Autonomic and endocrine factors in the regulation of energy balance

The regulation of energy reserves is modified by both the autonomic nervous system and the hormonal milieu. The activity of the two limbs of the autonomic nervous system shows a reciprocal response to stimulation or damage in either the ventromedial or the lateral hypothalamus. Ventromedial hypothalamic lesions decrease the activity of the sympathetic nervous system and increase the activity of the vagus nerve. Lateral hypothalamic lesions, on the other hand, increase the activity of the sympathetic nervous system. Central neurotransmitters involved in energy balance include the monoamines, amino acids, and peptides. Removal of adrenal steroids by adrenalectomy reverses or attenuates all forms of obesity by reducing food intake and possibly by increasing energy expenditure. Acute insulin injections increase food intake, but chronic injections may reduce it. A model showing the reciprocal relation of sympathetic activity to energy reserves is presented.     

Bone endocrine regulation of energy metabolism and male reproduction

Usually vertebrate physiology is studied within the confined limits of a given organ, if not cell type. This approach has progressively changed with the emergence of mouse genetics that has rejuvenated the concept of a whole body study of physiology. A vivid example of how mouse genetics has profoundly affected our understanding of physiology is skeleton physiology. A genetic approach to bone physiology revealed that bone via osteocalcin, an osteoblast-secreted molecule, is a true endocrine organ regulating energy metabolism and male reproduction. This ongoing body of work that takes bone out of its traditional roles is connecting it to a growing number of peripheral organs. These novel important hormonal connections between bone, energy metabolism and reproduction underscore the concept of functional dependence in physiology and the importance of genetic approaches to identify novel endocrine regulations.     

神经内分泌和免疫系统之间的相互调节作用(一)

我们一般认为机体各器官、系统的功能都处于神经系统和内分泌系统的调节和控制之下。神经系统和内分泌系统是机体内起主导作用的调节系统。它们密切联系 ,互相配合 ,维持内环境相对稳定。这一传统的观念近年来受到了挑战。新的观点认为 ,免疫系统也是机体内一个重要感受和调节系统。神经内分泌和免疫系统之间的相互作用 ,对机体在不同条件下稳态的维持起有决定性的作用。因此 ,在谈到机体的功能调节时 ,如果不谈免疫系统的作用 ,将是一种缺陷。目前这方面的研究已经发展成为一门独立的边缘学科 :神经免疫调节学、神经免疫内分泌学或神经免疫…     

The adipocyte: a model for integration of endocrine and metabolic signaling in energy metabolism regulation

The ability to ensure continuous availability of energy despite highly variable supplies in the environment is a major determinant of the survival of all species. In higher organisms, including mammals, the capacity to efficiently store excess energy as triglycerides in adipocytes, from which stored energy could be rapidly released for use at other sites, was developed. To orchestrate the processes of energy storage and release, highly integrated systems operating on several physiological levels have evolved. The adipocyte is no longer considered a passive bystander, because fat cells actively secrete many members of the cytokine family, such as leptin, tumor necrosis factor-alpha, and interleukin-6, among other cytokine signals, which influence peripheral fuel storage, mobilization, and combustion, as well as energy homeostasis. The existence of a network of adipose tissue signaling pathways, arranged in a hierarchical fashion, constitutes a metabolic repertoire that enables the organism to adapt to a wide range of different metabolic challenges, such as starvation, stress, infection, and short periods of gross energy excess.     

神经内分泌和免疫系统之间的相互作用(二)——神经免疫调节

(上接 2 0 0 0年第 3期第 3页 )1 .6.2　某些前激素 (prohormone)的作用　血液循环中的硫酸表甾酮 (dehydroepiandrosteronesulphate,DHEAS)受到 DHEA硫酸酶的作用变成 DHEA可增强 TH1的活性 ,此时 TH1/TH2 的比值趋向于 TH1占优势。随着年龄的增加 DHEA的水平也随之下降。这可能是机体随着年龄的增长免疫功能下降的重要原因之一。动物实验中也发现 ,老年鼠体内的 DHEA含量明显低于对照组。如果补充 DHEA后老年鼠的免疫缺损状态可以得到明显改善。此外 ,衰老时的免疫功能下降也与某些细胞因子分泌异常增高有关。例如 IL -6的…     

Interaction of cytoplasmic messenger-RNA with proteins: their possible function in the regulation of translation

In the present report we summarize recent results concerning our studies on messenger ribonucleoprotein particles and RNA-binding proteins from the cytoplasm of mouse erythroblasts and mouse Krebs II ascites cells.     

Cell volume regulation in the nervous system

There is good evidence that the three main compartments of the brain, i.e. extracellular space, neurones and glial cells, change their volume during physiological and pathophysiological neuronal activity. However, there is strikingly little knowledge about the mechanisms underlying such alterations in cell volume. For this purpose, a better understanding of the electrophysiological behavior of the neurones and glial cells during volume changes is necessary. Examples are discussed for which changes in cell volume can be derived from the underlying changes in membrane permeabilities. Volume regulatory mechanisms in the brain have not been described under isotonic conditions. However, a rapid volume regulatory decrease is occurring in cultured glial cells during exposure to hypotonic solutions. In contrast, in these cells no volume regulatory increase was found during superfusion with hypertonic media. On the other hand, the entire brain is able to compensate chronic hypertonic perturbations within hours to days. Interestingly, not only ion fluxes induce cellular volume changes but, in turn, water movements can also influence ion fluxes in both neurones and glial cells. With respect to this it should be considered that volume regulatory membrane processes might not exclusively be activated by changes in transmembranal ion gradient, but also by changes of membrane surface shape. Future studies on cellular mechanisms of volume regulation in the brain should imply a combined use of recent techniques such as computerized video-imaging, radiotracer flux measurements and ion-sensitive microelectrodes in defined cell cultures. Optical monitoring and ion-sensitive microelectrodes should enable measurements of volume changes in identified cellular elements of intact nervous structures such as brain slices.     

Interaction of chemokines and glycosaminoglycans: a new twist in the regulation of chemokine function with opportunities for therapeutic intervention

Despite their key role in inflammation, the apparent redundancy in the chemokine system is often cited as an argument against probing chemokines as therapeutic targets for inflammation. However, this in vitro redundancy frequently does not translate to the in vivo situation, as exemplified by the use of specific receptor antagonists, ligand neutralizing or receptor blocking antibodies and gene-deleted mice in models of human disease. Specificity may be conferred onto the chemokine system by fine-tuning of responses both temporally and spatially through their highly specific interactions with glycosaminoglycans (GAGs). In this survey, we present evidence for specificity in the interaction and introduce emerging technologies that enable detailed assessment of protein–GAG interactions. Finally, we address the issue of exploitation of this interaction for therapeutic advantage.     

Least energy regulation of the arterial system

The formulation and results of the Kalman State Regulator Problem are applied to a mathematical model of the arterial system of a dog to obtain an optimal control for blood pressure. The criterion for optimality is minimum energy per cycle. Presented at the Society for Mathematical Biology Meeting, University of Pennsylvania, Philadelphia, August 19–21, 1976.     

Postpartum reproductive function: association with energy,metabolic and endocrine status in high yielding dairy cows

This study evaluated the effect of metabolic, endocrine and energy status on onset of ovarian cycle, days open (DO), and conception at first service in 90 multiparous Holstein cows, housed at a research farm. Dry matter intake, milk yield and body weight were measured daily from Week 2 antepartum (a.p.) to Week 20 postpartum (p.p.). Milk composition was determined four times per week and milk acetone was measured weekly. Blood samples for the determination of glucose, non-esterified fatty acids, cholesterol, creatinine, albumin, urea, beta-hydroxybutyrate, leptin, insulin, insulin-like growth factor-1, growth hormone, 3,5,3'-triiodothyronine (T(3)), and thyroxine (T(4)) were taken 2 weeks a.p., in Weeks 1-16, and 20 p.p. between 7:30 and 9:00 h. The onset of ovarian cycle was specified by weekly gynecological examination and by skim milk progesterone determination by radioimmunoassay (twice per week). Energy balance (EB) traits were calculated and expressed as accumulated negative EB from calving to EB equilibrium, EB nadir (EBN), rate of EB recovery after EBN (EBR), and time from calving to EBN and to EB equilibrium, respectively. The onset of ovarian cycle p.p. was not related to EB. However, a low degree of EBN and a fast EBR were associated with fewer DO, and EB at first service was positively related to conception. High plasma levels of T(3) and T(4) p.p. were associated with an early start of ovarian cycle, and high concentrations of glucose and cholesterol with a short calving to conception interval. Conception at first service was positively related to EB at first service and progesterone concentration 10-13 days after first service. In conclusion, thyroid hormones may play an important role in resumption of ovarian cyclicity p.p., and a good energy status enhances the chance of conception at first service and shortens DO.     

Cardiac endocrine function is an essential component of the homeostatic regulation network: physiological and clinical implications

The discovery of cardiac natriuretic hormones required a profound revision of the concept of heart function. The heart should no longer be considered only as a pump but rather as a multifunctional and interactive organ that is part of a complex network and active component of the integrated systems of the body. In this review, we first consider the cross-talk between endocrine and contractile function of the heart. Then, based on the existing literature, we propose the hypothesis that cardiac endocrine function is an essential component of the integrated systems of the body and thus plays a pivotal role in fluid, electrolyte, and hemodynamic homeostasis. We highlight those studies indicating how alterations in cardiac endocrine function can better explain the pathophysiology of cardiovascular diseases and, in particular of heart failure, in which several target organs develop a resistance to the biological action of cardiac natriuretic peptides. Finally, we emphasize the concept that a complete knowledge of the cardiac endocrine function and of its relation with other neurohormonal regulatory systems of the body is crucial to correctly interpret changes in circulating natriuretic hormones, especially the brain natriuretic peptide.     

The effect of pheochromocytoma treatment on subclinical inflammation and endocrine function of adipose tissue

The aim of our study was to evaluate the influence of surgical removal of pheochromocytoma on the endocrine function of adipose tissue and subclinical inflammation as measured by circulating C-reactive protein (CRP) levels. Eighteen patients with newly diagnosed pheochromocytoma were included into study. Anthropometric measures, biochemical parameters, serum CRP, leptin, adiponectin and resistin levels were measured at the time of diagnosis and six months after surgical removal of pheochromocytoma. Surgical removal of pheochromocytoma significantly increased body weight, decreased both systolic and diastolic blood pressure, fasting blood glucose and glycated hemoglobin levels. Serum CRP levels were decreased by 50 % six months after surgical removal of pheochromocytoma (0.49+/-0.12 vs. 0.23+/-0.05 mg/l, p<0.05) despite a significant increase in body weight. Serum leptin, adiponectin and resistin levels were not affected by the surgery. We conclude that increased body weight in patients after surgical removal of pheochromocytoma is accompanied by an attenuation of subclinical inflammation probably due to catecholamine normalization. We failed to demonstrate an involvement of the changes in circulating leptin, adiponectin or resistin levels in this process.