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Insulin Target Tissue

Major Hormones: Origin, Target, Function

Major Hormones: Origin, Target, Function

Your online site for school work help and homework help. Science, English, History, Civics, Art, Business, Law, Geography, all free! Triggers secretion of hydrocortisone from the adrenal gland Stimulates female egg maturation and male sperm production Stimulates female ovulation and male secretion of testosterone Stimulates milk production in the breasts after childbirth Regulates water retention and blood pressure Triggers contraction of the uterus during labor Stimulates milk letdown for breast-feeding after childbirth Regulates circadian rhythm (awake/sleep patterns) and prevent jet lag Controls the level of calcium in the blood by depositing it in the bones Increases the bodys metabolic rate; promotes normal growth and development Promotes the growth and development of white blood cells, helping the body fight infection Regulates sodium and potassium levels in the blood to control blood pressure Plays key role in stress response; increases blood glucose levels and mobilizes fat stores; reduces inflammatation Increases blood pressure, heart and metabolic rate, and blood sugar levels; dilates blood vessels. Also released during exercise Continue reading >>

Histologic Distribution Of Insulin And Glucagon Receptors

Histologic Distribution Of Insulin And Glucagon Receptors

M. Watanabe, H. Hayasaki, T. Tamayama and M. Shimada Department of Anatomy, Osaka Medical College, Takatsuki, Osaka, Japan Insulin and glucagon are the hormonal polypeptides secreted by the B and A cells of the endocrine pancreas, respectively. Their major physiologic effects are regulation of carbohydrate metabolism, but they have opposite effects. Insulin and glucagon have various physiologic roles, in addition to the regulation of carbohydrate metabolism. The physiologic effects of insulin and glucagon on the cell are initiated by the binding of each hormone to receptors on the target cells. Morphologic studies may be useful for relating biochemical, physiologic, and pharmacologic information on the receptors to an anatomic background. Receptor radioautography techniques using radioligands to label specific insulin and glucagon receptors have been successfully applied to many tissues and organs. In this review, current knowledge of the histologic distribution of insulin and glucagon receptors is presented with a brief description of receptor radioautography techniques. Key words: radioautography, insulin, glucagon, receptor, distribution Introduction Insulin is a hormone secreted by B cells, and glucagon is secreted by A cells of the pancreas. The two hormones play an important role in carbohydrate metabolism. However, the actions of insulin and glucagon in carbohydrate metabolism are opposite. Furthermore, insulin and glucagon have various physiologic roles in addition to the regulation of carbohydrate metabolism. The physiologic effects of insulin and glucagon on the cell are initiated by the binding of each hormone to target cell receptors. To relate biochemical, physiologic, and pharmacologic information on receptors to an anatomic background, morphologic studies Continue reading >>

Insulin

Insulin

Insulin is a hormone, that means it is a chemical secreted into the blood by an endocrine organ and carried around the body to a target organ. Insulin helps to control the amount of glucose dissolved in the blood. Insulin prevents the blood sugar level from rising too high. It is also necessary to have insulin in your blood for respiration to take place. Without insulin cells can only get energy from fat and this causes serious problems. The control of blood sugar level is a homeostatic mechanism. How Insulin Works: Insulin is secreted by the Islets of Langerhans which are special groups of cells in the pancreas. The Islets (little islands) are endocrine organs. If you have a large carbohydrate meal, the level of glucose in the blood will start to rise as your digestive system turns all the starch and sugars in your food into glucose. If you have not had a meal for several hours your blood sugar level will fall because your cells use up the glucose in aerobic respiration. When your blood sugar level rises, the Islets of Langerhans secrete MORE insulin. When your blood sugar level falls, the Islets of Langerhans secrete LESS insulin. The main target organ for insulin is the liver. It is the liver which removes glucose from the blood by turning it into glycogen. All other tissues in your body need insulin to help then respire glucose, so in a way they are also target organs. If you eat, and eat, and eat, and eat, never mind how little exercise; there will come a time when there is no more room for glycogen in your liver. High levels of insulin will make you start to turn the excess glucose into FAT. Please balance your diet!!!!! When you fast for more than two days, your liver will run out of glycogen, so you will have to use fat and protein to get energy. When your blood Continue reading >>

Physiologic Effects Of Insulin

Physiologic Effects Of Insulin

Stand on a streetcorner and ask people if they know what insulin is, and many will reply, "Doesn't it have something to do with blood sugar?" Indeed, that is correct, but such a response is a bit like saying "Mozart? Wasn't he some kind of a musician?" Insulin is a key player in the control of intermediary metabolism, and the big picture is that it organizes the use of fuels for either storage or oxidation. Through these activities, insulin has profound effects on both carbohydrate and lipid metabolism, and significant influences on protein and mineral metabolism. Consequently, derangements in insulin signalling have widespread and devastating effects on many organs and tissues. The Insulin Receptor and Mechanism of Action Like the receptors for other protein hormones, the receptor for insulin is embedded in the plasma membrane. The insulin receptor is composed of two alpha subunits and two beta subunits linked by disulfide bonds. The alpha chains are entirely extracellular and house insulin binding domains, while the linked beta chains penetrate through the plasma membrane. The insulin receptor is a tyrosine kinase. In other words, it functions as an enzyme that transfers phosphate groups from ATP to tyrosine residues on intracellular target proteins. Binding of insulin to the alpha subunits causes the beta subunits to phosphorylate themselves (autophosphorylation), thus activating the catalytic activity of the receptor. The activated receptor then phosphorylates a number of intracellular proteins, which in turn alters their activity, thereby generating a biological response. Several intracellular proteins have been identified as phosphorylation substrates for the insulin receptor, the best-studied of which is insulin receptor substrate 1 or IRS-1. When IRS-1 is activa Continue reading >>

Sulfonylurea Effects On Target Tissues For Insulin.

Sulfonylurea Effects On Target Tissues For Insulin.

Diabetes Care. 1984 May-Jun;7 Suppl 1:42-6. Sulfonylurea effects on target tissues for insulin. McCaleb ML , Maloff BL , Nowak SM , Lockwood DH . We have examined the nonpancreatic actions of sulfonylureas on multiple aspects of insulin responsiveness in two target tissues for insulin, liver and fat. In vivo administration of tolazamide and glipizide reduced significantly the postabsorptive serum glucose levels in rats without altering the levels of insulin. This was consistent with extrapancreatic sites of drug action. The number and affinity of hepatic insulin receptors was not different from those of control rats. Using a tissue culture system for rat adipose tissue, a 20-h treatment with sulfonylureas markedly potentiated insulin action in fat cells. The primary augmentation was at the level of insulin-stimulated glucose transport. Again, there was no alteration of the insulin receptors located on the adipose tissue. Furthermore, consistent with the lack of an influence on insulin-induced receptor loss after in vitro treatment with sulfonylureas, the in vivo administration of these agents did not alter the transglutaminase activity in rat hepatic tissue. The data demonstrate that sulfonylureas potentiate the responsiveness of the target tissues for insulin. Thus, these hypoglycemic agents probably act by correcting some of the cellular lesions associated with the insulin resistance in type II diabetes mellitus. Continue reading >>

The Blood Vessel Wall As An Insulin Target Tissue.

The Blood Vessel Wall As An Insulin Target Tissue.

The blood vessel wall as an insulin target tissue. Find all citations in this journal (default).Or filter your current search Diabete & Metabolisme [01 Jul 1987, 13(3 Pt 2):294-300] Type: Research Support, Non-U.S. Gov't, Review, Journal Article Study of the effects of insulin and insulin-like growth factors on blood vessel walls has been expedited by the ability to isolate and grow components of large and small blood vessels in pure culture. This paper summarizes current knowledge about the effects of insulin and related molecules on blood vessel derived cells, with an emphasis on: (1) peptide receptors, their regulation, and transport and processing of molecules through the endothelium; (2) metabolic and (3) mitogenic effects of insulin and related peptides on the blood vessel wall, with a discussion of major differences between large and small vessel endothelia; and (4) interactions of insulin with barrier endothelia, for example cerebral microvascular endothelium, site of the blood-brain barrier. Continue reading >>

Adiponectin Signaling And Function In Insulin Target Tissues.

Adiponectin Signaling And Function In Insulin Target Tissues.

Adiponectin signaling and function in insulin target tissues. Department of Pharmacology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA [email protected] [email protected] Department of Cell and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA [email protected] [email protected] J Mol Cell Biol. 2016 Apr;8(2):101-9. doi: 10.1093/jmcb/mjw014. Epub 2016 Mar 18. Obesity-linked type 2 diabetes is one of the paramount causes of morbidity and mortality worldwide, posing a major threat on human health, productivity, and quality of life. Despite great progress made towards a better understanding of the molecular basis of diabetes, the available clinical counter-measures against insulin resistance, a defect that is central to obesity-linked type 2 diabetes, remain inadequate. Adiponectin, an abundant adipocyte-secreted factor with a wide-range of biological activities, improves insulin sensitivity in major insulin target tissues, modulates inflammatory responses, and plays a crucial role in the regulation of energy metabolism. However, adiponectin as a promising therapeutic approach has not been thoroughly explored in the context of pharmacological intervention, and extensive efforts are being devoted to gain mechanistic understanding of adiponectin signaling and its regulation, and reveal therapeutic targets. Here, we discuss tissue- and cell-specific functions of adiponectin, with an emphasis on the regulation of adiponectin signaling pathways, and the potential crosstalk between the adiponectin and other signaling pathways involved in metabolic regulation. Understanding better just why and how adiponectin and its downstream effector m Continue reading >>

Bbc Bitesize - Gcse Biology (single Science) - Coordination And Control - The Human Endocrine System - Aqa - Revision 1

Bbc Bitesize - Gcse Biology (single Science) - Coordination And Control - The Human Endocrine System - Aqa - Revision 1

is a chemical substance, produced by a gland and carried in the bloodstream, which alters the activity of specific target organs . An example of this is the release of the hormone adrenaline, which is released by the adrenal gland. One of its target organs is the heart, where it increases the heart rate. Once a hormone has been used, it is destroyed by the liver. Hormones can control the body, and the effects are much slower than the nervous system, but they last for longer. Contraceptive pills contain hormones to reduce the chances of becoming pregnant There are important differences between nervous and hormonal control. in the brain is known as a 'master gland'. It secretes several hormones into the blood in response to the body's condition, such as blood water levels. These hormones can also act on other glands to stimulate the release of different types of hormones and bring about effects. The body produces a range of different chemical hormones that travel in the bloodstream and affect a number of different organs or cells in the body. The diagram below shows this in detail. Important hormones released into the bloodstream include ADH (anti-diuretic hormone), adrenaline and insulin. Continue reading >>

Tissue Specificity On Insulin Action And Resistance: Past To Recent Mechanisms.

Tissue Specificity On Insulin Action And Resistance: Past To Recent Mechanisms.

Tissue specificity on insulin action and resistance: past to recent mechanisms. Departamento de Bioqumica y Biologa Molecular II, Facultad de Farmacia, Universidad Complutense, Madrid, Spain. [email protected] Acta Physiol (Oxf). 2011 Mar;201(3):297-312. doi: 10.1111/j.1748-1716.2010.02201.x. Insulin resistance is the most important pathophysiological feature in many pre-diabetic states. Type 2 diabetes mellitus is a complex metabolic disease and its pathogenesis involves abnormalities in both peripheral insulin action and insulin secretion by pancreatic -cells. The creation of monogenic or polygenic genetically manipulated mice models in a tissue-specific manner was of great help to elucidate the tissue specificity of insulin action and its contribution to the overall insulin resistance. However, a complete understanding of the molecular bases of insulin action and resistance requires the identification of intracellular pathways that regulate insulin-stimulated proliferation, differentiation and metabolism. Accordingly, cell lines derived from insulin target tissues such as brown adipose tissue, liver and beta islets lacking insulin resistance or sensitive candidate genes such as IRS-1, IRS-2, IRS-3, IR and PTP1B have been developed. Indeed, these cell lines have also been very useful to understand the tissue specificity of insulin action and inaction. Obesity is a risk factor for several components of the metabolic syndromes such as type 2 diabetes, dyslipidaemia and systolic hypertension, because white and brown adipose tissues as endocrine organs express and secrete a variety of adipocytokines that can act at both local and systemic levels, modulating the insulin sensitivity. Recent studies revealed that the subjects with the highest transcription rates of genes e Continue reading >>

Developmental Programming: Differential Effects Of Prenatal Testosterone Excess On Insulin Target Tissues

Developmental Programming: Differential Effects Of Prenatal Testosterone Excess On Insulin Target Tissues

Polycystic ovarian syndrome (PCOS) is the leading cause of infertility in reproductive-aged women with the majority manifesting insulin resistance. To delineate the causes of insulin resistance in women with PCOS, we determined changes in the mRNA expression of insulin receptor (IR) isoforms and members of its signaling pathway in tissues of adult control (n = 7) and prenatal testosterone (T)-treated (n = 6) sheep (100 mg/kg twice a week from d 3090 of gestation), the reproductive/metabolic characteristics of which are similar to women with PCOS. Findings revealed that prenatal T excess reduced (P < 0.05) expression of IR-B isoform (only isoform detected), insulin receptor substrate-2 (IRS-2), protein kinase B (AKt), peroxisome proliferator-activated receptor- (PPAR), hormone-sensitive lipase (HSL), and mammalian target of rapamycin (mTOR) but increased expression of rapamycin-insensitive companion of mTOR (rictor), and eukaryotic initiation factor 4E (eIF4E) in the liver. Prenatal T excess increased (P < 0.05) the IR-A to IR-B isoform ratio and expression of IRS-1, glycogen synthase kinase-3 and - (GSK-3 and -), and rictor while reducing ERK1 in muscle. In the adipose tissue, prenatal T excess increased the expression of IRS-2, phosphatidylinositol 3-kinase (PI3K), PPAR, and mTOR mRNAs. These findings provide evidence that prenatal T excess modulates in a tissue-specific manner the expression levels of several genes involved in mediating insulin action. These changes are consistent with the hypothesis that prenatal T excess disrupts the insulin sensitivity of peripheral tissues, with liver and muscle being insulin resistant and adipose tissue insulin sensitive. Polycystic ovary syndrome (PCOS) is the most common cause of infertility in reproductive-aged women ( 1 , 2 Continue reading >>

Insulin Receptor Substrate 2 Plays Diverse Cell-specific Roles In The Regulation Of Glucose Transport*

Insulin Receptor Substrate 2 Plays Diverse Cell-specific Roles In The Regulation Of Glucose Transport*

The insulin receptor substrate 2 (IRS-2) protein is one of the major insulin-signaling substrates. In the present study, we investigated the role of IRS-2 in skin epidermal keratinocytes and dermal fibroblasts. Although skin is not a classical insulin target tissue, we have previously demonstrated that insulin, via the insulin receptor, is essential for normal skin cell physiology. To identify the role of IRS-2 in skin cells, we studied cells isolated from IRS-2 knock-out (KO) mice. Whereas proliferation and differentiation were not affected in the IRS-2 KO cells, a striking effect was observed on glucose transport. In IRS-2 KO keratinocytes, the lack of IRS-2 resulted in a dramatic increase in basal and insulin-stimulated glucose transport. The increase in glucose transport was associated with an increase in total phosphatidylinositol (PI) 3-kinase and Akt activation. In contrast, fibroblasts lacking IRS-2 exhibited a significant decrease in basal and insulin-induced glucose transport. We identified the point of divergence, leading to these differences between keratinocytes and fibroblasts, at the IRS-PI 3-kinase association step. In epidermal keratinocytes, PI 3-kinase is associated with and activated by only the IRS-1 protein. On the other hand, in dermal fibroblasts, PI 3-kinase is exclusively associated with and activated by the IRS-2 protein. These observations suggest that IRS-2 functions as a negative or positive regulator of glucose transport in a cell-specific manner. Our results also show that IRS-2 function depends on its cell-specific association with PI 3-kinase. The insulin-signaling pathway exists in many cells, and is mediated through the insulin receptor (IR). 1 However, the effects it has on various tissues are diverse. It is well known that liver, m Continue reading >>

Target Tissues Of Insulin? Watch

Target Tissues Of Insulin? Watch

Q: What are the major target tissues/organs of insulin? Summarize briefly the PROCESSES controlled by insulin action on: liver, skeletal muscle, adipose (fat) tissue I know that insulin targets the liver to store glucose as glycogen (so the process is glycogenesis), but Im stuck on the muscle/fat tissue. I know that GLUT4 remains in vesicles until insulin causes them to fuse with the plasma membrane and allow glucose into the cell, but what would the answer to the processes question be? Thanks in advance the process is a negative feedback loop, so when blood glucose levels increase insulin lowers blood glucose levels. i have no idea if this is the correct answer~~ The PROCESSES mentioned by OP are correct - other processes affected by insulin include:- 1. It slows down the process of gluconeogenesis [Greek neo = new; genesis = production] - gluconeogenesis is the production of new glucose from amino acids (mainly) - slowing of this process obviously tends to lower blood glucose. 2. Insulin slows down glycogenolysis [opposite of glycogenesis: Greek lyse = breakdown as in lysosome, which is the organelle where acid hydrolases break down internal [e.g. dead mitochondria] or external [e.g. phagocytosed bacteria] waste]. Less decomposition of glycogen into glucose, once again, reduces blood glucose. 3. Increases protein synthesis in ribosomes 4. Increases ketone uptake (this explains the classical diagnostic smell of hyperglycaemic coma patient due to increased levels of e.g. alphaketobutyrate) 5. (In adipose tissue): - a) Activates lipoprotein lipase 6. Increases K+ uptake in muscle and adipose tissue An additional fact to remember is that the opposite(s) of these actions are brought about by the hormones that are called insulin antagonists, namely adrenaline, corticostero Continue reading >>

Human Physiology/the Endocrine System

Human Physiology/the Endocrine System

The endocrine system is a control system of ductless glands that secrete hormones within specific organs. Hormones act as "messengers," and are carried by the bloodstream to different cells in the body, which interpret these messages and act on them. It seems like a far fetched idea that a small chemical can enter the bloodstream and cause an action at a distant location in the body. Yet this occurs in our bodies everyday of our lives. The ability to maintain homeostasis and respond to stimuli is largely due to hormones secreted within the body. Without hormones, you could not grow, maintain a constant temperature, produce offspring, or perform the basic actions and functions that are essential for life. The endocrine system provides an electrochemical connection from the hypothalamus of the brain to all the organs that control the body metabolism, growth and development, and reproduction. There are two types of hormones secreted in the endocrine system: Steroidal (or lipid based) and non-steroidal, (or protein based) hormones. The endocrine system regulates its hormones through negative feedback, except in very specific cases like childbirth. Increases in hormone activity decrease the production of that hormone. The immune system and other factors contribute as control factors also, altogether maintaining constant levels of hormones. Exocrine Glands are those which release their cellular secretions through a duct which empties to the outside or into the lumen (empty internal space) of an organ. These include certain sweat glands, salivary and pancreatic glands, and mammary glands. They are not considered a part of the endocrine system. Endocrine Glands are those glands which have no duct and release their secretions directly into the intercellular fluid or into the blo Continue reading >>

Effects Of Vanadium On Insulin Target Tissues

Effects Of Vanadium On Insulin Target Tissues

DESCRIPTION: (Principal Investigator's Abstract): Vanadium is increasingly a source of possible toxic effects through the use of fossil fuels and its incorporation into metal alloys. Vanadium in the form of vanadate has been shown to have a number of insulin-mimetic properties when given acutely in vitro. However, the effects of chronic administration on insulin sensitive tissues in vivo is much less well studied. Therefore, the overall purpose of this proposal is to examine the effects of vanadium on insulin-sensitive activities at its target cell sites. The specific objectives are: 1) to determine if vanadate or vanadyl is preferentially accumulated and retained in tissues with insulin-sensitive glucose transport systems; 2) to determine if vanadium alters insulin receptor numbers, binding, or function; 3) to determine if vanadium has effects on insulin-stimulated activities in target tissues; and 4) to determine if vanadium affects insulin metabolism. Rats will be given vanadium, as sodium orthvanadate or vanadyl sulfate, in a liquid diet and a number of insulin-sensitive activities of target tissues measured and compared to control animals. Specifically, various organs will be harvested and the vanadium content determined by neutron activation analysis. Hepatocytes and adipocytes will be isolated from animals and insulin binding analyzed by Scatchard plots. Receptor function will be assessed by assaying its tyrosine kinase activity. Isolated hepatocytes will be assayed for the insulin-sensitive activities of: amino acid transport, inhibition of protein degradation, and glucose incorporation in glycogen. Isolated adipocytes will be assayed for the insulin-sensitive activities of: glucose uptake, glucose incorporation into lipids, glucose oxidation, and anti-lipolysi Continue reading >>

Insulin Target Tissues And Cells

Insulin Target Tissues And Cells

Rodent adipose tissue and cells represent the targets exhibiting the most prominent insulin sensitivity (i.e., lowest EC/IC50) and responsiveness (i.e., highest fold stimulation/inhibition above basal) of the relevant insulin signaling cascades (e.g., insulin receptor activation) and metabolic end effector systems (e.g., lipolysis) in comparison to liver (e.g., gluconeogenesis) and muscle cells (e.g., glucose transport). This might be based in part on technical advantages of the adipose tissue/adipocyte preparation in comparison to that of muscle/myocytes. But more likely, it reflects the exquisite physiological role of the adipose tissue in the regulation and coordination of glucose and lipid metabolism, i.e., insulin stimulation of lipid synthesis (lipogenesis) and insulin inhibition of lipolysis. On the basis of their relatively easy technical preparation, functional adipose tissue fragments (epididymal fat pads) and primary adipocytes (isolated epididymal adipocytes) from rats as well as adipocyte cell lines derived from mice (3T3-L1, F442A) are the first choice for the development of robust and reliable cell-/tissue-based assay systems for insulin-like activity. Do you want to read the rest of this chapter? Continue reading >>

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