A step towards developing the expertise to control hunger and satiety: Regulatory role of satiomem?A membrane proteoglycan

Abstract

Regulation of hunger and satiety is a complex process thought to be controlled by a complex interplay of neurotransmitters in the hypothalamic region of the brain. Reduced food intake or anorexia has also been observed under various disease or disorder conditions including AIDS and cancer. On the other hand, increased appetite because of some impairment of central mechanisms regulating the food intake could also cause/obesity. A large number of substances including neuropeptides, hormones, drugs, and synthetic peptides have been implicated in the regulation of appetite and food intake behavior in normal as well as disease or disorder conditions. Most of these substances are not directly involved in the regulation of normal hunger and satiety but exert their effect indirectly via other media. Some of them are involved under certain pathologic conditions and during the course they become involved directly or indirectly in the triggering of hunger and satiety regulatory mechanism. Recently, we have been able to isolate and purify an endogenous proteoglycan from membranes of animal and plant sources. This membrane anchored proteoglycan termed as 'Satiomem' reduces food intake without any rebound effects and has no apparent toxicity. It also fulfils all the criteria of a true satiety or anorexigenic substance. The release of satiomem from the cell surface could be mediated by a specific phospholipase-C. Satiomem seems to be involved in transducing activating signals and may also act as a source of second messenger for the regulatory mechanism of appetite. This article summarizes the regulatory aspects of hunger and satiety mechanisms controlled by endogenous substances with the emphasis on our present knowledge about satiomem.

Multiplexed Neurotransmission Emulated by a p–n Cross Nanowire Synaptic Transistor for Satiety, Depression, and Drug Withdrawal

“…[31][32][33] This phenomenon is similar to the nerve reactions of "satiety" (Figure 4f) and "drug withdrawal" (Figure 4g). [5,7,34,35] Nesfatin-1 is derived from the precursor of nucleobindin2 (NUCB2) and is a new peptide recently discovered in the stomach of rodents. Nesfatin-1 exerts gastric protection by activating the vagal nerve and sensory nerves to release calcitonin gene-related peptide (CGRP), which inhibits food intake and indicates "satiety."…”

“…These changes prevent the adverse effects of nicotine withdrawal and limit the escalation of nicotine intake. [5] The change in the synaptic weight of STs is similar to biological drug withdrawal.…”