Brain Hormone That Helps Regulate Food Intake May Dampen Drug Craving: Finding Exploits Possible Relationship Between Addiction and Eating Disorders

2001 ◽  
Author(s):  
Keyword(s):  
Eating Disorders ◽  
Food Intake ◽  
Drug Craving ◽  
Regulate Food Intake

Anorexia Nervosa and Depression in a Woman Blind since the Age of Nine Months

1993 ◽  
Vol 38 (7) ◽  
pp. 469-471 ◽  
Author(s):  
Clifford W. Sharp
Keyword(s):  
Eating Disorders ◽  
Body Image ◽  
Anorexia Nervosa ◽  
Eating Disorder ◽  
Major Depression ◽  
Food Intake ◽  
Older Women ◽  
The Body ◽  
Atypical Presentation ◽  
History Of

A woman aged 58 who has been blind since the age of nine months presented with major depression and a 40 year history of an eating disorder characterized by a restriction of food intake and body disparagement. The case is additional evidence that a specifically visual body image is not essential for the development of anorexia nervosa and supports the view that the concept of body image is unnecessary and unproductive in eating disorders. Greater emphasis should be placed on attitudes and feelings toward the body, and the possibility of an eating disorder should be considered in cases of older women with an atypical presentation.

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.

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)

Rational Design of Dual Peptides Targeting Ghrelin and Y2 Receptors to Regulate Food Intake and Body Weight

2015 ◽  
Vol 58 (10) ◽  
pp. 4180-4193 ◽  
Author(s):  
Tom-Marten Kilian ◽  
Nora Klöting ◽  
Ralf Bergmann ◽  
Sylvia Els-Heindl ◽  
Stefanie Babilon ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Rational Design ◽  
Regulate Food Intake

scholarly journals In vitro insulin treatment reverses changes elicited by nutrients in cellular metabolic processes that regulate food intake in fish

2020 ◽  
Vol 223 (8) ◽  
pp. jeb213454
Author(s):  
Ayelén M. Blanco ◽  
Juan I. Bertucci ◽  
José L. Soengas ◽  
Suraj Unniappan
Keyword(s):  
Food Intake ◽  
Insulin Treatment ◽  
Metabolic Processes ◽  
Regulate Food Intake

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 PACAP intraperitoneal treatment suppresses appetite and food intake via PAC1 receptor in mice by inhibiting ghrelin and increasing GLP-1 and leptin

2015 ◽  
Vol 309 (10) ◽  
pp. G816-G825 ◽  
Author(s):  
John P. Vu ◽  
Deepinder Goyal ◽  
Leon Luong ◽  
Suwan Oh ◽  
Ravneet Sandhu ◽  
...  
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Peptide Yy ◽  
Dark Phase ◽  
Dependent Manner ◽  
Pac1 Receptor ◽  
Intraperitoneal Treatment ◽  
Regulate Food Intake ◽  
Feeding Parameters ◽  
Glucagon Like Peptide 1

Pituitary adenylate cyclase-activating peptide (PACAP) is expressed within the gastroenteric system, where it has profound physiological effects. PACAP was shown to regulate food intake and thermogenesis centrally; however, PACAP peripheral regulation of appetite and feeding behavior is unknown. Therefore, we studied PACAP's effect on appetite and food intake control by analyzing feeding behavior and metabolic hormones in PAC1-deficient (PAC1−/−) and age-matched wild-type (WT) mice intraperitoneally injected with PACAP1–38 or PACAP1–27 before the dark phase of feeding. Food intake and feeding behavior were analyzed using the BioDAQ system. Active ghrelin, glucagon-like peptide-1 (GLP-1), leptin, peptide YY, pancreatic polypeptide, and insulin were measured following PACAP1–38 administration in fasted WT mice. PACAP1–38/PACAP1–27 injected into WT mice significantly decreased in a dose-dependent manner cumulative food intake and reduced bout and meal feeding parameters. Conversely, PACAP1–38 injected into PAC1−/− mice failed to significantly change food intake. Importantly, PACAP1–38 reduced plasma levels of active ghrelin compared with vehicle in WT mice. In PAC1−/− mice, fasting levels of active ghrelin, GLP-1, insulin, and leptin and postprandial levels of active ghrelin and insulin were significantly altered compared with levels in WT mice. Therefore, PAC1 is a novel regulator of appetite/satiety. PACAP1–38/PACAP1–27 significantly reduced appetite and food intake through PAC1. In PAC1−/− mice, the regulation of anorexigenic/orexigenic hormones was abolished, whereas active ghrelin remained elevated even postprandially. PACAP significantly reduced active ghrelin in fasting conditions. These results establish a role for PACAP via PAC1 in the peripheral regulation of appetite/satiety and suggest future studies to explore a therapeutic use of PACAP or PAC1 agonists for obesity treatment.

scholarly journals Regulation of food intake and body weight by recombinant proghrelin

2009 ◽  
Vol 297 (6) ◽  
pp. E1269-E1275 ◽  
Author(s):  
Weizhen Zhang ◽  
Arundhati Majumder ◽  
Xiaobin Wu ◽  
Michael W. Mulholland
Keyword(s):  
Body Weight ◽  
Amino Acid ◽  
Energy Metabolism ◽  
Food Intake ◽  
Normal Saline ◽  
Biological Function ◽  
Intraperitoneal Administration ◽  
Fat Consumption ◽  
Regulate Food Intake ◽  
Cumulative Food Intake

Ghrelin is a 28-amino-acid hormone derived from the endoproteolytic processing of its prehormone proghrelin. Although ghrelin has been reported to regulate food intake and body weight, it is still unknown whether proghrelin exercises any biological function. Here we show that recombinant proghrelin alters food intake and energy metabolism in mice. After intraperitoneal administration of recombinant proghrelin (100 nmol/kg body wt), cumulative food intake was significantly increased at days 1, 2, and 3 (6 ± 0.3, 13 ± 0.5, and 20 ± 0.8 g vs. 5 ± 0.2, 10 ± 0.2, and 16 ± 0.3 g of the control mice receiving normal saline, respectively, n = 6, P < 0.05). Twelve-hour cumulative food intake in the light photo period in mice treated with proghrelin increased significantly relative to the control (2.1 ± 0.04 vs. 1.3 ± 0.2 g, n = 6, P < 0.05). No change in 12-h cumulative food intake in the dark photo period was observed between mice treated with proghrelin and vehicle (4.2 ± 0.6 vs. 4.3 ± 0.6 g, n = 6, P > 0.05). This is associated with a decrease in body weight (0.42 ± 0.04 g) for mice treated with proghrelin, whereas control animals gained body weight (0.31 ± 0.04 g). Mice treated with proghrelin demonstrate a significant decrease in respiratory quotient, indicating an increase in fat consumption. Recombinant proghrelin is functionally active with effects on food intake and energy metabolism.

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