Influence of thyroidin on the condition of the viscera of the white rat (as indicated by vital staining of the tissues)

Summary Experiments were carried out on male albino rats which were given 0.25 g of thyroidin per 100 g body weight for 10 days. Vital staining with neutral red was used to study the interaction between the tissues of the different viscera (spleen, lungs, liver, kidneys, heart, testes, brain, small intestine, and skeletal muscle).In the animals receiving thyroidin there was a change in the sorptive property of the tissue of the liver, kidneys, heart, testes, brain, small intestine and skeletal muscle, which was thought to result from denaturation of cellular proteins.The results obtained reflect the nature and specific features of pathological and compensatory reactions occuring in tissues under the influence of thyroidin.Presented by Active Member AMN SSSR A. V. Lebedinskii Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 58, No. 10, pp. 108–110, October, 1964     

Porphyrobilinogen biosynthesis from δ-aminolevulinic acid by the viscera of albino rats

Ability to synthesize porphyrobilinogen (PBG) from -aminolevulinic acid (ALA) was determined in homogenates of tissues of the lungs, heart, liver, kidneys, spleen, pancreas, and small intestine of 77 albino rats. All these organs were found to be able to synthesize PBG. Highest ALA dehydratase activity was found in the liver tissue, followed in descending order by the kidneys, lungs, pancreas, small intestine, heart, and spleen. On the addition of a lead solution to the synthesizing system a significant decrease in enzyme activity was observed in the liver tissue, but in kidney tissue its activity was unchanged. On the addition of lead and D-penicillamine simultaneously no changes were found in the toxic effect of lead.M. F. Vladimirskii Moscow Regional Clinical Research Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR S. S. Debov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 12, pp. 687–689, December, 1978.     

Reduced mature size in progeny of swine severely restricted in protein intake during pregnancy.

The objective was to determine the effects of maternal gestation diet on mature body and organ size and composition of progeny. Female progeny of swine fed daily 1.8 kg (6,000 kcal DE) of a semipurified diet containing less than 0.5% protein (PR), 1.8 kg (6,000 kcal) of a standard maize-soybean meal-based gestation diet (C) or 0.6 kg (2,000 kcal DE) of C diet to d 70 of gestation and 1.8 kg (6,000 kcal DE) from d 71 to parturition (R) were used. They were fed ad libitum a standard maize-soybean meal-based growing diet to age 25 wk, then continued on limited feed intake to age 62 wk, then returned to ad libitum intake to age 119 wk. Body weight and ultrasonically determined subcutaneous backfat depth were recorded at 62, 79, 97, 105 and 119 wk of age and indices of body composition and organ weights were recorded on carcasses of animals killed at age 119 wk. Progeny of PR dams were permanently stunted in mature body weight and in weights of eviscerated carcass, heart, liver, kidneys, stomach and small intestine, but not in cerebrum, cerebellum weights or RNA and DNA content. It is concluded that severe protein restriction during gestation in swine resulted in permanent whole body weight stunting of progeny but that weights and total protein, RNA and DNA content of cerebrum, cerebellum and RNA and DNA concentration of longissimus muscle were unaffected.     

Immunohistochemical study of arginase 1 and 2 in various tissues of rats

Arginase 1 and arginase 2 catalyze the hydrolysis of arginine to ornithine and urea. The localization of these enzymes was studied in various tissues in Sprague-Dawley rats by immunohistochemistry and Western blotting. Western blot analysis showed that both arginase 1 and 2 were differentially expressed in the various organs examined. Arginase 1 was expressed at high levels in the liver, at moderate levels in the pancreas, and at low levels in the cerebrum, cerebellum, spinal cord, stomach, small and large intestines, kidneys, lungs, and spleen. The levels of arginase 2 immunoreactivity were high in the kidneys and pancreas, and moderate in the cerebrum, spinal cord, stomach, small intestine, large intestine, and lungs; the levels were very low in the liver and spleen compared with that in the cerebellum. Immunohistochemical analysis largely confirmed the results of the Western blot analysis. These findings indicate that the levels of arginase 1 and 2 varied among organs, suggesting that the arginase isoforms may play organ-specific roles in the urea cycle.     

“Structural autoregulation” of blood flow and GFR in the two renal vascular beds from two-kidney,one-clip renal hypertensive rats,as compared with kidneys from uni-nephrectomized and intact normotensive rats

Both kidneys from two-kidney, one-clip renal hypertensive rats (RHR) and the hypertrophied kidney of uni-nephrectomized rats (UNR) were investigated during artificial perfusion with 2% Dextran solution and kerosene at maximal vasodilatation, and studied with respect to organ weight, vascular resistance, preglomerular/postglomerular resistance ratio and glomerular filtration capacity. Paired perfusions were throughout used, isolated kidneys from age-matched normotensive rats serving as controls. The untouched, “high-pressure” RHR kidney had increased 40% in weight/100 g b. w. while its vascular resistance at maximal dilatation had increased almost 60%/g organ weight. Glomerular filtration capacity and preglomerular/postglomerular resistance ratio remained, however, largely unchanged.—The clipped “low-pressure”, RHR kidney was reduced 40% in weight and 45% in renal vascular resistance/g organ weight. It also showed a reduced pre/postglomerular resistance ratio and some reduction of filtration capacity.—The remaining hypertrophied kidney in UNR had increased 40% in weight, while its vascular resistance and filtration capacity/g organ weight, as well as its pre/postglomerular resistance ratio were unchanged. It is concluded that the kidney in renovascular hypertension rapidly adapts structurally not only in tissue mass, but also concerning total vascular resistance and pre/postglomerular resistance ratio, so as to chronically “autoregulate” GFR to match the altered pressure situation. Likewise, after unilateral nephrectomy the remaining, normotensive kidney increases in mass, with matched increases in blood flow and glomerular filtration capacity, while total resistance/g organ weight and the pre/postglomerular resistance ratio remain at normotensive levels.     

地尔硫卓对失血性休克犬肝、胰、小肠组织的保护作用（英文）

目的：探讨钙拮抗剂地尔硫卓（Diltiazem, Dil）对失血性休克犬肝、胰、小肠组织的保护作用及机理。方法：犬股动脉放血,平均动脉压（mean artery pressure, MAP）降至5.33-6.67 kPa（40-50 mmHg）,分别输Dil和生理盐水。休克90 min时将放出的血液全部回输。整个实验观察240 min。结果：从150 min到240 min,Dil明显提高MAP（P<0.01）;降低肝、胰、小肠组织中丙二醛（malondialdehyde, MDA）含量（P<0.01）;胰腺组织超氧化物歧化酶（SOD）活性升高。电镜显示：使用Dil后,休克犬肝、胰、小肠组织结构正常。结论：在犬失血性休克中,钙拮抗剂Dil能保护肝、胰、小肠组织结构和功能的完整性。     

Gross and microscopic visceral anatomy of the male Cape fur seal, Arctocephalus pusillus pusillus (Pinnipedia: Otariidae), with reference to organ size and growth

The gross and microscopic anatomy of the Cape fur seal heart, lung, liver, spleen, stomach, intestine and kidneys (n = 31 seals) is described. Absolute and relative size of organs from 30 male seals are presented, with histological examination conducted on 7 animals. The relationship between log body weight, log organ weight and age was investigated using linear regression. Twenty five animals were of known age, while 6 were aged from counts of incremental lines observed in the dentine of tooth sections. For the range of ages represented in this study, body weight changes were accurately described by the exponential growth equation, weight = w_or^t, with body weight increasing by 23% per annum until at least 9–10 y of age. Organ weight increased at a rate of between 25% and 33% per annum until at least 9–10 y of age, with the exception of the intestines, where exponential increase appeared to have ceased by about 7 y. The relationship between body weight and organ weight was investigated using logarithmic transformations of the allometric equation, y = ax^b, where the exponent b is 1 if organ weight is proportional to body weight. Most organs increased in proportion to the body. However, the heart, liver and spleen had exponents b > 1, suggesting that these organs increased at a faster rate than the body. The basic anatomical features of the viscera were similar to those of other pinnipeds, with some exceptions, including the arrangement of the multilobed lung and liver. Apart from the large liver and kidneys, relative size of the organs did not differ greatly from similar sized terrestrial carnivores. The histological features of the organs were generally consistent with those previously described for this species and other otariids. The heart, as in other pinnipeds, was unlike that of cetacea in not having unusually thick endocardium or prominent Purkinje cells. Notable histological features of the lungs included prominent fibrous septa, prominent smooth muscle bundles, cartilage extending to the level of the alveolar sacs and ample lymphoid tissue. The spleen had a thick capsule, well developed trabeculae and plentiful plasma cells. Abundant parietal cells were present in the fundic glands and lymphoid follicles were present in the gastric lamina propria, particularly in the pyloric region. Small intestinal villi were very long but this could have resulted from underlying chronic inflammation. Lymphoid follicles were prominent in the colon. The kidney reniculi each had a complete cortex, medulla and calyx, but a sportaperi medullaris musculosa was not identified.     

Growth of whole body and organs of growing rats during feed restriction and subsequent realimentation

Fifty-six Sprague-Dawley male rats (average body weight 70.6 +/- SD 11.6 g) were divided into two equal groups. One group was fed a 17% protein (N x 6.25) diet ad libitum for 42 d (Control). The second group was fed the same diet at 60% of the intake of the Control group for 14d (Restricted) and ad libitum for the remaining 28 d. Three rats per group were euthanized on d 1 and five rats per group on d 7, 14, 21, 28, and 42 and weights of the body, heart, spleen, liver, kidneys, epididymal fat, empty stomach, large and small intestines, and length of the left femur were recorded. The empty stomach, large and small intestines were dried to constant weight at 65 degrees C and assayed for crude protein content. Body weight, feed efficiency, weights of the heart, liver and epididymal fat were significantly reduced, while relative weight of the stomach and crude protein content of the small intestine were significantly increased in the restricted group during the period of feed restriction. Body and organ weights, however, compensated and caught up with control values within 14 d of feed rehabilitation and, by 28 d of realimentation, body weight, heart, liver and stomach weights were significantly greater in restricted than in control rats. Femur length was reduced by feed restriction, but continued to increase during restriction and realimentation. Gastrointestinal tract segments were less affected by feed restriction and responded more quickly to realimentation than the whole body.     

广州地区围产儿脏器重量及大小测量的研究

目的　探讨广州地区围产儿脏器重量及大小的发育规律 .方法　选择 6 2 5例胎龄准确的单胎 ,除外明显浸软、IUGR、水肿儿、巨大胎、有胸腹水者 ,新生儿除外先天性心脏病及有明显疾病的脏器 .根据胎龄分为 6组 ,分别测量围产儿体重、身长和各脏器重量、长度 .进行统计分析 .结果　胰腺、肺发育最早 ,肾脏与肺发育最快 ,出生后脑增长最少而胰腺增长最快 ,肠变异最大等规律 .结论　围产儿脏器资料用于围产儿病理研究有一定意义     

Role of Apelin/APJ axis in cancer development and progression

Apelin is an endogenous peptide, which is expressed in a vast board of organs such as the brain, placenta, heart, lungs, kidneys, pancreas, testis, prostate and adipose tissues. The apelin receptor, called angiotensin-like-receptor 1 (APJ), is also expressed in the brain, spleen, placenta, heart, liver, intestine, prostate, thymus, testis, ovary, lungs, kidneys, stomach, and adipose tissue. The apelin/APJ axis is involved in a number of physiological and pathological processes. The apelin expression is increased in various kinds of cancer and the apelin/APJ axis plays a key role in the development of tumors through enhancing angiogenesis, metastasis, cell proliferation and also through the development of cancer stem cells and drug resistance. The apelin also stops the apoptosis of cancer cells. The apelin/APJ axis was considered in this review as an attractive therapeutic target for cancer treatment.     

In vivo induction of H-2K/D antigens by recombinant interferon-gamma

B10.BR mice received i.v. increasing doses of recombinant interferon-gamma (rIFN-gamma) on three consecutive days. Using an immunoperoxidase technique the distribution of H-2K/D antigens was studied in frozen tissue sections of thirteen organs (kidney, liver, pancreas, esophagus, stomach, small intestine, colon, lungs, heart, brain, thymus, lymph node and spleen). Class I antigens were shown to be induced or enhanced in almost every organ after exposure to IFN-gamma. This effect was particularly conspicuous for renal tubular cells, hepatocytes, bronchiolar epithelial cells, gastric mucous cells, thymic cortical lymphocytes and capillary endothelial cells in heart and kidney. Neurons, glial cells, gastric chief and parietal cells, and pancreas cells were not inducible. The findings show that i.v. application of IFN-gamma leads to strong induction or enhancement of major histocompatibility complex class I antigens in a wide variety of tissues.     

Distribution of prolactin in selected rat organs and tissues

A single dose of 25 microg prolactin (PRL)/kg of rat body weight was administered to rats subcutaneously. At 1, 2, 3, 4 and 5 h after the injection, selected organs and tissues were taken for analysis. It was found that 1 h after administration, the highest amount of PRL accumulated in the milk (lactiferous) gland, the blood, the ovaries, the pituitary and the liver. Over time, the prolactin content in the selected organs and tissues decreased. PRL is selectively captured by the milk gland, the pituitary, the ovaries, the liver and the heart. Based on the value of the organ or tissue capacity index for PRL, the following order was established for the organs and tissues to which the hormone binds: milk gland > blood > pituitary > ovaries > lungs > liver > cranial bone > spleen > heart > kidneys > muscular tissue > adrenals > adipose tissue > brain.     

Cell number and size in selected organs of fetuses of rats malnourished and exposed to nitrofen

The effects of maternal exposure to nitrofen or protein-energy malnutrition on the number and sizes of cells in selected organs of the fetal rat have been studied. Pregnant rats were fed either an adequate (CON) or protein-energy deficient diet (PEM) throughout gestation. Each diet group was divided into two subgroups. One subgroup was gavaged with 25 mg nitrofen/kg body weight on gestational days 7-21 and the other, with corn oil carrier only. Fetal liver, kidneys, intestine, heart, lung, and brain were weighed and assayed for DNA, RNA, and protein. Maternal protein deficiency resulted in a reduction in organ weight and total DNA, RNA, and protein in all six organs. Maternal nitrofen exposure resulted in reduced weight and reduced protein in all organs except the brain. Total DNA and RNA were reduced in intestine, heart, and lung, and total RNA was also reduced in the liver following maternal nitrofen exposure. An interaction between diet and toxin affected lung weight, DNA, RNA, and protein, intestinal total protein, and heart DNA. Protein/DNA ratios were reduced in liver, intestine, and brain in the group fed the inadequate diet and in intestine only following nitrofen exposure. The deficient diet resulted in increased RNA/DNA ratio in the fetal liver and heart and a decreased ratio in the kidney and brain. Nitrofen exposure resulted in a lower RNA/DNA ratio in the liver. The data indicate that maternal protein-energy malnutrition results in smaller organs in the fetuses with fewer cells and containing less protein and RNA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamics and metabolism of the in vivo vascularly isolated canine pancreas.

Surgical procedures are detailed that have yielded for the first time an in vivo vascularly isolated, autoperfused preparation of the entire pancreas in anesthetized dogs. Previous studies had isolated only part of the pancreas or had resorted to blood-flow techniques not requiring pooled pancreatic venous blood, necessary for metabolic studies of the organ. Pancreatic blood flow (48 ml/min), O2 uptake (180 mumol/min), glucose uptake (51.0 mumol/min), lactate output (6.6 mumol/min), net free fatty acid uptake (2.23 mumol/min), all per 100 g tissue, and various other measured and calculated hemodynamic and metabolic variables were determined on the preparation during control conditions. The stability of the preparation was verified by serial determinations of these parameters and of blood alpha-amylase and beta-glucuronidase levels from 1 to 2.5 h postsurgery. Metabolic rate and glucose uptake were both found to be much higher than in intestinal tissues and approached values characteristic of liver tissue.     

衰老模型小鼠胰腺结构与功能的变化

目的探讨D-半乳糖(D-gal)致衰小鼠胰腺结构与功能变化。方法 2月龄雄性C57BL/6J小鼠随机分为两组,每组10只。衰老组:小鼠皮下注射D-gal(120mg/kg),每天1次,共42 d;对照组:小鼠皮下注射等时与等量生理盐水。衰老模型建立完成第2天,采外周血测定空腹血糖(FBG)与空腹胰岛素(FINS)水平;称小鼠体重(g)与胰腺湿重(mg)计算胰腺脏器指数;石蜡切片,HE染色观察胰腺光学显微镜下形态;制备胰腺冷冻切片,检测衰老相关β-半乳糖苷酶(SA-β-Gal)染色阳性胰腺细胞的相对吸光度(RA);免疫组织化学法观察胰腺组织晚期糖基化终产物(AGEs)的RA;制备胰腺组织匀浆检测超氧化物歧化酶(SOD)、总抗氧化能力(T-AOC)和丙二醛(MDA)的含量。结果衰老组小鼠FBG显著升高,FINS水平降低;胰腺湿重和胰腺脏器指数明显升高;胰腺光学显微镜下结构未见显著改变,但胰岛内单个有核细胞所占面积增加;胰腺SA-β-Gal染色阳性细胞数显著增加;AGEs阳性表达区域RA值明显升高;SOD与T-AOC含量显著降低,MDA含量显著升高。结论 D-gal复制衰老小鼠可致其胰腺损伤,其机制与D-gal致胰腺组织细胞的氧化应激损伤有密切关系。     

TdT缺口末端标记法检测大鼠石蜡切片内凋亡细胞

用末端转移酶介导的切口末端标记法（ＴＵＮＥＬ），检测了大鼠不同器官内的凋亡细胞。结果显示，凋亡细胞在光镜下多以核圆形、深染为特征，呈散在分布。有的凋亡细胞裂解成一个或多个凋亡小体。凋亡细胞数量因器官而异，在细胞增生活跃和细胞更替速度快的器官如小肠、大肠和淋巴结内，凋亡细胞较多，相对稳定的肝、胰等器官亡细胞较少。凋亡细胞通常被巨噬细胞或邻近细胞吞噬。该法的优点在于保存组织结构的同时，在原位到凋亡细胞     

Heme oxygenase -1 gene therapy: recent advances and therapeutic applications

Heme oxygenase-1 (HO-1) is regarded as a sensitive and reliable indicator of cellular oxidative stress. Studies on carbon monoxide (CO) and bilirubin, two of the three (iron is the third) end products of heme degradation have improved the understanding of the protective role of HO against oxidative injury. CO is a vasoactive molecule and bilirubin is an antioxidant, and an increase in their production through an increase in HO activity assists other antioxidant systems in attenuating the overall production of reactive oxygen species (ROS), thus facilitating cellular resistance to oxidative injury. Gene transfer is used to insert specific genes into cells that are either otherwise deficient in or that underexpress the gene. Successful HO gene transfer requires two essential elements to produce functional HO activity. Firstly, the HO gene must be delivered in a safe vector, e.g., adenoviral, retroviral or leptosome based vectors, currently being used in clinical trials. Secondly, with the exception of HO gene delivery to either ocular or cardiovascular tissue via catheter-based delivery systems, HO delivery must be site and organ specific. This has been achieved in rabbit ocular tissues, rat liver, kidney and vasculature, SHR kidney, and endothelial cells [Abraham et al., 1995a; Abraham et al., 1995b; Abraham et al., 2002c; Quan et al., 2004; Sabaawy et al., 2000; Sabaawy et al., 2001; Yang et al., 2004]. In this review, we discuss the functional significance of the HO system in various pathophysiological conditions and the beneficial therapeutic applications of human HO gene transfer and gene therapy in a variety of clinical circumstances.     

The distribution in the rabbit of choline administered by injection or infusion

1. The concentration of choline in plasma, erythrocytes, skeletal muscle, heart, lung, liver, small intestine and kidneys and the changes that follow the injection or infusion of choline have been measured in rabbits anaesthetized with pentobarbitone.2. The concentration of choline in the plasma of arterial blood was 11.8 +/- 0.6 n-mole/ml. and in the erythrocytes 28.4 +/- 1.3 n-mole/ml. blood.3. All tissues contained a higher concentration of free choline than did plasma. The values range from 19.1 +/- 2.2 n-mole/g in skeletal muscle to 500 +/- 25 n-mole/g in the kidney.4. In order of their choline concentrations the tissues were intestine (duodenal end) > kidney > intestine (caecal end) > liver > lung > brain > heart > erythrocytes > (blood) > skeletal muscle > plasma, while in order of the contribution to the total body choline they were liver > intestine > skeletal muscle > (blood) > kidney > erythrocytes > lung > brain > plasma > heart. The total free choline determined by these analyses was between 30-40 mumole/kg body weight, about one third being present in the liver.5. The choline content of the small intestine varied along its length. The lowest amount being present in the portion adjoining the caecum.6. Within 1 min of the injection of choline 100 or 300 mumole/kg, 70-90% had left the circulation. The proportionate loss was higher after 100 mumole/kg than after 300 mumole/kg.7. The loss following 300 mumole/kg was increased if that dose were preceded by a dose of 100 mumole/kg 40 min earlier; this suggests some additional disposal mechanism(s) had been activated by the first dose.8. Three minutes after the injection of choline 300 mumole/kg, about 60% was present as free choline in the tissues studied. The order of the concentration increases was kidneys > liver > muscle > lung > small intestine (caecal end) > heart > intestine > small intestine (duodenal end) > brain.9. Forty minutes after the injection of choline 300 mumole/kg, only 11% could be accounted for as free choline. Only the levels in the kidney, liver, muscle and lung were significantly above normal at this time.10. Infusion of choline 0.8 mumole/kg. min or greater produced rises in plasma choline that corresponded to a clearance of 32 ml. plasma/kg. min.11. After the infusion of 300 mumole/kg over a period of 1 hr, raised levels of choline were detected in all tissues assayed, but the amount found accounted for only 14% of the choline administered. The concentrations in the kidney, liver and lung were similar to those found 40 min after the injection of 300 mumole/kg.12. There was no change in the concentration of choline in the erythrocytes after the injection of choline 100 or 300 mumole/kg, nor during the infusion of choline at the rate of 5 mumole/kg. min for 1 hr.13. The plasma volume appeared to be affected by the injection of the large doses of choline; after choline 300 mumole/kg the plasma volume was reduced. No effect on the plasma volume was observed during the infusion of the same dose.     

Tissue distribution and toxicity of cyclosporin A in the mouse

Groups of mice were given cyclosporin A (CyA) subcutaneously for 6 wk at a dose of 12.5, 50 or 200 mg/kg/d. After 7, 21 and 42 days of CyA administration the CyA content of serum, thymus, mesenteric lymph nodes, spleen, kidney, liver, lung, small and large intestine and brain was measured, each organ was examined histologically, and the total viable nucleated cell content of thymus, mesenteric lymph nodes, spleen and femoral marrow was analysed. CyA was detected in every organ assayed at each concentration of CyA administered. The mean concentration of CyA per organ was consistently highest in organs of mice given CyA 200 mg/kg/d and lowest in those given 12.5 mg/kg/d at each time point, but there was pronounced variability in the concentration of CyA between individual mice. Repeated administration of CyA after the first week did not further elevate CyA tissue concentrations. At doses of 50 or 200 mg/kg/d CyA caused weight loss, diarrhea, intussusception and fatal neurotoxicity. In addition, the spleen, thymus and mesenteric lymph nodes of mice given CyA 50 or 200 mg/kg/d were hypocellular and disorganized, and all lymphoid organs contained numerous pyknotic lymphocytes. The liver showed fatty change and the kidney degeneration of proximal tubules. Femoral marrow showed enlarged and congested sinuses. No abnormalities were noted in mice given CyA 12.5 mg/kg/d.     

Adipose tissue and its role in organ crosstalk

The discovery of adipokines has revealed adipose tissue as a central node in the interorgan crosstalk network, which mediates the regulation of multiple organs and tissues. Adipose tissue is a true endocrine organ that produces and secretes a wide range of mediators regulating adipose tissue function in an auto‐/paracrine manner and important distant targets, such as the liver, skeletal muscle, the pancreas and the cardiovascular system. In metabolic disorders such as obesity, enlargement of adipocytes leads to adipose tissue dysfunction and a shift in the secretory profile with an increased release of pro‐inflammatory adipokines. Adipose tissue dysfunction has a central role in the development of insulin resistance, type 2 diabetes, and cardiovascular diseases. Besides the well‐acknowledged role of adipokines in metabolic diseases, and the increasing number of adipokines being discovered in the last years, the mechanisms underlying the release of many adipokines from adipose tissue remain largely unknown. To combat metabolic diseases, it is crucial to better understand how adipokines can modulate adipose tissue growth and function. Therefore, we will focus on adipokines with a prominent role in auto‐/paracrine crosstalk within the adipose tissue such as RBP4, HO‐1, WISP2, SFRPs and chemerin. To depict the endocrine crosstalk between adipose tissue with skeletal muscle, the cardiovascular system and the pancreas, we will report the main findings regarding the direct effects of adiponectin, leptin, DPP4 and visfatin on skeletal muscle insulin resistance, cardiovascular function and β‐cell growth and function.