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At least 19 recordsLinked to original sources
PubMed2003

An inhibitor of advanced glycation end product formation reduces N epsilon-(carboxymethyl)lysine accumulation in glomeruli of diabetic rats.

BACKGROUND: An inhibitor of advanced glycation, OPB-9195, retards the progression of nephropathy in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of non-insulin-dependent diabetes mellitus. The aim of this study is to evaluate histologically the role of N(epsilon)-(carboxymethyl)lysine (CML) in the development of diabetic nephropathy and investigate whether inhibition of CML accumulation by OPB-9195 is associated directly with the prevention of glomerular lesions in OLETF rats. METHODS: Kidneys of OLETF and Long-Evans Tokushima Otsuka rats were obtained at ages 7, 20, 50, and 68 weeks after collecting their blood and urine samples. OPB-9195 had been administered to the rats from age 24 weeks to the end of the experiments. CML in kidneys was detected by using a monoclonal antibody against CML according to an indirect immunofluorescence technique. CML-positive glomerular area was measured using NIH Image software (Research Services Branch of NIMH, Bethesda, MD). Hyalinized and/or sclerotic areas in glomeruli and mesangial and glomerular volume were measured using a point-counting technique. RESULTS: CML-positive area in glomeruli correlated closely not only with urinary albumin excretion (r = 0.912; P = 0.001), but also with volumes of mesangium and hyalinized and/or sclerotic lesions (r = 0.859; P = 0.0019 and r = 0.833; P = 0.0027, respectively). Treatment with OPB-9195 reduced CML-positive area and prevented the increase in mesangial volume, with no significant change in glomerular volume at age 68 weeks. The volume of hyalinized and/or sclerotic lesions also decreased by treatment with OPB-9195 in three of four rats at age 68 weeks. CONCLUSION: CML is a major advanced glycation end product contributing to the development of diabetic nephropathy, and inhibition of its accumulation by OPB-9195 results in amelioration of glomerular lesions in OLETF rats.

Age Factors↗
PubMed2000

Increased adrenocorticotropin responses to acute stress in Otsuka Long-Evans Tokushima Fatty (type 2 diabetic) rats.

The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is a new diabetic strain of rats whose disease closely resembles human type 2 diabetes. We measured plasma adrenocorticotropic hormone (ACTH) and corticostrone levels, and iodine-125-labeled ovine corticotropin-releasing factor ([125I]oCRF) binding in the anterior pituitary after ether-laparotomy stress in OLETF rats to examine the alteration of the hypothalamic-pituitary-adrenal (HPA) axis. In addition, we examined ACTH secretion following CRF administration in vivo and in vitro to characterize the mechanisms regulating the HPA axis in OLETF rats. Body weight, plasma glucose and insulin levels in OLETF rats were significantly higher than that in Long-Evans Tokushima Otsuka (LETO) rats. Basal plasma ACTH levels tended to be higher in OLETF rats than in LETO but it did not reach statistical significance. Ether-laparotomy stress dramatically increased plasma ACTH levels at 2 h after the stress both in either OLETF and LETO rats; the peak plasma ACTH level in OLETF rats following the stress was significantly greater than in LETO rats. Plasma ACTH levels following CRF (2 microg/kg, i.v.) in OLETF and LETO rats showed statistically significant increases at 10 and 30 min after CRF administration compared to ACTH levels at 0 min, however, the peak plasma ACTH level in OLETF rats at 10 min after CRF administration was significantly greater than in LETO rats. In contrast to ACTH levels, no significant differences in corticosterone levels between OLETF and LETO were observed at any of the time points. CRF (10 ng/ml) significantly increased ACTH secretion in pituitary cultures from OLETF compared to LETO rats. These data reveal a complex regulation of the endocrine system in this diabetic condition and suggest that HPA axis may be more stimulated during acute stress in diabetes mellitus than in unaffected subjects.

Acute Disease↗
PubMed1998

Centrally administered TRH-induced insulin secretion is impaired in the Otsuka-Long-Evans-Tokushima Fatty rats, a model of spontaneous non-insulin-dependent diabetes mellitus.

To investigate whether insulin secretion induced by stimulation of the vagus nerve is preserved or impaired in Otsuka-Long-Evans-Tokushima Fatty (OLETF) rats, we injected 10(-8) mol of thyrotropin-releasing hormone (TRH) into the third cerebral ventricle and determined the serum level of insulin in the unanesthetized, unrestrained rats. Intracerebroventricular (i.c.v.) injection increased the serum levels of glucose and insulin in both OLETF and Long-Evans-Tokushima-Otsuka (LETO) rats, a nondiabetic control strain, at 8-12 weeks of age. At 24-28 weeks of age, the increased level of glucose in OLETF rats was comparable to LETO rats but that of insulin was lower than control after the i.c.v. injection of TRH. Pretreatment with i.v. atropine had no significant effect on such hyperglycemia. However, the increases in the serum levels of insulin were suppressed in both OLETF and LETO rats. The plasma levels of epinephrine, norepinephrine, and glucagon rose significantly after TRH. There was no significant difference in the levels of any hormones between the two groups. In OLETF rats at 24-28 weeks of age, i.v. glucose load induced significantly higher serum levels of glucose and insulin than LETO rats. The results suggest that the vagus nerve-mediated insulin secretion is impaired in OLETF rats, similar to an autonomic diabetic neuropathy in the early stage of diabetes. This impairment may play some role in deteriorating glucose tolerance in this spontaneously developed diabetes model.

Animals↗
PubMed2001

Effect of obesity and troglitazone on expression of two glutathione peroxidases: cellular and extracellular types in serum, kidney and adipose tissue.

To determine the effect of obesity on expression of cellular- (C-) and extracellular (EC-) glutathione peroxidase (GPX) in serum, kidney and adipose tissue, we measured GPX in serum, kidneys and adipose tissue of the obese Otsuka-Long-Evans-Tokushima Fatty (OLETF) rat and its lean counterpart (LETO). We also investigated the effect of troglitazone. Five each of OLETF and LETO rats were fed diet with or without 0.2% troglitazone for 10 days. Final body weight, kidney weight, blood glucose and serum tumor necrosis factor-alpha (TNF-alpha) level were higher in OLETF rats than in LETO rats. Serum and kidney GPX activities were higher, but adipose tissue GPX activity was lower, in OLETF rats than in LETO rats. Troglitazone treatment decreased adipose tissue GPX activity and abolished overproduction of TNF-alpha in OLETF rats. Immunoblot analysis, for the first time, revealed that both obesity and troglitazone suppressed the protein signals for C-GPX and EC-GPX in adipose tissue. Serum protein carbonyl groups were increased in OLETF rats and troglitazone completely blocked this increase. Increased serum GPX activity in obese rat was due to the increased secretion of EC-GPX from the kidney. Troglitazone protected against the enhanced oxidative stress induced by obesity independently of the serum GPX concentration.

Adipose Tissue↗
PubMed2003

Morphological changes and increased sucrase and isomaltase activity in small intestines of insulin-deficient and type 2 diabetic rats.

The small intestine plays an important role in the digestion and absorption of many nutrients. To investigate the contribution of carbohydrate digestion to diabetes mellitus, we examined the morphological changes of the small intestine, and the expression of sucrase-isomaltase, which is one of the intestinal disaccharidases, in diabetic model rat, that is the streptozotocin-induced (STZ) diabetic rat (insulin-deficient model), and the Otsuka Long-Evans Tokushima Fatty (OLETF) rats and the Goto-Kakizaki (GK) rats (type 2 diabetic models). Intestinal hyperplasia was observed in STZ, OLETF, and GK rats. Moreover, in the small intestine of each diabetic strain, the proliferating cell nuclear antigen (PCNA)-labeling index, which is a marker of proliferation, was higher than in the respective control. Cdx1 and Cdx2, known to be transcriptional factors related to intestinal proliferation and differentiation, were more highly expressed in STZ, OLETF and GK rats than in the respective controls. These findings indicate that small intestinal hyperplasia, and thereby the resultant increase of total activity of disaccharidases such as sucrase and isomaltase in the entire small intestine, might be one of the reasons for postprandial hyperglycemia in diabetes mellitus.

Actins↗
PubMed2003

The effect of leptin, tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO) production on insulin resistance in Otsuka Long-Evans fatty rats.

Adipocytokines and nitric oxide (NO) play important roles in type 2 diabetes; however, the regulatory mechanism has not been fully clarified. To investigate the role of adipocytokines and NO production on insulin resistance in type 2 diabetes, the LETO rats and the OLETF rats were fed a control diet or a high-fat diet for 4 weeks. After 4 weeks the blood levels of leptin, tumor necrosis factor-alpha (TNF-alpha), and NO were measured. As an indicator of insulin resistance, the homeostasis model assessment for insulin resistance (HOMA-R) was applied. Food intake in high-fat diet group rats was lower than in control diet group rats. The high fat diet increased body weight (BW), but did not significantly affect the HOMA-R and blood pressure (BP). Leptin and TNF-alpha levels were significantly higher in the OLETF rats than in the LETO rats, while NO levels did not change between the two groups. The high-fat diet elevated blood leptin levels, but not TNF-alpha and NO levels. The HOMA-R in the OLETF rats was correlated with leptin, but not with BP, BW, TNF-alpha or NO. NO showed an inverse correlation with BP. In conclusion, leptin, TNF-alpha, and NO may each regulate insulin sensitivity through their own unique pathways. The elucidation of the regulatory mechanism of adipocytokines and NO may give a clue to clarify the pathophysiology of insulin resistance.

Adipose Tissue↗
PubMed2002

Correlation of functional and structural alterations of the coronary arterioles during development of type II diabetes mellitus in rats.

OBJECTIVE: Cardiac complications in diabetes mellitus (DM) are frequently ascribed to microangiopathy. Therefore, we sought to directly correlate the serial changes in coronary arterial function with the extent of coronary arteriolar remodeling in a model spontaneously developing type II DM. METHODS: Otsuka Long-Evans Tokushima Fatty (OLETF) rats and control Long-Evans Tokushima Otsuka (LETO) rats were used. At 5, 15 and 30 weeks of age, ten rats in each group were subjected to systemic and coronary hemodynamic measurements using the colored microsphere technique before and during maximal coronary hyperemia and histological assessment with Azan-Mallory stain of the coronary arterioles. RESULTS: As early as 15 weeks of age, at which time fasting plasma glucose concentration remained normal, OLETF rats exhibited a lower coronary flow reserve and a greater coronary vascular resistance during hyperemia than did LETO rats. On histomorphometry, OLETF rats exhibited a greater wall-to-lumen ratio and a greater degree of perivascular fibrosis of arterioles at 15 weeks of age and thereafter, both of which exhibited a significant correlation with the minimal coronary vascular resistance. CONCLUSIONS: The degree of functional deterioration in coronary circulation was directly correlated with the severity of coronary arteriolar structural remodeling during the development of microangiopathy in early stage of DM.

Animals↗
PubMed2001

Retinal vascular changes and systemic diseases: corrosion cast demonstration.

The purpose of the present study is to clarify the specific retinal vascular changes in rat models of single spontaneous or hereditary systemic diseases. We used Wistar Kyoto (WKy) rats 6 months of age as normal controls, 24-month-old Wistar Kyoto rats in studies of aging, 16-month-old spontaneously hypertensive rats (SHR), 18-month-old rats with inherited hypercholesterolemia (RICO) for arteriosclerosis, and 18-month-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats for diabetes mellitus. Retinal vascular corrosion casts were made and observed with a scanning electron microscope. The retinal vessels were also examined with a transmission electron microscope. Specific changes in the retinal vessels were: narrowing and thin thread-like capillaries in aging; capillary tortuosity, irregularity and narrowing in hypertension; straightening in hypercholesterolemia; and loop formation and microaneurysms in diabetes mellitus. These specific changes in the retinal vessels in each systemic disease can be clearly and easily revealed in a three-dimensional fashion by corrosion casts followed by scanning electron microscopy.

Aging↗
PubMed1999

DHEA improves glucose uptake via activations of protein kinase C and phosphatidylinositol 3-kinase.

We have examined the effect of adrenal androgen, dehydroepiandrosterone (DHEA), on glucose uptake, phosphatidylinositol (PI) 3-kinase, and protein kinase C (PKC) activity in rat adipocytes. DHEA (1 microM) provoked a twofold increase in 2-[3H]deoxyglucose (DG) uptake for 30 min. Pretreatment with DHEA increased insulin-induced 2-[3H]DG uptake without alterations of insulin specific binding and autophosphorylation of insulin receptor. DHEA also stimulated PI 3-kinase activity. [3H]DHEA bound to purified PKC containing PKC-alpha, -beta, and -gamma. DHEA provoked the translocation of PKC-beta and -zeta from the cytosol to the membrane in rat adipocytes. These results suggest that DHEA stimulates both PI 3-kinase and PKCs and subsequently stimulates glucose uptake. Moreover, to clarify the in vivo effect of DHEA on Goto-Kakizaki (GK) and Otsuka Long-Evans fatty (OLETF) rats, animal models of non-insulin-dependent diabetes mellitus (NIDDM) were treated with 0.4% DHEA for 2 wk. Insulin- and 12-O-tetradecanoyl phorbol-13-acetate-induced 2-[3H]DG uptakes of adipocytes were significantly increased, but there was no significant increase in the soleus muscles in DHEA-treated GK/Wistar or OLETF/Long-Evans Tokushima (LETO) rats when compared with untreated GK/Wistar or OLETF/LETO rats. These results indicate that in vivo DHEA treatment can result in increased insulin-induced glucose uptake in two different NIDDM rat models.

Adipocytes↗
PubMed2006

Mechanical and metabolic rescue in a type II diabetes model of cardiomyopathy by targeted gene transfer.

The Otsuka-Long-Evans Tokushima Fatty rat represents a model for spontaneous non-insulin-dependent type II diabetes mellitus (DM), characterized by diastolic dysfunction and associated with abnormal calcium handling and decrease in sarcoplasmic reticulum Ca2+ -ATPase (SERCA2a) expression. The aim of this study was to examine whether SERCA2a gene transfer can restore the energetic deficiency and left ventricular (LV) function in this model. DM rats were randomized to receive adenovirus carrying either the SERCA2a gene (DM + Ad.SERCA2a) or the beta-galactosidase gene (DM + Ad.betaGal) or saline (DM + saline). LV mechanoenergetic function was measured in cross-circulated heart preparations 3 days after infection. In DM, end-systolic pressure at 0.1 ml intraballoon water (ESP0.1) was low and end-diastolic pressure at 0.1 ml intraballoon water (EDP0.1) was high (22 mm Hg), compared with non-DM (EDP0.1 12 mm Hg). In DM + Ad.SERCA2a, however, ESP0.1 was increased over 200 mm Hg and EDP(0.1) was decreased to 7 mm Hg. LV relaxation rate was fast in DM + Ad.SERCA2a, but slow in the other DM groups. There was no difference in relation between cardiac oxygen consumption per beat and systolic pressure-volume area among all groups. Finally, the oxygen cost of LV contractility in DM was about three times as high as that of normal. In DM + Ad.SERCA2a, the oxygen cost decreased to control levels, but in DM + Ad.betaGal/DM + saline it remained high. In DM failing hearts, the high oxygen cost indicates energy wasting, which contributes to the contractile dysfunction observed in diabetic cardiomyopathy. SERCA2a gene transfer transforms this inefficient energy utilization into a more efficient state and restores systolic and diastolic function to normal.

Adenoviridae↗
PubMed2004

High-density rat radiation hybrid maps containing over 24,000 SSLPs, genes, and ESTs provide a direct link to the rat genome sequence.

The laboratory rat is a major model organism for systems biology. To complement the cornucopia of physiological and pharmacological data generated in the rat, a large genomic toolset has been developed, culminating in the release of the rat draft genome sequence. The rat draft sequence used a variety of assembly packages, as well as data from the Radiation Hybrid (RH) map of the rat as part of their validation. As part of the Rat Genome Project, we have been building a high-density RH map to facilitate data integration from multiple maps and now to help validate the genome assembly. By incorporating vectors from our lab and several other labs, we have doubled the number of simple sequence length polymorphisms (SSLPs), genes, expressed sequence tags (ESTs), and sequence-tagged sites (STSs) compared to any other genome-wide rat map, a total of 24,437 elements. During the process, we also identified a novel approach for integrating the RH placement results from multiple maps. This new integrated RH map contains approximately 10 RH-mapped elements per Mb on the genome assembly, enabling the RH maps to serve as a scaffold for a variety of data visualization tools.

Animals↗
PubMed2005

Development and application of rodent models for type 2 diabetes.

The increasing worldwide incidence of diabetes in adults constitutes a global public health burden. It is predicted that by 2025, India, China and the United States will have the largest number of people with diabetes. According to the 2003 estimates of the International Diabetes Federation, the diabetes mellitus prevalence in the USA is 8.0% and approximately 90-95% of diabetic Americans have type 2 diabetes - about 16 million people. Type 2 diabetes is a complex, heterogeneous, polygenic disease characterized mainly by insulin resistance and pancreatic beta-cell dysfunction. Appropriate experimental models are essential tools for understanding the molecular basis, pathogenesis of the vascular and neural lesions, actions of therapeutic agents and genetic or environmental influences that increase the risks of type 2 diabetes. Among the animal models available, those developed in rodents have been studied most thoroughly for reasons such as short generation time, inherited hyperglycaemia and/or obesity in certain strains and economic considerations. In this article, we review the current status of most commonly used rodent diabetic models developed spontaneously, through means of genetic engineering or artificial manipulation. In addition to these models, the Psammomys obesus, rhesus monkeys and many other species are studied intensively and reviewed by Shafrir, Bailey and Flatt and Hansen.

Animals↗
PubMed2000

Downregulation of melanocortin receptors in brain areas involved in food intake and reward mechanisms in obese (OLETF) rats.

The melanocortin (MC)4 receptor is important for food intake and weight homeostasis as it mediates the orexigenic and anorexigenic effects of the MCs. OLETF (Otsuka-Long-Evans-Tokushima-Fatty) rats are a selective inbred strain of polygenic variant rats which overeat and develop obesity with elevated leptin levels. We investigated by autoradiography if the expression of MC receptors were altered in ovariectomized estradiol-replaced female OLETF rats compared to their controls (Long-Evans-Tokushima-Otsuka (LETO) rats). We found that OLETF rats show a reduction in total [125I]NDP-MSH MC receptor binding in the ventromedial hypothalamic nucleus, perhaps reflecting an increased release of MC peptides in this region. The levels of MC receptors in the arcuate nucleus and the paraventricular hypothalamic nucleus were not changed. Interestingly, the OLETF rats also showed reduced MC-receptor binding in areas such as the nucleus accumbens shell, and the ventral tegmental area, both of which are believed to be involved in reward systems. Similarities in the changes of MC receptor expression in obese animals and in animals treated with opiates may suggest a neurobiological link between food intake mediated through the MC receptors and reward.

Animals↗
PubMed2003

Spatial memory impairment in OLETF rats without cholecystokinin - a receptor.

Cholecystokinin (CCK) is one of the most abundant neurotransmitter peptides in the brain. As Otsuka Long-Evans Tokushima Fatty (OLETF) rats lack CCK-A receptor because of a genetic abnormality, we examined whether learning and memory were impaired in these animals using both Morris water maze (MWM) and step-through type passive avoidance (PA) learning test. In the MWM test, memory impairment was observed in OLETF rats. The number of errors was also significantly higher, and that of the correct choices was significantly lower in OLETF rats compared to the controls [Long-Evans Tokushima Otsuka (LETO)] rats. In PA, OLETF rats did not show facilitating response 24 h after training. From these observations, we concluded that a spatial memory was impaired in the OLETF rats.

Animals↗
PubMed2000

Effects of systemic injection of interleukin-1beta on gastric vagal afferent activity in rats lacking type A cholecystokinin receptors.

We have shown that systemic administration of interleukin-1beta (IL-1beta) excites gastric vagal afferent activity in part via stimulation of type A cholecystokinin (CCK-A) receptors in rats. The present study was undertaken to determine whether the response of the gastric vagal afferent nerve to systemic IL-1beta is altered in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which lack CCK-A receptors. The response was compared with that of the control strain, Long-Evans Tokushima Otsuka (LETO) rats. All animals were anesthetized with pentobarbital and artificially ventilated. Intravenous administration of 4 microg/kg of IL-1beta increased gastric vagal afferent activity in both LETO and OLETF rats, whereas a smaller dose of 2 microg/kg of IL-1beta increased activity only in the OLETF rats. The present results demonstrate that the response of the gastric vagal afferent activity in CCK-A receptor deficient OLETF rats was more sensitive to intravenous administration of IL-1beta than was in control LETO rats.

Animals↗
PubMed2002

Different effects of castration and estrogen administration on glomerular injury in spontaneously hyperglycemic Otsuka Long-Evans Tokushima Fatty (OLETF) rats.

AIM: Non-insulin-dependent diabetic mellitus model rats, Otsuka-Long-Evans-Tokushima-Fatty (OLETF), develop diabetic nephropathy presenting with mesangial expansion leading to glomerular sclerosis and thickening of the glomerular basement membrane (GBM), especially in elderly males. The effects of sex hormones and castration on the incidence of diabetes mellitus (DM) have been studied in this strain rat. However, there have been no detailed studies on the effects of castration and sex hormone in the development of diabetic nephropathy. METHODS: In this study we examine the effect of castration or estrogen on the development of glomerular injury in OLETF rats. Thirty male OLETF rats and 10 male long-Evans Tokushima Otsuka (LETO) rats as a normal control were used. OLETF rats were divided into three groups: group 1 received sham-operation, group 2 was castrated at 6 weeks, and group 3 was administered 0.1 mg estrogen subcutaneously once a month from 6 weeks to 58 weeks of age and LETO rats were assigned to group 4. Body weight, urinary protein and fasting blood glucose, serum albumin and other serum constituents were investigated every 12 weeks from 12 weeks to 60 weeks of age. In groups 1-3, glucose tolerance test was performed at 38 weeks. Each group was studied morphologically at the end of the experiment (60 weeks of age). RESULTS: Castration attenuated proteinuria and glomerular sclerosis accompanied by an amelioration of glucose tolerance, a decrease in mesangial expansion and an attenuation of the GBM thickening. In contrast, although estrogen equally ameliorated glucose tolerance and attenuated the mesangial expansion and the GBM thickening, estrogen failed to attenuate proteinuria and glomerulosclerosis. A significant increase in glomerular tuft volume, and serum levels of growth hormone, total cholesterol and triglycerides was observed in the estrogen-treated rats as compared with the castrated rats. CONCLUSION: Besides the mechanisms involved in the development of diabetic nephropathy, other mechanisms may be involved and contribute to the development of glomerulosclerosis in the estrogen-treated rats, leading to a difference in glomerular injury between the castrated and estrogen-treated OLETF rats.

Animals↗
PubMed2004

Pepsinogen secretion in cholecystokinin-1 receptor-deficient rats.

We examined the roles of cholecystokinin (CCK)-2 receptors in the regulation of pepsinogen secretion in the CCK-1 receptor deficient Otsuka Long-Evans Tokushima Fatty (OLETF) rats. Pepsinogen secretion was determined in fasted acute fistula OLETF and control Long-Evans Tokusima Otsuka (LETO) rats. Pepsinogen secretion in OLETF rats under basal conditions as well as in response to CCK-8 stimulation was significantly higher than that in LETO rats. CCK-1 receptor specific agonist ARL 15849 was unable to stimulate pepsinogen secretion in OLETF rats, whereas it elicited pepsinogen secretion in LETO rats to levels similar to those obtained with equimolar CCK-8 stimulation. CCK-2 receptor antagonist reduced basal pepsinogen secretion and completely abolished CCK-8-stimulated pepsinogen output in OLETF rats, whereas in LETO rats, it reduced basal pepsinogen secretion but augmented CCK-8-stimulated pepsinogen output. CCK-1 receptor antagonist loxiglumide also greatly decreased CCK-8-stimulated pepsinogen secretion in OLETF rat, which indicates that loxiglumide is not a specific CCK-1 receptor antagonist. Intravenous infusion of somatostatin antagonist significantly increased CCK-8-stimulated pepsinogen secretion in LETO rats, whereas it had no significant influence on CCK-8-stimulated pepsinogen secretion in OLETF rats. These results indicate that CCK-8 stimulates pepsinogen secretion via CCK-2 receptors in CCK-1 receptor deficient OLETF rats and that the higher CCK-8-stimulated as well as basal pepsinogen secretion in OLETF rats might result from an elimination of tonic inhibition by somatostatin that is released from D cells through mainly CCK-1 receptors.

Animals↗