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)

Intermittent intraperitoneal infusion of peptide YY(3-36) reduces daily food intake and adiposity in obese rats

2007 ◽  
Vol 293 (1) ◽  
pp. R39-R46 ◽  
Author(s):  
Prasanth K. Chelikani ◽  
Alvin C. Haver ◽  
Roger D. Reidelberger
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Peptide Yy ◽  
Caloric Intake ◽  
Daily Food Intake ◽  
Daily Caloric Intake ◽  
Intraperitoneal Infusion ◽  
Daily Food ◽  
Sustained Reduction ◽  
Obese Rats

Peptide YY(3-36) [PYY(3-36)] is a gut-brain peptide that decreases food intake when administered by intravenous infusion to lean and obese humans and rats. However, chronic administration of PYY(3-36) by osmotic minipump to lean and obese rodents produces only a transient reduction in daily food intake and weight gain. It has recently been shown that 1-h intravenous infusions of PYY(3-36) every other hour for 10 days produced a sustained reduction in daily food intake, body weight, and adiposity in lean rats. Here, we determined whether intermittent delivery of PYY(3-36) can produce a similar response in diet-induced obese rats. During a 21-day period, obese rats (body fat >25%) received twice daily intraperitoneal infusion of vehicle ( n = 18) or PYY(3-36) ( n = 24) during hours 1–3 and 7–9 of the dark period. Rats had free access to both a 45% fat solid diet and a 29% fat liquid diet; intakes were determined from continuous computer recording of changes in food container weights. To sustain a 15–25% reduction in daily caloric intake, the initial PYY(3-36) dose of 30 pmol·kg−1·min−1 was reduced to 10 pmol·kg−1·min−1 on day 10 and then increased to 17 pmol·kg−1·min−1 on day 13. This dosing strategy produced a sustained reduction in daily caloric intake of 11–32% and prevented body weight gain (8 ± 6 vs. 51 ± 11 g) and fat deposition (4.4 ± 7.6 vs. 41.0 ± 12.8 g). These results indicate that intermittent intraperitoneal infusion of PYY(3-36) can produce a sustained reduction in food intake and adiposity in diet-induced obese rodents consuming palatable high-fat foods.

scholarly journals Cereals, calories and change: exploring approaches to quantification in Indus archaeobotany

2017 ◽  
Vol 10 (7) ◽  
pp. 1703-1716 ◽  
Author(s):  
J. Bates ◽  
C.A. Petrie ◽  
R.N. Singh
Keyword(s):  
Late Holocene ◽  
Caloric Intake ◽  
Relative Importance ◽  
Daily Lives ◽  
Daily Caloric Intake ◽  
The People ◽  
Alternative Approach ◽  
Perceived Importance ◽  
Indus Civilisation

Abstract Several major cereal groups have been identified as staples used by the pre-urban, urban and post-urban phase populations of the Indus Civilisation (3200–1500 BCE): wheat, barley, a range of small hulled millets and also rice, though their proportional exploitation is variable across space and over time. Traditional quantification methods examine the frequency, intensity and proportionality of the use of these crops and help ascertain the ‘relative importance’ of these cereals for Indus populations. However, this notion of ‘importance’ is abstracted from the daily lives of the people using these crops and may be biased by the differential production (as well as archaeological survival) of individual cereals. This paper outlines an alternative approach to quantifying Indus cereals by investigating proportions of calories. Cereals are predominantly composed of carbohydrates and therefore provided much of the daily caloric intake among many late Holocene farming populations. The four major cereal groups cultivated by Indus farmers, however, vary greatly in terms of calories per grain, and this has an impact on their proportional input to past diets. This paper demonstrates that, when converted to proportions of calories, the perceived ‘importance’ of cereals from five Indus sites changes dramatically, reducing the role of the previously dominant small hulled millet species and elevating the role of Triticoid grains. Although other factors will also have affected how a farmer perceived the role and importance of a crop, including its ecological tolerances, investments required to grow it, and the crop’s role in the economy, this papers suggests that some consideration of what cereals meant in terms of daily lives is needed alongside the more abstracted quantification methods that have traditionally been applied.

scholarly journals Role of VMH ketone bodies in adjusting caloric intake to increased dietary fat content in DIO and DR rats

2015 ◽  
Vol 308 (10) ◽  
pp. R872-R878 ◽  
Author(s):  
Christelle Le Foll ◽  
Ambrose A. Dunn-Meynell ◽  
Henry M. Miziorko ◽  
Barry E. Levin
Keyword(s):  
Food Intake ◽  
Potential Role ◽  
Ketone Bodies ◽  
Caloric Intake ◽  
High Energy ◽  
Leptin Resistance ◽  
Hypothalamic Nucleus ◽  
Diet Intake ◽  
Body Production

The objective of this study was to determine the potential role of astrocyte-derived ketone bodies in regulating the early changes in caloric intake of diet induced-obese (DIO) versus diet-resistant (DR) rats fed a 31.5% fat high-energy (HE) diet. After 3 days on chow or HE diet, DR and DIO rats were assessed for their ventromedial hypothalamic (VMH) ketone bodies levels and neuronal ventromedial hypothalamic nucleus (VMN) sensing using microdialysis coupled to continuous food intake monitoring and calcium imaging in dissociated neurons, respectively. DIO rats ate more than DR rats over 3 days of HE diet intake. On day 3 of HE diet intake, DR rats reduced their caloric intake while DIO rats remained hyperphagic. Local VMH astrocyte ketone bodies production was similar between DR and DIO rats during the first 6 h after dark onset feeding but inhibiting VMH ketone body production in DR rats on day 3 transiently returned their intake of HE diet to the level of DIO rats consuming HE diet. In addition, dissociated VMN neurons from DIO and DR rats were equally sensitive to the largely excitatory effects of β-hydroxybutyrate. Thus while DR rats respond to increased VMH ketone levels by decreasing their intake after 3 days of HE diet, this is not the case of DIO rats. These data suggest that DIO inherent leptin resistance prevents ketone bodies inhibitory action on food intake.

scholarly journals Altered acylated ghrelin response to food intake in congenital generalized lipodystrophy

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0244667
Author(s):  
Camilla O. D. Araújo ◽  
Renan M. Montenegro ◽  
Amanda P. Pedroso ◽  
Virgínia O. Fernandes ◽  
Ana Paula D. R. Montenegro ◽  
...  
Keyword(s):  
Food Intake ◽  
Analogue Scale ◽  
Caloric Intake ◽  
Acylated Ghrelin ◽  
Congenital Generalized Lipodystrophy ◽  
Meal Intake ◽  
Obese Subjects ◽  
Ad Libitum ◽  
Low Levels

Background Patients with congenital generalized lipodystrophy (CGL) have very low levels of leptin and are described as having a voracious appetite. However, a direct comparison between CGL and eutrophic individuals is lacking, regarding both appetite parameters and acylated ghrelin, the hormone form that is active in acute food intake stimulation. The objective of the present study was to address whether and in what extent the subjective appetite parameters and acylated ghrelin response to a meal are affected in CGL individuals, in comparison to eutrophic individuals. Additionally, an obese group was included in the study, to allow the comparison between a leptin-resistant and a leptin-deficient condition on these aspects. Methods Eutrophic controls (EUT, n = 10), obese subjects (OB, n = 10) and CGL (n = 11) were fasted overnight and then received an ad libitum meal. Blood was collected and the visual analogue scale was applied before and 90 minutes after the meal. An additional blood sample was collected at 60 minutes for ghrelin determination. Results The CGL patients showed low fasting levels of leptin and adiponectin, dyslipidemia, and insulin resistance. The caloric intake was similar among the 3 groups. However, both CGL (p = 0.02) and OB (p = 0.04) had shorter satiation times than EUT. The CGL patients also had lower satiety time (p = 0.01) and their sensation of hunger was less attenuated by the meal (p = 0.03). Fasting acylated ghrelin levels were lower in CGL than in EUT (p = 0.003). After the meal, the levels tended to decrease in EUT but not in CGL and OB individuals. Conclusion The data indicate that, although not hyperphagic, the CGL patients present appetite disturbances in relation to eutrophic individuals. Their low fasting levels of acylated ghrelin and the absence of the physiological drop after meal intake suggest a role of these disturbances in hunger attenuation and satiety but not in acute satiation.

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 Hypothalamic proinflammatory lipid accumulation, inflammation, and insulin resistance in rats fed a high-fat diet

2009 ◽  
Vol 296 (5) ◽  
pp. E1003-E1012 ◽  
Author(s):  
Kelly A. Posey ◽  
Deborah J. Clegg ◽  
Richard L. Printz ◽  
Jaeman Byun ◽  
Gregory J. Morton ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Food Intake ◽  
Inflammatory Responses ◽  
Neuronal Response ◽  
Caloric Intake ◽  
Reduce Food Intake ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Regulate Food Intake ◽  
The Brain

Weight gain induced by an energy-dense diet is hypothesized to arise in part from defects in the neuronal response to circulating adiposity negative feedback signals, such as insulin. Peripheral tissue insulin resistance involves cellular inflammatory responses thought to be invoked by excess lipid. Therefore, we sought to determine whether similar signaling pathways are activated in the brain of rats fed a high-fat (HF) diet. The ability of intracerebroventricular (icv) insulin to reduce food intake and activate hypothalamic signal transduction is attenuated in HF-fed compared with low-fat (LF)-fed rats. This effect was accompanied by both hypothalamic accumulation of palmitoyl- and stearoyl-CoA and activation of a marker of inflammatory signaling, inhibitor of κB kinase-β (IKKβ). Hypothalamic insulin resistance and inflammation were observed with icv palmitate infusion or HF feeding independent of excess caloric intake. Last, we observed that central IKKβ inhibition reduced food intake and was associated with increased hypothalamic insulin sensitivity in rats fed a HF but not a LF diet. These data collectively support a model of diet-induced obesity whereby dietary fat, not excess calories, induces hypothalamic insulin resistance by increasing the content of saturated acyl-CoA species and activating local inflammatory signals, which result in a failure to appropriately regulate food intake.

scholarly journals Serotonin as a Regulator of Leptin-Mediated Food Intake Control Within a Novel Neuronal Circuit Between the Hypothalamus and Raphe Nuclei

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A55-A56
Author(s):  
Alia T Sadek ◽  
Hanson B Cowan ◽  
Katie M Jimenez ◽  
Jesseca N Crawford ◽  
Nicholas D Maxwell ◽  
...  
Keyword(s):  
Food Intake ◽  
Time Course ◽  
Sprague Dawley ◽  
Anova Analysis ◽  
Guide Cannula ◽  
Post Hoc Analysis ◽  
Significant Difference ◽  
Regulate Food Intake ◽  
Post Hoc

Abstract The onset and exacerbation of obesity involves the overproduction of the adipocyte-derived hormone leptin, a key mediator of homeostatic appetite regulation and a signal for satiety. Although leptin’s hypothalamic regulation of food intake has been extensively investigated, its role in tandem with the anorectic neurotransmitter serotonin (5-HT) has been less characterized. 5-HT is synthesized in the dorsal raphe nucleus (DRN) where anatomical projections to many hypothalamic nuclei have previously been identified. Preliminary studies in our lab have: (1) identified serotonergic neurons responsive to leptin in the DRN that project to the arcuate nucleus (ARC) of the hypothalamus and (2) demonstrated leptin injected into the DRN significantly decreases food intake. The objective of the current study was to identify the role of 5-HT in leptin’s regulation of food intake first within the DRN, then between the DRN and the ARC. Adult male Sprague Dawley rats underwent stereotaxic surgery for guide cannula implantation in the DRN. After recovery, animals were administered 100 µg of p-chlorophenylalanine (PCPA), an inhibitor of 5-HT synthesis, in the DRN each day for four days. On the fourth day, leptin was also administered in the DRN (5 µg/rat) and food intake was measured over a 24-hour time course. ANOVA analysis revealed a significant difference in 24-hour food intake [F (3, 18) = 3.972; P = 0.0246] and post-hoc analysis showed that animals treated with leptin significantly decreased food intake (17.2 ± 2.0 g) compared to control rats (25.4 ± 0.9 g), whereas PCPA-treated rats did not differ from the control rats, suggesting that depletion of 5-HT attenuated leptin’s ability to regulate food intake within the DRN. To examine the role of 5-HT on leptin’s hypothalamic action, a subsequent experiment was conducted by implanting an additional cannula into the ARC for the administration of leptin or vehicle on the fourth day of treatment. ANOVA analysis revealed a significant difference in 24-hour food intake [F (3, 16) = 5.998; P = 0.0061] and post-hoc analysis showed that only rats treated with leptin in the ARC significantly decreased food intake (14.0 ± 1.5 g) compared to controls (21.8 ± 0.5 g). 5-HT depletion was assessed post-mortem using immunohistochemistry and was later quantified. Collectively, these results demonstrate that leptin’s ability to regulate food intake is dependent on 5-HT, regardless of the area of regulation (i.e. DRN or the hypothalamus).

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