Apolipoprotein Synthesis in Newborn Piglet Intestinal Explants

Black, Dennis D.; Ellinas, Herodotos

doi:10.1203/00006450-199211000-00014

Cited by 26 publications

(17 citation statements)

References 46 publications

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“…This observation was also confirmed in vivo by Doi et al (7). It has been recently demonstrated that intestinal apo A-IV synthesis and secretion are upregulated by insulin in both rodents and humans (3,5). Energy homeostasis in the body is accomplished by a highly integrated and redundant neurohumoral system that prevents the effect of short-term fluctuations in energy balance on fat mass (34).…”

Section: Does Apo A-iv Play a Role In The Regulation Of Food Intake Amentioning

confidence: 73%

Gastrointestinal Satiety Signals IV. Apolipoprotein A-IV

Tso¹,

Sun²,

Liu³

2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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The focus of this article is to review evidence that apolipoprotein A-IV (apo A-IV) acts as a satiety factor. Additionally, information regarding the general involvement of apo A-IV in the regulation of food intake and body weight is stated. Apo A-IV is a glycoprotein synthesized by the human intestine. In rodents, both the small intestine and liver secrete apo A-IV, but the small intestine is the major organ responsible for circulating apo A-IV. There is now solid evidence that the hypothalamus, especially the arcuate nucleus, is another active site of apo A-IV expression. Intestinal apo A-IV synthesis is markedly stimulated by fat absorption and does not appear to be mediated by the uptake or reesterification of fatty acids to form triglycerides. Rather, the local formation of chylomicrons acts as a signal for the induction of intestinal apo A-IV synthesis. Intestinal apo A-IV synthesis is also enhanced by a factor from the ileum, probably peptide tyrosine-tyrosine (PYY). The inhibition of food intake by apo A-IV is mediated centrally. The stimulation of intestinal synthesis and secretion of apo A-IV by lipid absorption are rapid; thus apo A-IV likely plays a role in the short-term regulation of food intake. Other evidence suggests that apo A-IV may also be involved in the long-term regulation of food intake and body weight, as it is regulated by both leptin and insulin. Chronic ingestion of a high-fat diet blunts the intestinal as well as the hypothalamic apo A-IV response to lipid feeding. It also suppresses apo A-IV gene expression in the hypothalamus. Whereas it is tempting to speculate that apo A-IV may play a role in diet-induced obesity, we believe the confirmation of such a proposal awaits further experimental evidence.

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Section: Does Apo A-iv Play a Role In The Regulation Of Food Intake Amentioning

confidence: 73%

Gastrointestinal Satiety Signals IV. Apolipoprotein A-IV

Tso¹,

Sun²,

Liu³

2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Black and Ellinas [24] have also investigated the effects of insulin on apo B synthesis in jejunal explants from newborn piglets. No influence of insulin was recorded in these experiments, suggesting that the modulation of apo B synthesis by insulin may depend on both the stage of development and the species studied.…”

Section: Resultsmentioning

confidence: 99%

Insulin modulation of newly synthesized apolipoproteins B‐100 and B‐48 in human fetal intestine: Gene expression and mRNA editing are not involved

et al. 1996

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We investigated insulin's effect on intestinal lipid transport and, particularly, the biogenesis of apolipoproteins crucial to lipoprotein secretion. Adding insulin (3 mU) to the serum-free medium of cultured jejunal explants from human fetuses (17-20 weeks) reduced triglyceride and chylomicron production and inhibited apo B-48 and apo B-100 secretion. When apo B mRNA was assayed by RT-PCR and its editing by primer extension, no change was detectable following the addition of insulin. HDL lipid content, apo A-1 synthesis and RNA level were unaffected by insulin. Collectively, these results suggest that the insulin-stimulated decline in intestinal chylomicron output may involve apo B co-or post-translational modifications.

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“…ApoA-IV synthesis and secretion by the gastrointestinal tract are upregulated by insulin (25)(26)(27). ApoA-IV enhances basolateral TG secretion in a association between apoB48 concentrations and body mass index (BMI).…”

Section: Association Between Jejunal Lipid Content and Other Variablesmentioning

confidence: 99%

Jejunal wall triglyceride concentration of morbidly obese persons is lower in those with type 2 diabetes mellitus

Soriguer

García‐Serrano

Garrido‐Sánchez

et al. 2010

Journal of Lipid Research

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This article is available online at http://www.jlr.orgThe insulin-resistance state and type 2 diabetes mellitus (T2DM) are closely related with an increase in cardiovascular disease. Factors conditioning this increase in cardiovascular disease include metabolic dyslipidemia associated with insulin resistance. It has recently been suggested that the overproduction of intestinally derived apolipoprotein (apo)B48-containing lipoproteins may contribute greatly to the dyslipidemia found in both the fasting and postprandial states in insulin resistance ( 1-3 ). However, the underlying mechanisms are still not fully understood.Most studies undertaken in this area have been carried out in the postprandial state ( 3, 4 ). The intestine maintains a basal production of apoB48, even in fasting states, synthesizing small triglyceride-rich lipoprotein (TRL) particles ( 4, 5 ). Animal studies have shown that the contribution of intestinal lipoproteins to the total fasting plasma triglycerides is from 10% to 20% ( 4, 5 ), increasing in the case of diabetes ( 4, 6, 7 ). Fructose-fed hamsters experience an increase in the assembly and secretion of apoB48-containing lipoproteins in insulin-resistant states ( 2 ). Duez et al. showed that the production of chylomicrons (CM) was upregulated in humans with insulin resistance ( 8 ). Studies undertaken in fructose-fed, insulin-resistant Syrian golden hamsters in both the fasted and fed states found that, in these insulin-resistant animals, the increased production of small TRL was greater in the fasted state than the fed state ( 1 ). Nevertheless, caution should be exercised when extrapolating results from experimental animal models to humans, due to the differences between species.Abstract The overproduction of intestinal lipoproteins may contribute to the dyslipidemia found in diabetes. We studied the infl uence of diabetes on the fasting jejunal lipid content and its association with plasma lipids and the expression of genes involved in the synthesis and secretion of these lipoproteins. The study was undertaken in 27 morbidly obese persons, 12 of whom had type 2 diabetes mellitus (T2DM). The morbidly obese persons with diabetes had higher levels of chylomicron (CM) triglycerides ( P < 0.001) and apolipoprotein (apo)B48 ( P = 0.012). The jejunum samples obtained from the subjects with diabetes had a lower jejunal triglyceride content ( P = 0.012) and angiopoietin-like protein 4 (ANGPTL4) mRNA expression ( P = 0.043). However, the apoA-IV mRNA expression was signifi cantly greater ( P = 0.036). The jejunal triglyceride content correlated negatively with apoA-IV mRNA expression ( r = ؊ 0.587, P = 0.027). The variables that explained the jejunal triglyceride content in a multiple linear regression model were the insulin resistance state and the apoA-IV mRNA expression. Our results show that the morbidly obese subjects with diabetes had lower jejunal lipid content and that this correlated negatively with apoA-IV mRNA expression. These fi ndings show that the jejunum appears to play an act...

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Apolipoprotein Synthesis in Newborn Piglet Intestinal Explants

Cited by 26 publications

References 46 publications

Gastrointestinal Satiety Signals IV. Apolipoprotein A-IV

Gastrointestinal Satiety Signals IV. Apolipoprotein A-IV

Insulin modulation of newly synthesized apolipoproteins B‐100 and B‐48 in human fetal intestine: Gene expression and mRNA editing are not involved

Jejunal wall triglyceride concentration of morbidly obese persons is lower in those with type 2 diabetes mellitus

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