Subdiaphragmatic vagotomy fails to inhibit intravenous leptin-induced IL-1β expression in the hypothalamus

2002 ◽  
Vol 282 (2) ◽  
pp. R627-R631 ◽  
Author(s):  
Toru Hosoi ◽  
Yasunobu Okuma ◽  
Atsushi Ono ◽  
Yasuyuki Nomura
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Vagus Nerve ◽  
Rt Pcr ◽  
Subdiaphragmatic Vagotomy ◽  
Infection And Inflammation ◽  
The Brain ◽  
Afferent Vagus

Leptin is known to be an important circulating signal for regulation of food intake and body weight. Recent evidence has suggested that leptin is involved in infection and inflammation. The afferent vagus nerve is known to be an important component for transmitting peripheral immune signals to the brain, such as interleukin (IL)-1β expression in the brain, anorexia, and fever responses. In the present study, we investigated whether intravenous leptin-induced IL-1β expression in the hypothalamus is mediated via afferent vagus nerve. IL-1β transcripts in the hypothalamus were significantly increased on RT-PCR assessment 1 h after the administration of leptin (1 mg/kg iv) to mice. Subdiaphragmatic vagotomy did not significantly modify intravenous leptin-induced IL-1β expression in the hypothalamus compared with that in sham-treated mice. These data suggest that circulating leptin directly acts in the brain independently of afferent vagus nerve input originating from the subdiaphragmatic organs.

Electrical stimulation of afferent vagus nerve induces IL-1β expression in the brain and activates HPA axis

2000 ◽  
Vol 279 (1) ◽  
pp. R141-R147 ◽  
Author(s):  
Toru Hosoi ◽  
Yasunobu Okuma ◽  
Yasuyuki Nomura
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Hpa Axis ◽  
Vagus Nerves ◽  
Rt Pcr ◽  
Protein Levels ◽  
Infection And Inflammation ◽  
The Brain ◽  
Stimulation Of ◽  
Afferent Vagus

Possible roles of the afferent vagus nerve in regulation of interleukin (IL)-1β expression in the brain and hypothalamic-pituitary-adrenal (HPA) axis were examined in anesthetized rats. Levels of IL-1β mRNA and protein in the brain were measured by comparative RT-PCR and ELISA. Direct electrical stimulation of the central end of the vagus nerve was performed continuously for 2 h. The afferent stimulation of the vagus nerve induced increases in the expression of mRNA and protein levels of IL-1β in the hypothalamus and the hippocampus. Furthermore, expression of corticotropin-releasing factor mRNA was increased in the hypothalamus 2 h after vagal stimulation. Plasma levels of ACTH and corticosterone were also increased by this stimulation. The present results indicate that activation of the afferent vagus nerves itself can induce production of IL-1β in the brain and activate the HPA axis. Therefore, the afferent vagus nerve may play an important role in transmitting peripheral signals to the brain in the infection and inflammation.

Role of the hepatic branch of the vagus nerve in liver regeneration in rats

1987 ◽  
Vol 253 (4) ◽  
pp. G439-G444 ◽  
Author(s):  
K. Tanaka ◽  
S. Ohkawa ◽  
T. Nishino ◽  
A. Niijima ◽  
S. Inoue
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Vagus Nerve ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Specific Effect ◽  
The Body ◽  
Subdiaphragmatic Vagotomy ◽  
Hepatic Branch

The role of the vagus nerve in liver regeneration after partial hepatectomy was examined by comparing the effects of hepatic vagotomy (sectioning of the hepatic branch of the vagus nerve) with those of subdiaphragmatic vagotomy in rats. Hepatic vagotomy delayed but did not suppress the increase in the rate of hepatic DNA synthesis and the activity of thymidine kinase after partial hepatectomy. On the other hand, subdiaphragmatic vagotomy delayed and suppressed these indices. The time courses of restoration of liver DNA content after partial hepatectomy were not affected by hepatic vagotomy. However, this index was both delayed and suppressed in subdiaphragmatic vagotomized rats. Hepatic vagotomy did not affect the daily food intake or the body weight increase after partial hepatectomy. However, subdiaphragmatic vagotomy caused considerably more loss of food intake and body weight. There were no differences in the plasma insulin levels after partial hepatectomy among three groups. We concluded that a vagal specific effect is evident in the delay but fails to suppress liver regeneration.

scholarly journals The Vagus Nerve Mediates the Physiological but not Pharmacological Effects of PYY3-36 on Food Intake

2020 ◽  
Author(s):  
A Martin Alonso ◽  
SC Cork ◽  
Y Ma ◽  
M Arnold ◽  
H Herzog ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Vagus Nerve ◽  
Peptide Yy ◽  
Therapeutic Potential ◽  
Pharmacological Effects ◽  
Gut Hormone ◽  
Reducing Activity ◽  
Higher Doses ◽  
Afferent Vagus

AbstractPeptide YY (PYY3-36) is a post-prandially released gut hormone with potent appetite-reducing activity mediated by the neuropeptide Y (NPY) Y2 receptor (Y2R). However, the neuronal pathways by which PYY3-36 acts to supress appetite are unclear. Determining how the PYY3-36 system physiologically regulates food intake may help exploit its therapeutic potential. Here we demonstrate that germline and post-natal targeted knockdown of the Y2R in the afferent vagus nerve inhibits the anorectic effects of physiologically-released PYY3-36, but not peripherally-administered higher doses. Post-natal knockdown of the Y2R results in a transient body weight phenotype that is compensated for in the germline model. Loss of vagal Y2R signalling also alters meal patterning and accelerates gastric emptying. These results may facilitate the design of PYY-based anti-obesity agents.Abstract Figure

scholarly journals The Gut Microbiome Derived From Anorexia Nervosa Patients Impairs Weight Gain and Behavioral Performance in Female Mice

Endocrinology ◽  
2019 ◽  
Vol 160 (10) ◽  
pp. 2441-2452 ◽  
Author(s):  
Tomokazu Hata ◽  
Noriyuki Miyata ◽  
Shu Takakura ◽  
Kazufumi Yoshihara ◽  
Yasunari Asano ◽  
...  
Keyword(s):  
Body Weight ◽  
Anorexia Nervosa ◽  
Weight Gain ◽  
Food Intake ◽  
Brain Stem ◽  
Body Weight Gain ◽  
Field Tests ◽  
Compulsive Behavior ◽  
The Brain ◽  
Poor Weight Gain

Abstract Anorexia nervosa (AN) results in gut dysbiosis, but whether the dysbiosis contributes to AN-specific pathologies such as poor weight gain and neuropsychiatric abnormalities remains unclear. To address this, germ-free mice were reconstituted with the microbiota of four patients with restricting-type AN (gAN mice) and four healthy control individuals (gHC mice). The effects of gut microbes on weight gain and behavioral characteristics were examined. Fecal microbial profiles in recipient gnotobiotic mice were clustered with those of the human donors. Compared with gHC mice, gAN mice showed a decrease in body weight gain, concomitant with reduced food intake. Food efficiency ratio (body weight gain/food intake) was also significantly lower in gAN mice than in gHC mice, suggesting that decreased appetite as well as the capacity to convert ingested food to unit of body substance may contribute to poor weight gain. Both anxiety-related behavior measured by open-field tests and compulsive behavior measured by a marble-burying test were increased only in gAN mice but not in gHC mice. Serotonin levels in the brain stem of gAN mice were lower than those in the brain stem of gHC mice. Moreover, the genus Bacteroides showed the highest correlation with the number of buried marbles among all genera identified. Administration of Bacteroides vulgatus reversed compulsive behavior but failed to exert any substantial effect on body weight. Collectively, these results indicate that AN-specific dysbiosis may contribute to both poor weight gain and mental disorders in patients with AN.

Feeling Sick

2020 ◽  
pp. 63-78
Author(s):  
Pamela K. Keel
Keyword(s):  
Eating Disorders ◽  
Body Weight ◽  
Eating Disorder ◽  
Food Intake ◽  
Genetic Factors ◽  
Twin Studies ◽  
Nausea And Vomiting ◽  
Purging Disorder ◽  
Biological Responses ◽  
The Brain

Eating is fundamental to our survival and subject to numerous biological regulators that influence when, what, and how much we eat. This makes biological factors central to any answer for why someone develops purging disorder. Genetic factors impact body weight and temperament and may even influence a person’s susceptibility to nausea and vomiting. Yet data from family and twin studies suggest that genes may play a slightly smaller role in risk for purging disorder compared to other eating disorders. Instead, biological responses to food intake may explain the unique configuration of purging after consuming normal amounts of food in purging disorder. Compared to those with bulimia, individuals with purging disorder have greater release of hormones that trigger the brain to stop eating. Compared to those with bulimia and those without an eating disorder, individuals with purging disorder release excessive amounts of a hormone that triggers feelings of nausea and stomachache.

scholarly journals Therapeutic Effects of Licorice and Dried Ginger Decoction on Activity-Based Anorexia in BALB/c AnNCrl Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Do-Hyun Kim ◽  
Joong Sun Kim ◽  
Jeongsang Kim ◽  
Jong-Kil Jeong ◽  
Hong-Seok Son ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
Body Weight Loss ◽  
Drop Out ◽  
Therapeutic Effects ◽  
Excessive Sweating ◽  
Dopamine Concentration ◽  
Wheel Activity ◽  
The Brain

Licorice and dried ginger decoction (Gancao-ganjiang-tang, LGD) is used for nausea and anorexia, accompanied by excessive sweating in Traditional Chinese Medicine. Herein, we investigated the therapeutic effects of LGD using the activity-based anorexia (ABA) in a mouse model. Six-week-old female BALB/c AnNCrl mice were orally administered LGD, water, licorice decoction, dried ginger decoction, or chronic olanzapine, and their survival, body weight, food intake, and wheel activity were compared in ABA. Additionally, dopamine concentration in brain tissues was evaluated. LGD significantly reduced the number of ABA mice reaching the drop-out criterion of fatal body weight loss. However, LGD showed no significant effects on food intake and wheel activity. We found that in the LGD group the rise of the light phase activity rate inhibited body weight loss. Licorice or dried ginger alone did not improve survival rates, they only showed longer survival periods than chronic olanzapine when combined. In addition, LGD increased the dopamine concentration in the brain. The results from the present study showed that LGD improves the survival of ABA mice and its mechanism of action might be related to the alteration of dopamine concentration in the brain.

Capsaicin-sensitive fibers are required for the anorexic action of systemic but not central bombesin

1999 ◽  
Vol 276 (6) ◽  
pp. R1617-R1622 ◽  
Author(s):  
David Michaud ◽  
Hymie Anisman ◽  
Zul Merali
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Neural Circuits ◽  
Body Weight Gain ◽  
Systemic Effects ◽  
Neuronal System ◽  
Afferent Neurons ◽  
The Brain

Bombesin (BN) suppresses food intake in rats whether given centrally or systemically. Although the brain BN-sensitive receptors are known to be essential for the anorexic effect of systemic BN, the mode of communication between the gut and the brain remains unclear. This study assessed whether the anorexic effect of systemic BN is mediated humorally or via neural circuits. Afferent neurons were lesioned using capsaicin (50 mg/kg sc) on postnatal day 2, and responses to BN were assessed during adulthood. Capsaicin treatment decreased body weight gain significantly from postnatal age 4–7 wk. Peripheral BN (4–16 μg/kg ip) dose dependently suppressed food intake in control animals. However, this effect was completely blocked in capsaicin-treated rats. In contrast to systemic effects, feeding-suppressant effects of centrally administered BN (0.01–0.5 μg icv) were not affected by capsaicin treatment. This research suggests that peripheral BN communicates with the brain via a neuronal system(s) whose afferent arm is constituted of capsaicin-sensitive C and/or Aδ-fibers, whereas the efferent arm of this satiety- and/or anorexia-mediating circuitry is capsaicin resistant.

scholarly journals Pancreatic signals controlling food intake; insulin, glucagon and amylin

2006 ◽  
Vol 361 (1471) ◽  
pp. 1219-1235 ◽  
Author(s):  
Stephen C Woods ◽  
Thomas A Lutz ◽  
Nori Geary ◽  
Wolfgang Langhans
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Homeostasis ◽  
Endocrine Pancreas ◽  
Situational Factors ◽  
Meal Size ◽  
Vagus Nerves ◽  
Social Emotional ◽  
Short Term ◽  
The Brain

The control of food intake and body weight by the brain relies upon the detection and integration of signals reflecting energy stores and fluxes, and their interaction with many different inputs related to food palatability and gastrointestinal handling as well as social, emotional, circadian, habitual and other situational factors. This review focuses upon the role of hormones secreted by the endocrine pancreas: hormones, which individually and collectively influence food intake, with an emphasis upon insulin, glucagon and amylin. Insulin and amylin are co-secreted by B-cells and provide a signal that reflects both circulating energy in the form of glucose and stored energy in the form of visceral adipose tissue. Insulin acts directly at the liver to suppress the synthesis and secretion of glucose, and some plasma insulin is transported into the brain and especially the mediobasal hypothalamus where it elicits a net catabolic response, particularly reduced food intake and loss of body weight. Amylin reduces meal size by stimulating neurons in the hindbrain, and there is evidence that amylin additionally functions as an adiposity signal controlling body weight as well as meal size. Glucagon is secreted from A-cells and increases glucose secretion from the liver. Glucagon acts in the liver to reduce meal size, the signal being relayed to the brain via the vagus nerves. To summarize, hormones of the endocrine pancreas are collectively at the crossroads of many aspects of energy homeostasis. Glucagon and amylin act in the short term to reduce meal size, and insulin sensitizes the brain to short-term meal-generated satiety signals; and insulin and perhaps amylin as well act over longer intervals to modulate the amount of fat maintained and defended by the brain. Hormones of the endocrine pancreas interact with receptors at many points along the gut–brain axis, from the liver to the sensory vagus nerve to the hindbrain to the hypothalamus; and their signals are conveyed both neurally and humorally. Finally, their actions include gastrointestinal and metabolic as well as behavioural effects.

scholarly journals Chronic immunoneutralization of brain angiotensin-(1-12) lowers blood pressure in transgenic (mRen2)27 hypertensive rats

2009 ◽  
Vol 297 (1) ◽  
pp. R111-R115 ◽  
Author(s):  
Katsunori Isa ◽  
Maria Antonia García-Espinosa ◽  
Amy C. Arnold ◽  
Nancy T. Pirro ◽  
Ellen N. Tommasi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Food Intake ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Rat Tissues ◽  
Pressure Regulation ◽  
Hypertensive Rats ◽  
Male Adult ◽  
The Brain

Angiotensin-(1-12) [ANG-(1-12)] is a newly identified peptide detected in a variety of rat tissues, including the brain. To determine whether brain ANG-(1-12) participates in blood pressure regulation, we treated male adult (mRen2)27 hypertensive rats (24–28 wk of age) with Anti-ANG-(1-12) IgG or Preimmune IgG via an intracerebroventricular cannula for 14 days. Immunoneutralization of brain ANG-(1-12) lowered systolic blood pressure (−43 ± 8 mmHg on day 3 and −26 ± 7 mmHg on day 10 from baseline, P < 0.05). Water intake was lower on intracereroventricular day 6 in the Anti-ANG-(1-12) IgG group, accompanied by higher plasma osmolality on day 13, but there were no differences in urine volume, food intake, or body weight during the 2-wk treatment. In Preimmune IgG-treated animals, there were no significant changes in these variables over the 2-wk period. The antihypertensive effects produced by endogenous neutralization of brain ANG-(1-12) suggest that ANG-(1-12) is functionally active in brain pathways regulating blood pressure.

scholarly journals Prolactin-releasing peptide: a new tool for obesity treatment

2016 ◽  
Vol 230 (2) ◽  
pp. R51-R58 ◽  
Author(s):  
Jaroslav Kuneš ◽  
Veronika Pražienková ◽  
Andrea Popelová ◽  
Barbora Mikulášková ◽  
Jana Zemenová ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Binding Affinity ◽  
Subcutaneous Administration ◽  
Obesity Treatment ◽  
Noninvasive Therapy ◽  
Food Intake Regulation ◽  
Intake Regulation ◽  
Prolactin Releasing Peptide ◽  
The Brain

Obesity is an escalating epidemic, but an effective noninvasive therapy is still scarce. For obesity treatment, anorexigenic neuropeptides are promising tools, but their delivery from the periphery to the brain is complicated because peptides have a low stability and limited ability to cross the blood–brain barrier. In this review, we summarize results of several studies with our newly designed lipidized analogs of prolactin-releasing peptide (PrRP). PrRP is involved in feeding and energy balance regulation as demonstrated by obesity phenotypes of both PrRP- and PrRP-receptor-knockout mice. Lipidized PrRP analogs showed binding affinity and signaling in PrRP receptor-expressing cells similar to natural PrRP. Moreover, these analogs showed high binding affinity also to anorexigenic neuropeptide FF (NPFF)-2 receptor. Acute peripheral administration of myristoylated and palmitoylated PrRP analogs to mice and rats induced strong and long-lasting anorexigenic effects and neuronal activation in the brain areas involved in food intake regulation. Two-week-long subcutaneous administration of palmitoylated PrRP31 and myristoylated PrRP20 lowered food intake, body weight, improved metabolic parameters and attenuated lipogenesis in mice with diet-induced obesity. A strong anorexigenic, body weight-reducing and glucose tolerance-improving effect of palmitoylated-PrRP31 was shown also in diet-induced obese rats after its repeated 2-week-long peripheral administration. Thus, the strong anorexigenic and body weight-reducing effects of palmitoylated PrRP31 and myristoylated PrRP20 make these analogs attractive candidates for antiobesity treatment. Moreover, PrRP receptor might be a new target for obesity therapy.

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