanIberica, Barcelona, Spain) containing16.6% of energy as protein, 73.1% ofenergy as carbohydrate and 10.3% of

D. F. GARCÍA-DÍAZ, J. CAMPION, F. I. MILAGRO, et al.338

J. Physiol. Biochem., 63 (4), 2007

energy as lipid by dry weight. The secondgroup of animals (Cafeteria, n=20) was fedon a high-fat diet in order to generate adiet induced obesity model as previouslyreported (13, 32). The composition of thiscafeteria diet was 9.3% of energy as pro-tein, 31.5% as carbohydrates and 59.2%as lipids by dry weight (462 kcal per 100 gin the cafeteria diet vs. 349 kcal per 100 gin the pelleted diet). Later, control andcafeteria rats were randomized by weightinto unstressed (control diet (C), n=10,and cafeteria diet (Caf), n=10) and stressed(control diet (CS), n=10, and cafeteria diet(CafS), n=10) groups, respectively. Ani-mals had ad libitum access to water andfood during the experimental trial. Bodyweight was recorded daily. Animals wereindividually housed overnight for measur-ing food intake in days 72-73. At the endof the experimental period (77 days), ratswere anaesthetized after overnight fastingwith Ketamine (50 mg/kg i.p., Parke-Davis, Madrid, Spain) and Medetomidine(0.025 mg/kg i.p., Pfizer SA, Madrid,Spain) for the analysis of the body com-position by using a non-invasive electro-magnetic apparatus devised for rodents(EM-SCAN model SA-2, Springfield, IL,USA) as described elsewhere (8). Then,the animals were sacrificed by decapita-tion and blood and tissue samples wereimmediately collected for further analy-ses. All the procedures were performedaccording to national and institutionalguidelines of the Animal Care and UseCommittee at the University of Navarra.

Serum measurements.– Circulating glu-cose was measured with a HK-CP kit(ABX diagnostic, Montpellier, France) inan automatized COBAS MIRA equip-ment (Roche, Basel, Switzerland). Serumleptin (Linco Research, Missouri, USA)and insulin levels (Mercodia AB, Uppsala,Sweden) were determined by ELISA.

Stress paradigm.– A stress protocol, aspreviously described (18) was applied toinduce moderate, random and chronicstress, three times per week in the after-noon (17:00). The stressors included were:1) Crowded conditions: animals werehoused 5 per cage on darkness during1 hour in a relatively small space (25 cm Hx 25 cm D x 15 cm H), 2) Immobilization:animals were restrained during 15 minuteson a transparent cylinder (8 cm diameter x22 cm length), 3) Dirty cage: animals weremoved to an unclean cage of anothergroup of rats during 45 minutes, 4) Salineinjection: i.p. saline injection (0.2 ml),5) Bath immersion: swim stress in a buck-et of water, which was deep enough thatthe animals could not touch bottom, at22-24 ºC during 8 minutes, 6) Dominantmale: the animals were exposed during 10minutes to another conspecific male ratplaced in the home cage of the experimen-tal rats.

Locomotor activity.– Horizontal andvertical locomotive activity was measuredfor 30 min in an open field, which consist-ed of nine square arenas (43 cm H x 51 cmD x 45 cm H) made of black wood, usinga video tracking system (Ethovision 3.0,Noldus Information Technology BV,Wageningen, The Netherlands), in a soft-ly illuminated room according to a previ-ously reported protocol (1). The trackingsystem was set to determine the positionof the animal five times per second. Totaldistance moved (cm), meander (degrees/cm) and rearing (frequency) were ana-lyzed according to manufacturer’s soft-ware. These measures were realized in themorning, at days 23-30 of treatment.

Indirect calorimetry.– Oxygen (O2)consumption and carbon dioxide (CO2)production were measured using anOxylet 00 O2/CO2 indirect calorimeter

LOCOMOTIVE AND METABOLIC CHANGES BY STRESS IN OBESITY 339


(Panlab SL, Barcelona, Spain) as describedelsewhere (12). Each animal was placedinto one of four acrylic chambers (350mm H x 200 mm D x 180 mm H each).Room air was drawn through each cham-ber at a rate of 670 mL/min, and then TheO2 and CO2 levels from each chamberand room air were measured on 3-minsampling periods (8 sampling periods per2 hr of data collection with four cham-bers). Respiratory quotient (RQ) was cal-culated as the ratio of the volume of CO2produced by the volume of O2 consumed.EE was calculated according to the for-mula for non-fasted animals: EE(kcal/day/body weight3/4) = O2 volume x1.44 x (3.815 + (1.232 x RQ)). Experimen-tal measures were performed in the morn-ing in non-fasted animals between days 58and 66 of dietary treatment.

Rectal temperature.– Colonic tempera-ture was measured using a petroleum jellycovered YSI 400 series rectal probe ther-mocouple thermometer (Panlab SL,Barcelona, Spain) inserted at a standard-ized distance (6 cm) until a stable temper-ature reading was obtained.

Statistical analysis.– All results areexpressed as mean ± standard error of themean (SEM). Data and interactions wereevaluated by factorial two-way ANOVA(Diet, Stress, and Diet x Stress) followedby U Mann-Whitney test. The level ofprobability was set at P<0.05 as statistical-ly significant. All statistic analyses wereperformed using SPSS 13.0 packages forWindows (Chicago, IL, USA).

Results

Effects of the high fat diet and CMS onbody and biochemical variables of the ani-mals.– Cafeteria diet actually established

the expected overweight model necessaryfor the present study. Thus, the weight ofthe rats fed on high fat diet was statistical-ly augmented in comparison to controlgroups (Fig. 1 and Table I). These differ-ences were statistically significant fromday 13 of treatment (Fig. 1). At the end ofthe treatment, data confirmed that cafete-ria intake induced metabolic alterationsthat drive to the common features of obe-sity (Table I). On the other hand, noeffects of the stress protocol on bodyweight (Fig. 1), corporal and biochemicalmarkers (Table I), with the exception ofglucose levels, were detected. Further-more, post-hoc analysis between controland high fat fed stressed and non-stressedrats showed no statistical differences, withthe exception for the weight/lenght2 ratio,total white adipose tissue (WAT) weightand leptin/body weight ratio, which weresignificantly decreased by the stress modelbut only on the chow fed animals. Finally,



Fig. 1. Body weight evolution for the four experi-mental groups of animals.

Each data point is expressed by the mean ± SEM.Dotted lines indicates when the stress protocol startsand when metabolic or activity measures were per-formed (C, Control; CS, Control – Stress; Caf, Cafe-teria; CafS, Cafeteria – Stress; Different letters (a,b)indicate significant differences between groups of at

least p<0.05).



Tab

le I.

Bod

y an

d b

ioch

emic

al m

easu

rem

ents

and

sta

tistic

al a

naly

ses

of t

he f

our

die

tary

gro

ups.

Mea

n ±

SE

MTw

o w

ay A

NO

VA

Con

trol

Con

trol

-Str

ess

Caf

eter

iaC

afet

eria

-Str

ess

Die

t*n

= 5

n =

5n

= 1

0n

= 9

Die

tS

tres

sS

tres

sB

ody/

Tiss

ue m

easu

rem

ents

Fina

l bod

y w

eigh

t (g

)40

4.80

±11

.80a

388.

60 ±

10.6

3a50

8.50

±18

.22b

486.

67 ±

14.5

1b<

0.00

1n.

s.

n.s.

Wei

ght/

leng

ht 2 r

atio

7.60

±0.

14a

7.25

±0.

04b

8.54

±0.

20c

8.42

±0.

26c

<0.

001

n.s.

n.

s.To

tal W

AT

wei

ght

(g)

60.6

5 ±

4.18

a43

.28

±2.

93b

94.9

1 ±

5.51

c10

1.24

±9.

30c

<0.

001

n.s.

n.

s.S

ubcu

tane

ous

WA

T w

eigh

t(g)

6.86

±

0.82

a5.

12 ±

0.50

a14

.08

±1.

20b

12.9

6 ±

1.84

b<

0.00

1n.

s.

n.s.

Vis

cera

l WA

T w

eigh

t (g

)22

.91

±1.

930a

18.5

4 ±

1.67

a46

.90

±4.

00b

43.5

0 ±

3.91

b<

0.00

1n.

s.

n.s.

Mus

cle/

tota

l WA

T ra

tio0.

033

±0.

003a

0.04

2 ±

0.00

4a0.

024

±0.

002b

0.02

1 ±

0.00

2b<

0.00

1n.

s.

<0.

05

Bio

chem

ical

mea

sure

men

tsG

luco

se (m

g/d

l)82

.40

±5.

48ab

70.8

0 ±

2.13

a87

.10

±2.

31b

81.6

7±2.

59b

<0.

05<

0.05

n.s.

Insu

lin (m

g/l)

0.21

±0.

03a

0.18

±0.

03a

0.38

±0.

09b

0.33

±0.

04b

<0.

05n.

s.n.

s.Le

ptin

/bod

y w

eigh

t ra

tio (%

)10

0 ±

11.8

80a

63.9

6 ±

7.95

b19

4.06

±25

.48c

195.

23 ±

25.0

5c<

0.00

1n.

s.n.

s.

Tab

le II

. Lo

com

otiv

e ac

tivity

, foo

d in

take

, ene

rgy

effic

ienc

y an

d r

ecta

l tem

per

atur

e an

d s

tatis

tical

ana

lyse

s of

the

fou

r d

ieta

ry g

roup

s.

Mea

n ±

SE

MTw

o w

ay A

NO

VA

Con

trol

Con

trol

-Str

ess

Caf

eter

iaC

afet

eria

-Str

ess

Die

t*n

= 1

0/5

n =

10/

5n

= 1

0n

= 1

0/9

Die

tS

tres

sS

tres

sLo

com

otio

n va

riab

les

Tota

l dis

tanc

e m

oved

(cm

)84

.24

±6.

74a

99.3

1 ±

5.72

ab86

.56

±72

3a10

8.52

±73

5bn.

s.<

0.05

n.s.

Mea

nder

(deg

rees

/cm

)–8

1.38

±5.

75a

–67.

97 ±

5.85

b–8

3.64

±76

8ab–6

3.93

±55

9abn.

s.<

0.05

n.s.

Rea

ryng

fre

cuen

cy3.

13 ±

023ab

4.36

±02

3c2.

83 ±

022b

4.26

±04

2acn.

s.<

0.00

1n.

s.

Res

t of

var

iab

les

Food

inta

ke (k

cal/d

ay)

80.2

7 ±

4.13

a78

.18

±6.

10a

247.

63 ±

29.1

1b20

4.31

±15

41b

<0.

001

n.s.

n.s.

Ene

rgy

effic

ienc

y (g

/kca

l)1.

26 ±

0.05

a1.

07 ±

0.08

ab0.

82 ±

008b

0.89

±0.

09ab

<0.

01n.

s.n.

s.R

ecta

l tem

per

atur

e (°

C)

37.1

2 ±

0.07

a37

.14

±0.

12a

37.5

9 ±

0.13

b37

.51

±0.

07b

<0.

001

n.s.

n.s.

Diff

eren

t le

tter

s (a

, b

, c)

ind

icat

es s

igni

ficat

ive

diff

eren

ces

bet

wee

n gr

oup

s of

at

leas

t p

<0.

05.

WA

T, w

hite

ad

ipos

e tis

sue;

BA

T, b

row

n ad

ipos

e tis

sue;

n.s

.no

t si

gnifi

cativ

e. R

esul

ts a

re e

xpre

ssed

by

mea

n ±

SE

M.



no interactions between the dietary treat-ment and the stress protocol were found,with the exception of the muscle/totalWAT ratio.

Effects of the cafeteria diet and stress onthe locomotive activity.– An open-fieldtest was used to assess locomotive activityof the rats and evaluate a possible rela-tionship between dietary treatment andthe stress undertaken by the animals.Regarding the diet, it was not a modulat-ing factor of the activity behavior of theanimals, presenting no effects on horizon-tal movement (total distance moved), sin-uosity of movement (meander) and verti-cal movement (rearing) of the animals(Table II). More interestingly, stressappears to be a critical factor that effec-tively increases the general activity of therats, reaching statistical significances forall variables analyzed.

Effects of the high fat diet and the stressprotocol on food intake, energy efficiencyand rectal temperature.– Food intake, effi-ciency of weight gain and rectal tempera-ture of the four groups of animals werealso measured at the end of the study(Table II). Again, the three analyzed vari-ables were clearly and significantly affect-ed by high-fat diet. However, the stressparadigm did not alter these variables, andno interactions were found between thedietary treatment and the stress model.

Effects of the high fat diet and stressparadigm on the respiratory quotient andenergy expenditure of the rats.– Indirectcalorimetry determination performed onweeks 8 and 9 of treatment showed signif-icant effects of the diet and the stress onthe RQ of the animals (Fig. 2), beingaffected this variable by both experimen-tal models. Experimental measurements

showed also that the animals that wereexposed to the stress protocol presentedsignificant more energy expenditure thanthe non-stressed animals, without chang-ing effects by dietary treatment. No inter-actions between the cafeteria and stressmodel were observed neither for RQ nor

Fig. 2. Calorimetric determinations for the fourexperimental groups of animals.

(A) Respiratory quotient and (B) Energy expendi-ture. Each value represents the mean ± SEM of threeminute data recollection. Dotted line in graph (A)corresponds to the 0.73 limit that indicates alcoholicmetabolism for data below this value. (C, Control;CS, Control – Stress; Caf, Cafeteria; CafS, Cafeteria- Stress; RQ, Respiratory quotient; EE; Energyexpenditure; bw, body weight; Different letters (a, b,c) indicate statistical significant differences between

groups of at least p<0.05; n.s., not significant).

for the EE determinations for all theexperimental groups of animals.

Discussion

High fat cafeteria feeding is a validatedmodel of diet-induced obesity in rats thatshares common features with Westerndiet (13, 26). As expected, the consump-tion of a high saturated fat diet inducedbody weight gain and adiposity in Wistarrats, which was accompanied by hyper-phagia, hyperthermia, insulin resistance(measured as HOMA index) and hyper-leptinemia. On the other hand, specificmeasurements performed in this studycomparing cafeteria rats with chow fedrats have shown a lower respiratory quo-tient and increased total energy expendi-ture. These results are in agreement withothers studies using a similar model ofhigh-fat diet (20, 44). In addition, locomo-tive measurements have been performedin the rats to analyze possible changes insome behavioral stress-dependent vari-ables. However, although chronic high fatdiet has been described as an inductor ofstress-response by several authors (17,24), it was unable to modify any of themarkers analyzed, leading to the conclu-sion that cafeteria diet was not able tomodify stress responsivity.

The CMS paradigm employed in thiswork has been criticized in the past forbeing difficult to replicate, posses a highvalidity, but a large number of recent pub-lications have confirmed that CMS causesbehavioral changes in rodents that parallelsymptoms of depression (45) and could bean excellent model for studying diet-induced obesity (17, 18). In this work,lean mass, estimated as gastrocnemiusmuscle weight, was decreased in stressedanimals in comparison to non-stressedrats. This effect is a common feature, and

a role for glucocorticoids in the reductionof muscle mass by stress has beendescribed (16). On the other hand,although it has been reported that CMSprocedure causes hyperthermia (22)together with disturbance of circadianrhythms and hypercortisolism (43), in thiswork the stress model did not provokeany changes in body temperature. Thislack of results could be due to a differentmanipulation of the animals or the type ofstress paradigm used. Moreover, as cafete-ria diet induces hyperthermia per se (27),high fat diet intake could lead to a differ-ent thermoresponse to stress in the ani-mals (7).

In contrast, locomotive analysisshowed after 4 weeks of stress paradigman increase in activity, measured as run-ning distance, meander and rearing, instressed animals in comparison to non-stressed animals. According to otherauthors, open field studies reportedstress-induced increases in locomotoractivity in rats (18, 21), and therefore,stress paradigm was efficient to inducebiological changes in the animals. Fur-thermore, CMS induced significantdecrease in the RQ of the rats in both thecontrol and high-fat fed groups, showinga preference for fat oxidation instead ofcarbohydrates. Different kind of stressprotocols cause increased or decreasedRQ, confirming the importance of typeand duration of the stress (23). In thispaper we describe that energy expenditureis increased by chronic stress, being theeffect independent of the type of diet, aspreviously reported (23). This effect couldbe due to several biological mechanisms(16), possibly including a metabolic adap-tation of the animals facilitating the fightor flight reaction (42).

Finally, the purpose of this paper wasto investigate a role of the CMS paradigm



in a possible interaction with a model ofcafeteria diet in Wistar rats (18) by specif-ically analyzing basal metabolic rates. Atthis respect, only a statistical interactionbetween diet and stress was found on themuscle/total WAT ratio, confirming apossible role of the stress in energy parti-tioning and mobilization of fatty acids(37). On the other hand, in-depth post-hoc analysis show a more marked effect ofchronic stress model in chow fed animals(C vs. CS groups). Thus, total and retro-peritoneal WAT weight and serum leptinwere decreased significantly in controlstressed rats in comparison to non-stressed rats, according to TAMASHIRO etal. (39). In this sense, it has been proposedby other authors a decisive role of leptinin cross-talk between signals derived fromboth skeletal muscle and adipose tissue (2)and energy partitioning (33). In this way,although a role of basal metabolism couldbe present in this effect, post-hoc analysisrevealed no impact on metabolic rate orlocomotive activity. On the other hand,despite of no changes in adiposity, high-fat fed rats showed an altered metabolicrate and locomotive activity as comparedto their stressed counterparts. This find-ing suggests a possible protective role ofthis kind of diet on the weight loweringeffect of stress. This metabolic differencebetween both dietary groups could beexplained by the high intake of total ener-gy and dietary fat of cafeteria animals.

In summary, this experimental workinvestigates how the combination of achronic stress model with a high fat dietaffects the development of diet-inducedobesity in rats, analyzing speciallychanges in locomotive activity, thermoge-nesis, basal metabolism and energy expen-diture. In such context, CMS affectedenergy metabolism by increasing EE anddecreasing RQ, and these changes could

be involved in the reduction of muscle andvisceral fat weights in chow fed animals.However, this weight lowering effect wasnot observed in cafeteria animals despitethe occurrence of similar metabolic alter-ations. Because chronic stress is increas-ingly and convincingly being attributedfor causing metabolic, cardiovascular, andother complex diseases in large compo-nents of the adult population, it is essen-tial to investigate approaches – dietary, lifestyle, and even pharmacological – foravoiding undesirable synergic effects ofstress and obesity

Acknowledgements

The authors wish to thank to Línea Especial(LE/97) from the University of Navarra, NavarraGovernment funds from 2000, as well as to theComunidad de Trabajo de los Pirineos CTP (Nava-rra) for financial support. Also we wish to thank theDepartment of Pharmacology of the University ofNavarra for lending us kindly the Ethovision videotracking system for the open field locomotive activi-ty measures.

D. F. GARCÍA-DÍAZ, J. CAMPION, F. I.MILAGRO, A. LOMBA, F. MARZO y J. A.MARTÍNEZ. El estrés crónico moderadoinduce variación en el comportamiento motor yel metabolismo de ratas alimentadas con dietaalta en grasas. J. Physiol. Biochem., 63 (4), 337-346, 2007.

El estrés crónico moderado se ha asociado amenudo con la patogénesis de diversas enfer-medades, como la obesidad. La obesidad visce-ral, por su parte, se ha relacionado con el desa-rrollo de síndrome metabólico, enfermedadescardiovasculares y diabetes. Con el fin de estu-diar una posible relación entre el estrés y elestablecimiento de obesidad, se analizó duran-te 11 semanas un modelo de ingesta alta en gra-sas (dieta de cafetería) junto con un estrés cró-nico moderado en ratas Wistar macho. Duran-te este período experimental, se analizó el



metabolismo basal por calorimetría indirecta,la temperatura rectal, la ingesta calórica y laactividad motora de los animales. Tras los 77días, los animales se sacrificaron y se analiza-ron diversas medidas corporales y de adiposi-dad, así como el perfil bioquímico de las ratas.Como se esperaba, la dieta de cafetería en ani-males no estresados indujo un aumento signifi-cativo del peso corporal, la adiposidad y losniveles de marcadores de insulino-resistencia.Las medidas de actividad motora, específica-mente el movimiento horizontal, vertical y lasinuosidad de movimiento, aumentaron signi-ficativamente con el estrés, lo que se observóen las primeras semanas del experimento. Ade-más, estrés crónico moderado en ratas Wistarincrementó significativamente el gasto energé-tico y parece jugar un papel conjunto con eltratamiento con dieta alta en grasa en la modu-lación del índice peso del músculo/peso de lagrasa de los animales. En resumen, este mode-lo de estrés crónico moderado no afectó signi-ficativamente al peso corporal, tanto de los ani-males controles como de los alimentados condieta de cafetería, pero indujo una interaccióncon la alta ingesta de grasa concerniente a larepartición metabólica músculo/grasa.

Palabras clave: Obesidad, Estrés, Dieta de cafetería,Actividad motora, Calorimetría.

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Chronic mild stress induces variations in locomotive behavior and metabolic rates in high fat fed...

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