2016
DOI: 10.1016/j.biochi.2016.03.009
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Studies on the influence of CCK-8 on the ability of obestatin to reduce food intake, gain in body weight and related lipid parameters

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Cited by 9 publications
(4 citation statements)
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“…A possible hypothesis indicates that increased fat intake (exceeding the animal's metabolic capacity) may limit feed intake through fat‐induced feedback signals. Cholecystokinin (CCK) is the body's signal for satiety in many kinds of mammals (Nagaraj & Manjappara, 2016). Previous studies have shown that CCK significantly reduced the feed intake of HFD rats (Covasa & Ritter, 1998).…”
Section: Discussionmentioning
confidence: 99%
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“…A possible hypothesis indicates that increased fat intake (exceeding the animal's metabolic capacity) may limit feed intake through fat‐induced feedback signals. Cholecystokinin (CCK) is the body's signal for satiety in many kinds of mammals (Nagaraj & Manjappara, 2016). Previous studies have shown that CCK significantly reduced the feed intake of HFD rats (Covasa & Ritter, 1998).…”
Section: Discussionmentioning
confidence: 99%
“…Cholecystokinin (CCK) is the body's signal for satiety in many kinds of mammals (Nagaraj & Manjappara, 2016). Previous studies have…”
Section: Discussionmentioning
confidence: 99%
“…The results were expressed as means ± SEM (n = 6 animals/group). *P < 0.05; **P < 0.01. regulation of appetite and energy absorption (Nagaraj and Manjappara, 2016;ten Kulve et al, 2016;Dardzińska et al, 2017). Combining the expression characteristics of the chicken PCSK1 gene in the present study and the function of PC1/3 reported in mammals, it is reasonable to speculate that the function of PC1/3 in the chicken may be similar to that in mammals; therefore, chicken PC1/3 may process a variety of proneuropeptides and prohormones into functional hormones involved in the regulation of central and peripheral energy metabolism.…”
Section: Discussionmentioning
confidence: 99%
“…As mentioned earlier, the possible involvement of GHS/ghrelin receptor signaling in the mediation of obestatin"s action was also suggested in correlation to its anorexigenic role and interaction with ghrelin on feeding behavior(26,78). This idea was further supported by an in vitro study, in which the administration of the ghrelin receptor antagonist [D-Lys3]-GHRP6 reduced the survival of β cells and human islet cells induced by obestatin(95). Furthermore, the administration of obestatin stimulated GHSR expression in vitro in pituitary cell cultures from baboons and mice, while it downregulated in mice, in vivo(160).Taken together, the present resultsthat the anxiogenic-and depressive-like effects of obestatin where reversed by the administration of a ghrelin receptor antagonistindicate that obestatin may act through GHSR signaling.…”
mentioning
confidence: 69%