The Effect of Insulin on Food Intake After Vagotomy and Sympathectomy

Pentapeptide (Proctolin) Associated with an Identified Neuron

“…In particular, tumor-induced anorexia could be caused by a circulating peptide that exerts a depressant effect on appetite. The hypothesis is supported by investigations demonstrating that many peptides affect appetite (10). Clinical experience also is consonant with the concept of an anorexigenic peptide, as the tumors often associated with anorexia commonly produce ectopic peptide hormones (11).…”

“…Extracts of the LW neuron (P. americana) were prepared by dissecting the neuron's cell body from both sides of the living abdominal ganglion under isotonic physiological saline (10). The dissected and isolated cells were transferred to 50 plJ of 2N acetic acid at room temperature.…”

Control of food intake during continuous injection of glucose into the upper duodenum and the upper ileum of rats

“…Evidence of adequate regulation of food intake in the absence of oropharingeal sensations (Epstein & Teitelbaum, 1962) and after gastrectomy (McDonald, Ingelfinger, & Belding, 1947) suggests that intestinal factors may be inyolved; continued regulation following vagotomy (Snowdon & Epstein, 1970) or after complete gastrointestinal denervation (Grossman, Cummins, & Ivy, 1947) points to a humoral mechanism. The participation of humoral factors in induction of satiety has, indeed, been reported in recent years (Davis, Campbell, Gallagher, & Zurakov, 1971;Seoane, Baile, & Martin, 1972).…”

The State of Research into the Mechanisms of Appetites for Energy (first published in French in 1956)

“…The small reserves of glycogen in the liver and the concentration of glucose in the blood vary rapidly during a fast. The immediate activity of insulin (Andik & Donhoffer, 1950;Grossman et al, 1947;Grossman & Stein, 1948;Long & Bisschoff, 1930;Mackay et al, 1940;Morgan & Morgan, 1940;Richter, 1942) and of exogenous adrenaline (Mayer & Bates, 1952) on food intake, and numerous other data now support the hypothesis that reduction in blood glucose level or, more precisely, in the level of cellular glucose utilization, acts as an internal humoral stimulus of the hunger state Bulatao & Carlson, 1924;Mayer & Bates, 1952;Stunkard & Wolf, 1954;. This stimulus is thought to act directly at the level of the extreme lateral hypothalamic nuclei (Anand & Brobeck, 1951a;Anand & Brobeck, 1951b;Anand & Dua, 1955;Anand et al, 1955;Delgado & Anand, 1953), which are therefore described as food intake initiation system or the hunger centre.…”