scholarly journals The Central Effects of Thyroid Hormones on Appetite

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Anjali Amin ◽  
Waljit S. Dhillo ◽  
Kevin G. Murphy
Keyword(s):  
Thyroid Hormone ◽  
Food Intake ◽  
Public Health Issue ◽  
Major Public Health Issue ◽  
The Central Nervous System ◽  
Regulate Food Intake ◽  
Clinically Significant ◽  
Hpt Axis ◽  
New Treatments

Obesity is a major public health issue worldwide. Current pharmacological treatments are largely unsuccessful. Determining the complex pathways that regulate food intake may aid the development of new treatments. The hypothalamic-pituitary-thyroid (HPT) axis has well-known effects on energy expenditure, but its role in the regulation of food intake is less well characterised. Evidence suggests that the HPT axis can directly influence food intake. Thyroid dysfunction can have clinically significant consequences on appetite and body weight. Classically, these effects were thought to be mediated by the peripheral effects of thyroid hormone. However, more recently, local regulation of thyroid hormone in the central nervous system (CNS) is thought to play an important role in physiologically regulating appetite. This paper focuses on the role of the HPT and thyroid hormone in appetite and provides evidence for potential new targets for anti-obesity agents.

scholarly journals Neuropeptide Y1 and Y5 Receptors Mediate the Effects of Neuropeptide Y on the Hypothalamic-Pituitary-Thyroid Axis

Endocrinology ◽  
2002 ◽  
Vol 143 (12) ◽  
pp. 4513-4519 ◽  
Author(s):  
Csaba Fekete ◽  
Sumit Sarkar ◽  
William M. Rand ◽  
John W. Harney ◽  
Charles H. Emerson ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Paraventricular Nucleus ◽  
Receptor Agonist ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Ad Libitum ◽  
Thyroid Hormone Levels ◽  
Hpt Axis

Abstract Neuropeptide Y (NPY) is one of the most important hypothalamic-derived neuropeptides mediating the effects of leptin on energy homeostasis. Central administration of NPY not only markedly stimulates food intake, but simultaneously inhibits the hypothalamic-pituitary-thyroid axis (HPT axis), replicating the central hypothyroid state associated with fasting. To identify the specific NPY receptor subtypes involved in the action of NPY on the HPT axis, we studied the effects of the highly selective Y1 ([Phe7,Pro34]pNPY) and Y5 ([chicken pancreatic polypeptide1–7, NPY19–23, Ala31, Aib32 (aminoisobutyric acid), Q34]human pancreatic polypeptide) receptor agonists on circulating thyroid hormone levels and proTRH mRNA in hypophysiotropic neurons of the hypothalamic paraventricular nucleus. The peptides were administered continuously by osmotic minipump into the cerebrospinal fluid (CSF) over 3 d in ad libitum-fed animals and animals pair-fed to artificial CSF (aCSF)-infused controls. Both Y1 and Y5 receptor agonists nearly doubled food intake compared with that of control animals receiving aCSF, similar to the effect observed for NPY. NPY, Y1, and Y5 receptor agonist administration suppressed circulating levels of thyroid hormones (T3 and T4) and resulted in inappropriately normal or low TSH levels. These alterations were also associated with significant suppression of proTRH mRNA in the paraventricular nucleus, particularly in the Y1 receptor agonist-infused group [aCSF, NPY, Y1, and Y5 (density units ± sem), 97.2 ± 8.6, 39.6 ± 8.4, 19.9 ± 1.9, and 44.6 ± 8.4]. No significant differences in thyroid hormone levels, TSH, or proTRH mRNA were observed between the agonist-infused FSanimals eating ad libitum and the agonist-infused animals pair-fed with vehicle-treated controls. These data confirm the importance of both Y1 and Y5 receptors in the NPY-mediated increase in food consumption and demonstrate that both Y1 and Y5 receptors can mediate the inhibitory effects of NPY on the HPT axis.

Suppression of food intake by intravenous nutrients and insulin in the baboon

1984 ◽  
Vol 247 (2) ◽  
pp. R393-R401 ◽  
Author(s):  
S. C. Woods ◽  
L. J. Stein ◽  
L. D. McKay ◽  
D. Porte
Keyword(s):  
Food Intake ◽  
Caloric Intake ◽  
Glucose Infusion ◽  
Base Line ◽  
Papio Cynocephalus ◽  
Insulin Levels ◽  
Daily Caloric Intake ◽  
Total Base ◽  
Regulate Food Intake

Intravenous nutrients were infused at 25 and 50% of total base-line daily caloric intake to determine the role of circulating factors on spontaneous food ingestion in young adult male baboons (Papio cynocephalus). Glucose infusion suppressed food intake (15.1%) when 25% of total calories was infused (P less than 0.05) and 41.8% when 50% of total calories was infused (P less than 0.05) for 14-21 days. Both infusions produced basal hyperglycemia (82-172 mg/dl during 25% glucose and 120-239 mg/dl during 50% glucose). Both infusions also caused an increase in circulating insulin (48.1-63.1 microU/ml during 25% glucose and 68.5-77.2 microU/ml during 50% glucose). The simultaneous infusion of exogenous insulin (0.33 mU X kg-1 X min-1) prevented hyperglycemia (85.8-87.9 mg/dl during 25% glucose) but maintained raised basal peripheral insulin levels (52.4-84.4 microU/ml). The 13% suppression of food intake (P less than 0.05) was similar to glucose infusion alone. Comparable infusions of Intralipid as 25 and 50% of total daily calories also suppressed spontaneous food intake but did not produce hyperglycemia or elevated insulin levels. The magnitude of suppression was similar to that of glucose: 16% when 25% of basal calories was infused (P less than 0.05) and 31.3% when 50% of basal calories was infused (P less than 0.05). However, the pattern was different with a more rapid effect, which tended to diminish in time, rather than the slow effect found with glucose, which was maintained for 14 days. We conclude that circulating nutrients can regulate food intake independent of gastrointestinal absorption in primates.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevention and Mitigation of Intimate-Partner Violence: The Role of Community Leaders in Tanzania

2019 ◽  
Vol 26 (3-4) ◽  
pp. 359-378
Author(s):  
Elizabeth Simmons ◽  
Nafisa Halim ◽  
Maria Servidone ◽  
Ester Steven ◽  
Naomi Reich ◽  
...  
Keyword(s):  
Intimate Partner Violence ◽  
Partner Violence ◽  
Intimate Partner ◽  
Community Level ◽  
Community Leaders ◽  
Public Health Issue ◽  
Valuable Insight ◽  
Major Public Health Issue ◽  
Key Informant

Intimate-partner violence (IPV) is a major public health issue that disproportionately affects women, especially in Tanzania where 40% of women report experiencing IPV. While IPV research has focused on IPV victims and perpetrators, community leaders can provide valuable insight on IPV at the community level. We conducted 50 key informant interviews with community leaders in nine villages in the Karatu district. These leaders identified common themes regarding IPV causes and consequences, reporting methods, and future recommendations. This information can help mitigate IPV at the community level in future interventions and shows community leaders themselves could be powerful tools in future IPV programming.

scholarly journals Glucocorticoids attenuate the central sympathoexcitatory actions of insulin

2014 ◽  
Vol 112 (10) ◽  
pp. 2597-2604 ◽  
Author(s):  
Jennifer L. Steiner ◽  
Megan E. Bardgett ◽  
Lawrence Wolfgang ◽  
Charles H. Lang ◽  
Sean D. Stocker
Keyword(s):  
Food Intake ◽  
Mammalian Target Of Rapamycin ◽  
Chronic Administration ◽  
Sprague Dawley ◽  
Sympathetic Function ◽  
Sprague Dawley Rats ◽  
Access To Water ◽  
The Central Nervous System ◽  
Regulate Food Intake ◽  
Few Data

Insulin acts within the central nervous system to regulate food intake and sympathetic nerve activity (SNA). Strong evidence indicates that glucocorticoids impair insulin-mediated glucose uptake and food intake. However, few data are available regarding whether glucocorticoids also modulate the sympathoexcitatory response to insulin. Therefore, the present study first confirmed that chronic administration of glucocorticoids attenuated insulin-induced increases in SNA and then investigated whether these effects were attributed to deficits in central insulin-mediated responses. Male Sprague-Dawley rats were given access to water or a drinking solution of the glucocorticoid agonist dexamethasone (0.3 μg/ml) for 7 days. A hyperinsulinemic-euglycemic clamp significantly increased lumbar SNA in control rats. This response was significantly attenuated in rats given access to dexamethasone for 7, but not 1, days. Similarly, injection of insulin into the lateral ventricle or locally within the arcuate nucleus (ARC) significantly increased lumbar SNA in control rats but this response was absent in rats given access to dexamethasone. The lack of a sympathetic response to insulin cannot be attributed to a generalized depression of sympathetic function or inactivation of ARC neurons as electrical activation of sciatic afferents or ARC injection of gabazine, respectively, produced similar increases in SNA between control and dexamethasone-treated rats. Western blot analysis indicates insulin produced similar activation of Akt Ser473 and rpS6 Ser240/244 in the ventral hypothalamus of control and dexamethasone-treated rats. Collectively, these findings suggest that dexamethasone attenuates the sympathoexcitatory actions of insulin through a disruption of ARC neuronal function downstream of Akt or mammalian target of rapamycin (mTOR) signaling.

scholarly journals Analysis of Hypothalamic TRH Neurons in Regulating Thyroid Hormone Levels

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A849-A849
Author(s):  
Ricardo H Costa e Sousa ◽  
Rodrigo Rorato ◽  
Anthony Neil Hollenberg ◽  
Kristen R Vella
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormone Receptor ◽  
Designer Drugs ◽  
Mrna Levels ◽  
Hormone Levels ◽  
Males And Females ◽  
Thyroid Hormone Levels ◽  
Hpt Axis ◽  
Tsh Levels

Abstract Thyroid hormone (TH) is a major regulator of development and metabolism. An important mechanism controlling TH production is the negative feedback at the hypothalamic and pituitary level and it has been suggested that thyroid hormone receptor β (TRβ) is the main mediator of TH actions in the hypothalamic paraventricular nucleus (PVN). Nevertheless, the direct actions of TH and TRβ in the negative regulation of TRH have yet to be demonstrated in vivo. Here we used two approaches to investigate the TRH neuron. First, we used a chemogenetic tool to directly investigate the role of TRH neurons on the regulation of thyroid hormone levels. Mice expressing Cre-recombinase in TRH neurons received bilateral injections of the activating designer receptors exclusively activated by designer drugs (DREADD) directly into the PVN. Activation of TRH neurons produced a rapid and sustained increase in circulating TSH levels in both males and females. TSH levels increased approximately 10-fold from baseline within 15 minutes of injection of CNO, returning to baseline within 2.5 hours. TH levels were increased approximately 2-fold in males and females. Therefore, using a chemogenetic approach, we were able to directly evaluated the role of PVN TRH neurons on the control of thyroid activity, for the first time. Next, we generated mice deficient in TRβ specifically in neurons expressing melanocortin 4 receptor (MC4R), which overlaps with TRH expression in the PVN. Knockout mice (KO) developed normally and showed no change in TH and TSH levels. TRH mRNA levels in the PVN of KO mice were similar to control mice. To investigate if the deletion of TRβ in the PVN changes the sensitivity of the HPT axis to T3, mice were rendered hypothyroid and given increasing doses of T3 for 2 weeks. Results show no difference in TRH mRNA or serum TSH between controls and KO. Surprisingly, despite the presence of detectable genomic recombination on the TRβ gene in the PVN, there was no difference in TRβ mRNA expression between control and KO mice, suggesting that either MC4R-positive neurons do not express TRβ or they represent a very small population of TRβ-positive cells in the PVN. Present data show that TRH neuron activation rapidly stimulates TSH release and increases TH levels, demonstrating a major role of these neurons in the regulation of the hypothalamic-pituitary-thyroid (HPT) axis. Nevertheless, deletion of TRβ from MC4R neurons had no major effect on either TRH or TH levels in in mice. Additionally, TRβ in MC4R-positive TRH neurons in the PVN is not necessary for TH-induced suppression of TRH mRNA. Although further studies are necessary, these data suggest that there are distinct populations of hypophysiotropic TRH neurons in the PVN, some of which are not regulated by thyroid hormone and TRβ.

Depression, Anxiety and Stress Among Arsenic-Induced Cancer Patients in Indo-Gangetic Plains of Bihar: Role of Proactive Coping

2021 ◽  
pp. 0272684X2110334
Author(s):  
Shishu Kesh Kumar ◽  
Das Ambika Bharti
Keyword(s):  
Cancer Patients ◽  
Proactive Coping ◽  
Anxiety And Depression ◽  
Public Health Issue ◽  
Depression And Anxiety ◽  
Research Attention ◽  
Major Public Health Issue ◽  
Gangetic Plains ◽  
The Relationship

Arsenic induced cancer is a major public health issue in Indo-Gangetic plains of Bihar, India where 22 out of 38 districts report arsenic contamination of groundwater. Its psychological aspect is under studied in contrast to the physiological and social. This baseline correlational survey research explores the relationship and role of proactive coping on depression, anxiety and stress among this population. Depression, anxiety and stress were assessed in 77 consenting arsenic induced cancer patients with depression, anxiety and stress scales. Proactive Coping was assessed with proactive coping inventory. Results demonstrated negative association and influence of proactive coping on stress, anxiety and depression. Avoidance coping associated positively with depression and reflective coping predicted for depression and anxiety. The findings advocate for more research attention on psychological aspects of arsenic induced cancer. Timely psychological interventions to build proactive coping are warranted to alleviate depression, anxiety and stress among this population.

scholarly journals Central Neurocircuits Regulating Food Intake in Response to Gut Inputs—Preclinical Evidence

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 908
Author(s):  
Kirsteen N. Browning ◽  
Kaitlin E. Carson
Keyword(s):  
Food Intake ◽  
Vagus Nerve ◽  
Sensory Information ◽  
Specific Reference ◽  
Motor Nucleus ◽  
Dorsal Motor Nucleus ◽  
The Central Nervous System ◽  
Complex Integration ◽  
The Many

The regulation of energy balance requires the complex integration of homeostatic and hedonic pathways, but sensory inputs from the gastrointestinal (GI) tract are increasingly recognized as playing critical roles. The stomach and small intestine relay sensory information to the central nervous system (CNS) via the sensory afferent vagus nerve. This vast volume of complex sensory information is received by neurons of the nucleus of the tractus solitarius (NTS) and is integrated with responses to circulating factors as well as descending inputs from the brainstem, midbrain, and forebrain nuclei involved in autonomic regulation. The integrated signal is relayed to the adjacent dorsal motor nucleus of the vagus (DMV), which supplies the motor output response via the efferent vagus nerve to regulate and modulate gastric motility, tone, secretion, and emptying, as well as intestinal motility and transit; the precise coordination of these responses is essential for the control of meal size, meal termination, and nutrient absorption. The interconnectivity of the NTS implies that many other CNS areas are capable of modulating vagal efferent output, emphasized by the many CNS disorders associated with dysregulated GI functions including feeding. This review will summarize the role of major CNS centers to gut-related inputs in the regulation of gastric function with specific reference to the regulation of food intake.

scholarly journals Differential effects of fasting vs food restriction on liver thyroid hormone metabolism in male rats

2014 ◽  
Vol 224 (1) ◽  
pp. 25-35 ◽  
Author(s):  
E M de Vries ◽  
H C van Beeren ◽  
M T Ackermans ◽  
A Kalsbeek ◽  
E Fliers ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Food Intake ◽  
Caloric Restriction ◽  
Food Restriction ◽  
Male Rats ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism ◽  
Limited Food ◽  
Fasted Rats

A variety of illnesses that leads to profound changes in the hypothalamus–pituitary–thyroid (HPT) are axis collectively known as the nonthyroidal illness syndrome (NTIS). NTIS is characterized by decreased tri-iodothyronine (T3) and thyroxine (T4) and inappropriately low TSH serum concentrations, as well as altered hepatic thyroid hormone (TH) metabolism. Spontaneous caloric restriction often occurs during illness and may contribute to NTIS, but it is currently unknown to what extent. The role of diminished food intake is often studied using experimental fasting models, but partial food restriction might be a more physiologically relevant model. In this comparative study, we characterized hepatic TH metabolism in two models for caloric restriction: 36 h of complete fasting and 21 days of 50% food restriction. Both fasting and food restriction decreased serum T4concentration, while after 36-h fasting serum T3also decreased. Fasting decreased hepatic T3but not T4concentrations, while food restriction decreased both hepatic T3and T4concentrations. Fasting and food restriction both induced an upregulation of liver D3 expression and activity, D1 was not affected. A differential effect was seen inMct10mRNA expression, which was upregulated in the fasted rats but not in food-restricted rats. Other metabolic pathways of TH, such as sulfation and UDP-glucuronidation, were also differentially affected. The changes in hepatic TH concentrations were reflected by the expression of T3-responsive genesFasandSpot14only in the 36-h fasted rats. In conclusion, limited food intake induced marked changes in hepatic TH metabolism, which are likely to contribute to the changes observed during NTIS.

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