Differential expression of the mouse cholecystokinin gene during brain and gut development.

Friedman, Jeffrey M.; Schneider, B; Powell, D. J.

doi:10.1073/pnas.82.17.5593

Cited by 48 publications

(19 citation statements)

References 36 publications

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“…In com parison, marked development of CCK fibers was somewhat delayed with appreciable numbers appearing at postnatal day 5 and reaching a maximum by adulthood, a pattern similar to the development of CCK immunoreactivity. Recently, a similar pattern has been reported for mouse brain [26].…”

Section: Discussionsupporting

confidence: 48%

Expression of the Cholecystokinin Gene in Rat Brain during Development

et al. 1987

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The expression of the gene encoding for cholecystokinin (CCK) was studied pre- and postnatally in rat brain with a preproCCK-specific cDNA probe to quantitate mRNA. In addition, a C-terminal-specific radioimmunoassay was used to measure CCK-immunoreactive peptides. Poly(A)⁺-enriched RNA from rat brain was analyzed for the presence of CCK mRNA by agarose gel electrophoresis, followed by transfer to nitrocellulose and hybridization to a ³²P-labeled CCK cDNA probe. An RNA of approximately 700 nucleotides was observed and there were no obvious CCK mRNA differences between samples taken at the different developmental stages. Brain preproCCK mRNA was detectable by embryonic day 14 and increased continuously until postnatal day 14 when it reached maximal concentrations. In young adult rats, levels were slightly decreased. CCK-immunoreactive peptides began to be detected in the samples from embryonic day 21, but marked development was seen only postnatally with a rajjid increase occurring during the first 2 weeks after birth. The highest content of the peptide was present in young adult rats.

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Section: Discussionsupporting

confidence: 48%

Expression of the Cholecystokinin Gene in Rat Brain during Development

et al. 1987

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“…(3) Some mRNAs show a high concentration at birth, which then falls during the suckling period from 4 to 17 days, and rises again to adult levels in the enterocyte. mRNAs encoding apolipoprotein B [8] and cholecystokinin (CCK) [9] are examples of this pattern. (4) Some ente rocyte mRNAs are present at high levels at birth, and fall rapidly post-natally.…”

Section: Pre-translational Mechanismsmentioning

confidence: 99%

Pre-Translational, Translational, and Post-Translational Mechanisms in Adaptation of Intestinal Proteins

Alpers

1990

Digestion

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The enterocyte exhibits remarkable short-term adaptation to a meal, complementing the well recognized adaptation of the stomach and pancreas. The mechanisms utilized include increased protein synthesis by pre-translational and translational events, and post-translational alterations in protein degradation and secretion. All of these events occur within a few hours after the meal. These adaptations are compared with the more long-term events in post-natal development that occur over a period of days, at least in the rat. They contrast even more with the macroscopic changes that also occur over days and weeks following intestinal resection, the model most commonly associated with the concept of intestinal adaptation. The demonstration of cellular and molecular adaptation within a few hours of a meal represents an expansion of the definition of intestinal adaptation and may provide clues to the explanation of more delayed events.

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“…2G7 was a clone that mapped to the region of chromosome 6 where the ob gene had been found to reside (Friedman et al 1991, Bahary et al 1993. The development of this film was the culmination of a 12-year odyssey that began with the demonstration that cholecystokinin, then considered to be a candidate for the ob gene, mapped to chromosome 9 and could not be ob (Friedman et al 1985(Friedman et al , 1989, to the identification of 2G7 from an exon-trapping experiment in which 182 different clones from an w100-kB P1 clone in the region of the ob gene on mouse chromosome 6 were arrayed on two microtiter plates (the ob gene was on plate 2, row G, column 7) (Zhang et al 1994).…”

Section: Introductionmentioning

confidence: 99%

20 YEARS OF LEPTIN: Leptin at 20: an overview

Friedman¹

2014

Journal of Endocrinology

204

146

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Historically, adipose tissue was considered to be a passive storage vessel discharging nutrients in times of famine and accumulating fat in times of surfeit. This view changed with the identification of leptin as an adipocyte hormone. Leptin functions as an afferent signal in a negative feedback loop that regulates food intake and metabolism to maintain homeostatic control of adipose tissue mass. Before this, the existence of a system maintaining homeostatic control of energy balance was unclear. The identification of leptin has thus uncovered a new endocrine system that also links changes in nutrition to adaptive responses in most if not all other physiologic systems. Further studies have revealed a set of clinical syndromes caused by leptin deficiency, including lipodystrophy and hypothalamic amenorrhea. This work has led to new therapeutic approaches for a number of human conditions and has also established a conceptual framework for studying the pathogenesis of obesity.

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Differential expression of the mouse cholecystokinin gene during brain and gut development.

Cited by 48 publications

References 36 publications

Expression of the Cholecystokinin Gene in Rat Brain during Development

Expression of the Cholecystokinin Gene in Rat Brain during Development

Pre-Translational, Translational, and Post-Translational Mechanisms in Adaptation of Intestinal Proteins

20 YEARS OF LEPTIN: Leptin at 20: an overview

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