The Hypothalamus and Drinking

Jt, Fitzsimons

doi:10.1093/oxfordjournals.bmb.a070479

Cited by 29 publications

(5 citation statements)

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“…Previous research already showed that drinking water separately with the meal vs. water consumption in the food suppressed thirst more [15]. When thirst is not quenched by water in the meal, this could be due to a different mouth feel, which leads to secondary thirst as described according to Fitzsimons [33], [34].…”

Section: Discussionmentioning

confidence: 99%

Satiating Capacity and Post-Prandial Relationships between Appetite Parameters and Gut-Peptide Concentrations with Solid and Liquefied Carbohydrate

et al. 2012

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BackgroundDifferences in satiating capacity of liquid and solid meals are unclear.ObjectiveInvestigating appetite parameters, physiological measurements and within-subject relationships after consumption of a single macronutrient, subject-specific carbohydrate meal in liquefied versus solid form, controlled for energy density, weight and volume.DesignIn a cross-over design, ten male subjects (age = 21.1±3.9 y, BMI = 22.4±1.2 kg/m2) consumed a solid (CS, whole peaches +750 ml water) and liquefied carbohydrate (CL, peach blended in 500 ml water +250 ml water) lunch. Appetite profiles, insulin-, glucose- and ghrelin concentrations were measured over three hours. Post-prandial relationships between appetite and blood parameters were calculated using subject-specific regression analyses.ResultsFullness ratings were higher in the CL (85±5 mm) compared to the CS condition (73±8 mm) at 20 min (p<0.03). Glucose concentrations peaked 20 to 30 min after the start of the lunch in the CL condition, and 30 to 40 min after start of the CS condition. Correspondingly, insulin concentrations were peaked at 20–30 min in the CL condition, and at 30–40 min in the CS condition. AUC or condition x time interactions were not different comparing the CL and the CS condition. Insulin was significantly higher in the CS compared to the CL condition 40 min after the start of the lunch (p<0.05). Fullness scores were significantly related to insulin concentrations but not to glucose concentrations; desire to eat scores were significantly associated with ghrelin concentrations in both, the CL and the CS condition. The relationship between fullness scores and glucose concentrations was not statistically significant.ConclusionLiquefied and solid carbohydrate meals do not differ in satiating capacity, supported by appetite profile and relevant blood parameters. Postprandially, fullness and desire to eat were associated with respectively insulin and ghrelin concentrations.

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Section: Discussionmentioning

confidence: 99%

Satiating Capacity and Post-Prandial Relationships between Appetite Parameters and Gut-Peptide Concentrations with Solid and Liquefied Carbohydrate

et al. 2012

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“…Although other osmosensitive areas have been identified in the C.N.S. (Fitzsimons, 1966), it seems probable that there is a direct link between osmoreception and ADH release only in the SON and PVN of the hypothalamus. In the present experiments, a slight and inconsistent fall was obtained after injecting hypertonic saline into the area preopticus and fasciculus mammillothalamicus.…”

Section: Discussionmentioning

confidence: 97%

A microinjection study of the control of antidiuretic hormone release by the supraoptic nucleus of the hypothalamus in the cat

Milton¹,

Paterson²

1974

The Journal of Physiology

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SUMMARY1. The release of antidiuretic hormone (ADH) has been studied in the chloralose anaesthetized cat after microinjection of various agents directly into the brain, in particular the supraoptic nucleus of the hypothalamus (SON). The concentration of ADH in jugular venous blood was determined using the waterloaded, alcohol anaesthetized rat assay. The position of the microinjection cannula was located post mortem in stained brain sections.2. Nicotine, noradrenaline (NA) and hypertonic saline caused release of ADH, whereas microinjections of isotonic saline did not affect the blood level of the hormone.3. Nicotine administered to other sites in the central nervous system (c.N.s.) could also cause ADH release. Hypertonic saline proved to be an ineffective stimulus at all the tested sites outside the supraoptic region. 4. The ganglion-blocking agents hexamethonium and pempidine inhibited the releasing action of nicotine at the SON in most of the experiments. These blocking drugs had no effect on osmotic release. When administered alone, both hexamethonium and pempidine had variable, but analogous effects on the hormone output.5. The a-adrenoreceptor blocking drug, phentolamine, stimulated ADH release, but the fl-receptor blocking drug, propranolol, had no such effect.Both drugs appeared to have inhibitory action on noradrenergic release of AIDH, but neither had a consistent effect on the osmotic release of the hormone.

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“…The hypothalmic region, close to the third ventricule, shows the highest level of angiotensin found, and about one-third of it is angiotensin II. This may have important physiological and physiopathological consequences in areas related to the biosynthesis of catecholamines, the regulation of the cardiovascular system (20), the mechanism of thirst (21), and the over-all behavior of the autonomic nervous system. The finding of renin and angiotensin in brain tissue is an important clue to its local formation.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin and Renin in Rat and Dog Brain

Fischer-Ferraro

Nahmod

Goldstein

et al. 1971

The Journal of Experimental Medicine

351

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Since the discovery of the angiotensins a link was sought in vain between these polypeptides and the physiological mechanism that regulates the systemic blood pressure (1). This search, however, was rich in surprises as soon as the amazing diversity of pharmacological actions of angiotensin II was established. Besides being the most powerful vasopressor molecule known, the polypeptide is the hormone for aldosterone release (2) and has several effects on the autonomic nervous system: (a) it inhibits the uptake of catecholamines by sympathetic nerve endings (3); (b) it has a direct action on cholinergic ganglionic cells (4); (c) it accelerates the rate of biosynthesis of norepinephrine (5); and (d) it acts directly or indirectly on central sympathetic structures inducing a prolonged increase in blood pressure and heart rate (6). Even if this versatility shattered the early ideas concerning the function of the polypeptide, the classical scheme that accounted for angiotensin I production was not challenged until very recently. The liberation of the polypeptide was supposed to be restricted to the plasma, where a circulating alpha-2 globulin synthetized by the liver, angiotensinogen, is split by a proteolytic enzyme, renin, synthesized by the granular cells of the juxtaglomerular apparatus of the kidney. This proteolytic step releases a 10-residue long polypeptide from angiotensinogen, denominated angiotensin I, which is itself the substrate for a specific, Cl-activated carboxipeptidase, the converting enzyme, giving rise to the octapeptide angiotensin II. This scheme was first questioned after the finding that isolated rat renal glomeruli, devoid of plasma contamination and incubated in a simple salt medium, were able to secrete angiotensin I in great amounts (7-8). The release of the polypeptide was suppressed with protein-synthesis inhibitors. I The tissue synthesis of angiotensin I was strongly supported by the finding of a polypeptide in several tissues of the rat and the dog with pharmacological and

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The Hypothalamus and Drinking

Cited by 29 publications

References 0 publications

Satiating Capacity and Post-Prandial Relationships between Appetite Parameters and Gut-Peptide Concentrations with Solid and Liquefied Carbohydrate

Satiating Capacity and Post-Prandial Relationships between Appetite Parameters and Gut-Peptide Concentrations with Solid and Liquefied Carbohydrate

A microinjection study of the control of antidiuretic hormone release by the supraoptic nucleus of the hypothalamus in the cat

Angiotensin and Renin in Rat and Dog Brain

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