SEARCH · PubMed Health

Results for “peripheral response”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

PubMed1989

Interplay and interference of the carotid baroreceptors, central command, ergoreceptors on the peripheral vascular responses during static exercise.

1. The aim of the present study was to examine the influence of the carotid baroreceptors on the peripheral vascular responses during static exercise and its interference with the 'central command' and the ergoreceptors. 2. Ten healthy subjects performed an isometric handgrip with 30% of maximal voluntary contraction for 1.5 min. Five seconds prior to the end of the exercise the arterial circulation to the exercising forearm muscles was occluded for 1.5 min. The carotid baroreceptors were stimulated by neck suction at -40 mmHg for 0.5 min in each period, and also during control and recovery phase. Contralateral forearm and calf blood flow were measured simultaneously with ECG-triggered venous occlusion plethysmography. 3. The present findings suggest that there are 'central command' and ergoreceptors which modulate carotid baroreflex function to the afferent output to the heart and the peripheral circulation.

Adult↗

PubMed1995

A possible screening test for inherited p53-related defects based on the apoptotic response of peripheral blood lymphocytes to DNA damage.

The cellular response, in terms of cell cycle arrest(s) and apoptosis, to radiation-induced DNA damage was studied. Experiments were performed on both mitogen-stimulated and resting peripheral blood lymphocytes (PBLs) from normal and cancer-prone (C-P) individuals. The C-P individuals comprised three patients carrying germline p53 mutations and three members of two families apparently without such mutations, but with an inherited defect which results in p53 deregulation as shown by high levels of stabilised p53 protein in normal tissues. Interestingly, mitogen-stimulated PBL, from both normal and C-P individuals failed to demonstrate a G1 arrest after gamma radiation. However, a clear difference was seen in the apoptotic response to DNA damage, of PBL from normal and C-P individuals; PBLs from C-P individuals with inherited p53-related defects had a reduced apoptotic response (P = 0.0003). There was a wide margin of separation, with no overlap between the two groups, supporting the possibility of using this altered apoptotic response as a screening test. This simple and rapid procedure could be used to identify those individuals in a C-P family who carry germline p53-related defects. The method appears to detect both individuals with p53 mutations and those apparently without mutations but with other p53-related defects.

Adult↗

PubMed2005

Physical activity alters the brain Hsp72 and IL-1beta responses to peripheral E. coli challenge.

Physically active rats have facilitated heat shock protein 72 (Hsp72) responses after stressor exposure in both brain and peripheral tissues compared with sedentary rats. This study verifies that physically active animals do not have elevated Hsp72 levels compared with sedentary animals in the hypothalamus, pituitary, or dorsal vagal complex. We then examined whether 1) physically active rats respond more efficiently than sedentary rats to a bacterial challenge; 2) peripheral immune challenge elicits brain induction of Hsp72; 3) this induction is facilitated by prior freewheel running; and 4) Hsp72 upregulation produced by peripheral immune challenge results in a commensurate decrease in the proinflammatory cytokine IL-1beta. Adult male Fischer 344 rats were housed with either a mobile or locked running wheel. Six weeks later, rats were injected intraperitoneally with saline or Escherichia coli and killed 30 min, 2.5 h, 6 h, and 24 h later. Serum endotoxin and IL-1beta, and peritoneal fluid endotoxin and E. coli colony-forming units (CFUs) were measured. Hsp72 and IL-1beta were measured in hypothalamus, pituitary, and dorsal vagal complex. The results were that physically active rats had a faster reduction in endotoxin and E. coli CFUs and lower levels of circulating endotoxin and cytokines compared with sedentary rats. E. coli challenge elicited significantly greater time-dependent increases of both Hsp72 and IL-1beta in hypothalamus, pituitary, and dorsal vagal complex of physically active animals but not sedentary animals. Contrary to our hypothesis, increases in Hsp72 were positively correlated with IL-1beta. This study extends our findings that physical activity facilitates stress-induced Hsp72 to include immunological stressors such as bacterial challenge and suggests that brain Hsp72 and IL-1beta responses to peripheral immune challenge may contribute to exercise-mediated resistance to long-term sickness.

Adaptation, Physiological↗

PubMed1999

Peptide length-dependent TCR antagonism on class II HLA-restricted responses of peripheral blood mononuclear cells and T cell clones.

T cell clonal recognition of peptide ligands is highly diverse. To investigate how peptide mixtures with diverse sequences affect polyclonal responses of peripheral blood mononuclear cells (PBMC), we synthesized Xn (n = 9-19) peptides that consist of 9 to 19 residues with random sequences. We found that: (1) in antagonism assays, Xn peptides inhibit polyclonal responses of PBMC induced by purified protein derivative (PPD) and crude mite extracts as well as mixed lymphocyte reaction (MLR), in which intermediate-length peptides (n = 13 or 15) show the largest inhibitory effects; and (2) a high-affinity HLA-DR4-binding peptide is devoid of inhibitory activity against MLR to DR4, indicating that these effects are not caused by inhibition of peptide binding to HLA. Furthermore, X15 did not abrogate PBMC proliferation induced by phorbol 12-myristate 13-acetate + ionomycin, or anergize PBMC by preculture. All these observations indicate that TCR antagonism does exist at peripheral T cell levels in humans, and that Xn peptides, depending on peptide length, are capable of antagonizing T cell polyclonal responses. Indeed, even with cloned T cells, certain non-agonistic peptides shorter (but not too short) than the wild type in their C termini, function as TCR antagonists, findings which corroborate the observation that X13-15 antagonizes T cell responses more efficiently than does X17-19 or X9-11.

Amino Acid Sequence↗

PubMed1979

Non-specific effects of avian retrovirus co-incubation on lymphocyte function: abrogation of antigen- and mitogen-induced proliferative responsiveness.

Peripheral blood lymphocytes from chickens bearing tumours induced by avian retroviruses can be stimulated to divide by group-specific antigens present in supernatant fluids of avian retrovirus-infected but not normal chicken embryo fibroblast (CEF) cells. Centrifugation studies revealed that the relevant antigenic activity is non-virion in nature. Indeed, the presence of avian retrovirus particles was found to be inhibitory to the capacity of sensitized lymphocytes to be stimulated in this antigen-driven blastogenesis assay. Similar results were obtained in lymphocyte mitogenesis experiments in which any of peripheral chicken lymphocytes or mouse splenic, lymph node or thymic lymphocytes were co-incubated with either concanavalin A or phytohaemagglutinin in the presence of numerous types of virus particles. This inhibitory effect was not due to infection of lymphocytes by the viruses tested, and was obtained in the case of lymphocyte-virus combinations for which the cells lacked the surface receptors required for viral entry. Virus could be added to lymphocyte cultures as late as 26 h after co-incubation with mitogen, and still inhibit the usual mitogenic response. In addition, co-addition of virus to lymphocytes in the presence of concanavalin A was found to block the capping of ligand-bound receptors which normally ensues. Pre-added virus did not, however, affect the ability of lectins to bind to cells.

Alpharetrovirus↗

PubMed2002

Expression of c-fos, rather than c-jun or glucocorticoid-receptor mRNA, correlates with decreased glucocorticoid response of peripheral blood mononuclear cells in asthma.

Resolution of the molecular mechanism(s) underlying glucocorticoid (GC) resistance is an important clinical problem when performing individualized GC therapy according to the GC response of peripheral cells in asthma. In order to investigate the mechanism(s) underlying the individual differences of lymphocyte GC response, we examined the relationship between lymphocyte sensitivity to GC in vitro and the expression of mRNAs for GC receptor (GR) alpha, GRbeta, c-fos and c-jun, which are reported to be implicated in the regulation of the pharmacological effects of GCs in asthma patients. Twenty-seven patients with bronchial asthma and 14 healthy subjects were included in the study. IC50s of prednisolone and methylprednisolone on blastogenesis of peripheral blood mononuclear cells (PBMCs) stimulated with concanavalin A in vitro were estimated. Transcripts for GRalpha, c-fos, c-jun and beta-actin genes in PBMCs were quantitatively determined by reverse transcription-competitive polymerase chain reaction (RT-cPCR) procedures. GRbeta mRNA expression was examined with an RT-PCR technique. A statistically significant positive correlation was observed between the IC50s for prednisolone (p <0.002) or methylprednisolone (p <0.001) and expression of c-fos mRNA in PBMCs of asthma patients (n = 27). Thus, the increased expression of c-fos mRNA correlated with the decreased responses of PBMCs to prednisolone and methylprednisolone in vitro. In contrast, the expression of GRalpha and c-jun mRNAs did not correlate with the IC50 for prednisolone and methylprednisolone in asthma patients. In addition, no statistically significant difference in IC50s of GCs between asthma patients with PBMCs exhibiting GRbeta mRNA and those without GRbeta mRNA expression was observed. The increased expression of c-fos mRNA suggests to attenuate PBMC response to GCs, which may contribute to progression of GC resistance in asthma. On the other hand, c-jun and GC receptor mRNA expression appears to have less influence on poor GC-response establishment.

Adult↗

PubMed1997

Sucrose consumption in mice: major influence of two genetic loci affecting peripheral sensory responses.

Individual variability in sucrose consumption is prominent in humans and other species. To investigate the genetic contribution to this complex behavior, we conducted behavioral, electrophysiological, and genetic studies, using male progeny of two inbred mouse strains (C57BL/6ByJ [B6] and 129/J [129]) and their F2 hybrids. Two loci on Chromosome (Chr) 4 were responsible for over 50% of the genetic variability in sucrose intake. These loci apparently modulated intake by altering peripheral neural responses to sucrose. One locus affected the response threshold, whereas the other affected the response magnitude. These findings suggest that the majority of difference in sucrose intake between male B6 and 129 mice is due to polymorphisms of two genes that influence receptor or peripheral nervous system activity.

Animals↗

PubMed1991

In vitro effect of interleukin-2 on proliferative responses of peripheral blood T cells from leprosy patients.

Because of the important role played by interleukin-2(IL-2) in T cell growth and differentiation, we investigated the effect of exogenous IL-2 on the proliferative response of peripheral blood mononuclear cells(PBMCs) from 77 leprosy patients. The proliferative responses of PBMCs from lepromatous leprosy(LL) or borderline lepromatous leprosy(BL) patients to M. leprae were significantly lower(cpm 6,051 +/- 803 for LL type; 4,951 +/- 2,529 for BL type) than those from tuberculoid leprosy(TT) or borderline tuberculoid leprosy(BT) patients (28,853 +/- 28,916 for TT type; 15,884 +/- 334 for BT type). To investigate the effect of exogenous IL-2, purified IL-2 was added at the start of culture at 100 unit/ml. There was an apparent increase in 3H-thymidine incorporation of M. leprae-stimulated PBMCs(18,723 +/- 6,503) in the presence of IL-2 compared to the results without IL-2(6,051 +/- 803) in LL patients. Twenty nine out of 33 LL patients belonged to the responders to IL-2 and four patients were nonresponders. Therefore we conclude that the defective cell mediated immune response in LL patients may result from diminished production of IL-2, but we can not exclude the possibility of diminished expression of the IL-2 receptor. And we suggest that the immunologic heterogeneous response of an individual to M. leprae is important to the pathogenesis of clinical disease in the same LL patients.

Cells, Cultured↗

PubMed1987

Amplification of HTLV-III/LAV infection by antigen-induced activation of T cells and direct suppression by virus of lymphocyte blastogenic responses.

Peripheral blood mononuclear cells (PBMNC) from healthy donors immune to the soluble antigens tetanus toxoid (TT) and/or keyhole limpet hemocyanin (KLH) were exposed to infectious human T lymphotropic virus, type III/lymphadenopathy-associated virus (HTLV-III/LAV) with and without prior activation by TT or KLH. After exposure to the virus, PBMNC that had been activated by antigen were 10 to 100 times more susceptible to viral replication, as estimated by measurement of production of reverse transcriptase and viral antigens, than PBMNC that had been preincubated without antigen. In addition, exposure of PBMNC to HTLV-III/LAV led to a loss of lymphocyte blastogenic responses after 2 to 3 wk in culture. HTLV-III/LAV-induced inhibition of lymphocyte blastogenic responses occurred in the absence of detectable production of RT but required the use of live rather than heat-inactivated virus. These results demonstrate that HTLV-III/LAV infection is amplified by antigen-induced activation of PBMNC, and that low levels of HTLV-III/LAV infection in vitro can suppress lymphocyte blastogenic responses. This study provides an in vitro model for the analysis of HTLV-III/LAV-induced immune defects.

Acquired Immunodeficiency Syndrome↗

PubMed1995

Prominent proliferative response of peripheral blood mononuclear cells to a recombinant non-structural (NS3) protein of hepatitis C virus in patients with chronic hepatitis C.

The proliferative response of peripheral blood mononuclear cells (PBMC) to a recombinant non-structural (NS3) protein of hepatitis C virus (HCV) was studied in 41 patients with chronic hepatitis C. Of them, 28 had chronic persistent hepatitis (CPH) and 13 chronic active hepatitis (CAH). The positive proliferation rate of PBMC to the recombinant NS3 protein, T9Ag, was 66% in the 41 patients (77% in CAH versus 61% in CPH; P > 0.05) when stimulation index (SI) = 4 was set as the cut-off value. However, mean SI of CAH patients was significantly higher than that of CPH patients (8.3 +/- 5.2 versus 5.1 +/- 3.6; P < 0.05). Six other chronic hepatitis patients who were repeatedly negative for anti-HCV antibody but positive for serum HCV RNA also had an SI of > or = 4.0. The frequency of cellular immune response to the T9Ag is among the highest results obtained by using HCV antigens tested so far. Our studies thus indicate that NS3 is an immunologically important region of HCV for T cells. Moreover, the proliferative response to T9Ag may help to establish hepatitis C etiology in chronic hepatitis patients who are seronegative with currently available anti-HCV assays.

Adult↗

PubMedDate not supplied

Analysis of responses of peripheral blood lymphocytes from sarcoidosis patients to purified protein derivative.

PURPOSE: Negative skin test reaction against purified protein derivative (PPD) is one of the important diagnostic criteria for sarcoidosis. The purpose of this study was to investigate the relationship between negative skin test reaction against PPD and the responses of peripheral blood lymphocytes (PBLs) against PPD in sarcoidosis patients. METHODS: Sarcoidosis patients (n = 14) with ocular changes were selected for this study. As a control, blood was collected from volunteers without uveitis (n = 10). All subjects in both groups had a history of bacille de Calmette-Guerin vaccination, and 8 of the 14 patients underwent the PPD skin test. Peripheral blood lymphocytes were obtained from all patients and separated by gradient centrifugation. Peripheral blood lymphocytes were tested for their proliferative responses to PPD. To determine the frequency of PPD-specific precursor cells in blood, limiting dilution analysis was used. The frequency was calculated following the Poisson model. The culture supernatants were harvested 3 days after incubation and assayed for interferon (IFN)-gamma production by ELISA. RESULTS: Four of the 8 patients showed a negative skin test reaction against PPD, while all the healthy volunteers had a positive reaction. Compared to PBLs from healthy volunteers, PBLs from sarcoidosis patients showed weaker responses to PPD. There was no clear difference between these two groups about frequency of precursor cells against PPD and production of IFN-gamma. CONCLUSIONS: Negative skin test for PPD in sarcoidosis patients does not seem to have any relationship to the low precursor frequency of PPD-specific cells in patient blood.

Adult↗

PubMed1999

Free radicals contribute to the reduction in peripheral vascular responses and the maintenance of thermal hyperalgesia in rats with chronic constriction injury.

We previously reported that the time frame and the extent of the changes in the peripheral neurogenic inflammatory response in the skin area, innervated by an injured nerve, coincide with those of pain behaviours. We raised the possibility that common factors might operate to modulate neuropathic pain and peripheral neurogenic processes in rats with chronic constriction nerve injury (CCI). In the present study we examined the role of free radicals in modulating the neurogenic vascular response and thermal hyperalgesia in rats with CCI of the sciatic nerve. Free radicals, via an interaction with nitric oxide (NO) to form peroxynitrite, have previously been implicated in the maintenance of thermal hyperalgesia in CCI rats. In this study, we induced CCI of the sciatic nerve and the activity of xanthine oxidase (XO), which catalyzes the formation of superoxide anions, was measured in the injured nerve. In addition, we examined the effect of antioxidants on thermal hyperalgesia and on the neurogenic vascular response to substance P (SP) perfused over the base of a blister induced on the hind footpad skin which is innervated by the injured sciatic nerve. Compared with the sham operated group, CCI rats had a significantly higher XO activity in the injured sciatic nerve and significantly reduced thermal threshold and peripheral neurogenic vascular response to SP. Treatment with antioxidants, superoxide dismutase (SOD) or tirilazad significantly improved the neurogenic vascular response while tirilazad treatment significantly alleviated thermal hyperalgesia. The results therefore, suggest that free radicals are elevated in CCI animals and that they contribute to the maintenance of thermal hyperalgesia and the reduction in peripheral microvascular blood flow in the area innervated by the injured nerve. We raise the possibility that common mechanisms may govern the changes in neuropathic pain and in the peripheral neurogenic vascular responses in tissues innervated by the injured nerve.

Animals↗

PubMed1989

Intracerebroventricular infusion of interleukin 1 rapidly decreases peripheral cellular immune responses.

Low doses (50-200 pg or 3.1-12.4 fmol) of interleukin 1 (IL-1) infused into the brain of rats produced rapid suppression of various cellular immune responses in peripheral lymphocytes of rats. Fifteen minutes after infusion of purified IL-1 beta into the lateral ventricle, natural killer cell activity, response to phytohemagglutinin stimulation, and interleukin 2 production were markedly suppressed in lymphocytes isolated from blood and spleen. These effects were due to infusion of IL-1 into brain since they did not occur when IL-1 was infused into the cisterna magna (essentially posterior to brain) or was injected intraperitoneally. Effects of IL-1 in brain could be blocked by simultaneous infusion of alpha-melanocyte-stimulating hormone, which is known to block the biological actions of IL-1. To stimulate release of endogenous IL-1 in brain, lipopolysaccharide was infused; this produced similar effects as IL-1, and these effects also were blocked by alpha-melanocyte-stimulating hormone. At longer intervals after infusion of IL-1 and lipopolysaccharide (3, 6, and 24 hr), immune responses returned to baseline or remained suppressed; i.e., "rebound" immunopotentiation did not occur. Finally, IL-1 infusion suppressed cellular immune responses in adrenalectomized animals, thereby showing that the effects of central IL-1 on peripheral cellular immune responses were, at least in part, independent of the stimulatory effect of IL-1 on secretion of adrenal hormones. These results indicate a link from brain to peripheral immune responses by means of action of a cytokine acting in the brain.

Animals↗

PubMed2003

Effect of age on peripheral vascular response to transverse aortic banding in mice.

The placement of a ligature to constrict the transverse aorta has become a standard procedure to induce cardiac hypertrophy in mice. Apart from cardiac response, there are adaptive changes in the proximal and distal arterial system that function to maintain adequate peripheral perfusion. The purpose of this study was to characterize the peripheral vascular response by measuring the carotid blood flow using noninvasive Doppler methods, and to investigate the effect of aging on the adequacy and timing of the response after aortic banding in mice. Five 16-month-old and 9 4-month-old male B6D2F1 mice underwent transverse aortic banding. Blood flow velocity was measured with Doppler in the right and left carotid arteries (RCA and LCA) before, 1 day after, and 7 days after, banding. Pulsatility index defined as (peak - minimum)/mean velocity was used to estimate local compliance and distal arterial resistance. The RCA/LCA mean velocity ratio was lower and pulsatility index ratio was higher at 1 day after banding in older mice. However, at 7 days, the RCA/LCA mean velocity ratio and pulsatility index ratio were similar between the 2 age groups. Our data indicate that there is an age-related delay in the development of vascular adaptations in carotid arteries after aortic banding. Older mice take a longer time for adaptation to establish adequate and equal mean flow velocity in the carotid arteries.

Aging↗

PubMed1987

Almitrine bismesylate and the central and peripheral ventilatory response to CO2.

Effects of almitrine bismesylate on the peripheral and central chemoreflex to a CO2 challenge during normoxia were studied in nine alpha-chloralose-urethan anesthetized cats. With the dynamic end-tidal CO2 forcing technique the ventilatory response after a square-wave change in end-tidal PCO2 (PETCO2) was partitioned into a central and a peripheral part using a two-compartment model. With almitrine administered intravenously (0.6 mg/kg followed by a maintenance dose of 0.4 mg.kg-1 X h-1) the CO2 sensitivity of the peripheral chemoreflex increased on the average from 0.315 to 0.564 l.min-1 X kPa-1 (P less than 0.001, 6 cats, 73 runs), whereas the CO2 sensitivity of the central chemoreflex remained the same (P = 0.87). The extrapolated PETCO2 at zero ventilation (apneic threshold) of the (total) steady-state response curve decreased on the average from 3.50 to 2.36 kPa (P less than 0.001). With the artificial brain stem perfusion technique it was confirmed that almitrine did not affect ventilation by administering it to the blood perfusing the brain stem. We conclude that almitrine bismesylate during normoxia enhances the CO2 sensitivity of the peripheral chemoreflex loop and decreases the apneic threshold due to an action located outside the brain stem.

Almitrine↗

PubMed1993

Comparison of peripheral chemoreceptor responses in monozygotic and dizygotic twin infants.

The peripheral chemoresponses of infant twin pairs were determined using a single-breath hyperoxic stimulus. A total of 43 twin pairs of comparable gestation and birth weight were studied during sleep at a mean (SD) age of 8 wk (1.4) while alternately breathing either air or 16% oxygen in nitrogen. Infants responded to a single breath of 100% oxygen by a reduction in ventilation; the mean (SEM) reduction in air was 273 ml/min (10.6) and in 16% oxygen 560 ml/min (18.4). Within-pair variances were compared in 14 monozygotic and 28 dizygotic pairs utilizing combined responses (air + 16% oxygen) computed for measurements made in behavioral quiet sleep and in 9 monozygotic and 20 dizygotic pairs for whom data were complete in polygraphically confirmed quiet sleep. The variance of responses within dizygotic twin pairs was greater than in monozygotic pairs when expressed in ml/min: F ratio 4.11 (p = 0.005) for all data and F ratio 7.67 (p = 0.003) in quiet sleep. Expressed in ml/min/kg the difference was less significant: F ratio 1.83 (p = 0.126) for all data and F ratio 3.46 (p = 0.039) in quiet sleep. Gender, birth weight, and birth order had no effect on these findings. This closer similarity of response in monozygotic twin pairs is explained by proposing a high degree of heritability for the response.

Chemoreceptor Cells↗

PubMedDate not supplied

Effect of lymphoproliferative disease virus and of niridazole on the in vitro blastogenic response of peripheral blood lymphocytes of turkeys.

Turkeys inoculated at 5 weeks of age with lymphoproliferative disease (LPD) virus developed typical lesions in the spleen, thymus, and pancreas. The in vitro blastogenic response of peripheral blood lymphocytes to the mitogens phytohemagglutinin and concanavalin A was drastically (up to 90%) suppressed in the inoculated turkeys 1 to 4 weeks postinoculation compared with uninoculated controls, and even at 11 weeks the response was about 50% inhibited. A lethal (about LD33) dose of antihelminthic drug niridazole, 100 mg/kg given each day for 3 days to 4-week-old turkeys, caused a transient inhibition of the blastogenic response within 32 days of treatment, which was less pronounced than that observed in turkeys inoculated with LPD virus, whether pretreated with niridazole or not. Virus-associated reverse transcriptase activity in the plasma was significantly higher in the turkeys pretreated with niridazole, and LPD lesions developed to the same extent in the untreated and treated groups, as determined 9 weeks post virus inoculation. A sublethal dose of niridazole, 50 mg/kg given each day for 4 days, did not suppress the blastogenic response to mitogens at any time determined (starting 10 days post-treatment) and did not affect the pathogenesis of LPD and the viremia. Body weights were significantly decreased by virus infection and by treatment with lethal doses of niridazole.

Animals↗

PubMed2001

Acute changes in the response to peripheral leptin with alteration in the diet composition.

Dietary induced obesity in rodents is associated with a resistance to leptin. We have investigated the hypothesis that dietary fat per se alters the feeding response to peripheral leptin in rats that were fed either their habitual high- or low-fat diet or were naively exposed to the alternative diet. Osborne-Mendel rats were adapted to either high- or low-fat diet. Food-deprived rats were given either leptin (0.5 mg/kg body wt ip) or saline, after which they were provided with either their familiar diet or the alternative diet. Food intake of rats adapted and tested with the low-fat diet was reduced 4 h after leptin injection, whereas rats adapted and tested with a high-fat diet did not respond to leptin. Leptin was injected again 1 and 5 days after the high-fat diet-adapted rats were switched to the low-fat diet. Leptin reduced the food intake on both days. In contrast, when low-fat diet-adapted rats were switched to a high-fat diet, the leptin inhibitory response was present on day 1 but not observed on day 5. Peripheral injection of leptin increased serum corticosterone level and decreased hypothalamic neuropeptide Y mRNA expression in rats fed the low-fat but not the high-fat diet for 20 days. The data suggest that dietary fat itself, rather than obesity, may induce leptin resistance within a short time of exposure to a high-fat diet.

Animals↗