In vivo regulation of low-density lipoprotein receptor and apolipoprotein B gene expressions by dietary fat and cholesterol in inbred strains of mice

Srivastava, Rai Ajit K.; Jiao, Sheng; Tang, Jingjing; Pfleger, Barbara; Kitchens, Robert T.; Schonfeld, Gustav

doi:10.1016/0005-2760(91)90151-7

Cited by 76 publications

(32 citation statements)

References 38 publications

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“…Similar conclusions were drawn from animal studies, e.g. rats (Davidson et al 1988), mice (Srivastava et al 1991), African green monkeys (Sorci-Thomas et al 1989), suggesting that apoB gene transcription is not influenced by metabolic factors. However, evidence has been accumulating to suggest that pretranslational effects on apoB synthesis are also important.…”

Section: A M S a L T E R A N D D A W H I T E R E G U L A T I O N supporting

confidence: 69%

Effects of Dietary Fat on Cholesterol Metabolism: Regulation of Plasma LDL Concentrations

Salter

White²

1996

Nutr. Res. Rev.

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Section: A M S a L T E R A N D D A W H I T E R E G U L A T I O N supporting

confidence: 69%

Effects of Dietary Fat on Cholesterol Metabolism: Regulation of Plasma LDL Concentrations

Salter

White²

1996

Nutr. Res. Rev.

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“…Liver LDL-r removes LDL-cholesterol from circulation, thereby maintaining cholesterol homeostasis (12). A high-SFA intake during the postnatal time period has been reported to lower the expression of hepatic LDL-r in several animal models (19,30,31,55) and in human studies (29). The LDL-r mRNA expression was significantly reduced in the female S/S and C/S offspring.…”

Section: Discussionmentioning

confidence: 99%

Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor

Chechi

McGuire²,

Cheema³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Chechi K, McGuire JJ, Cheema SK. Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor. Am J Physiol Regul Integr Comp Physiol 296: R1029 -R1040, 2009. First published February 4, 2009 doi:10.1152/ajpregu.90932.2008We have previously shown that a maternal high-fat diet, rich in saturated fatty acids (SFA), alters the lipid metabolism of their adult offspring. The present study was designed to investigate 1) whether alterations in hepatic LDL-receptor (LDL-r) expression may serve as a potential mechanism of developmental programming behind the altered lipid metabolism of the offspring, 2) whether altered lipid metabolism leads to aortic vascular dysfunction in the offspring, 3) whether deleterious effects of SFA exposure preweaning are influenced by postweaning diet, and 4) whether gender-specific programming effects are observed. Female C57Bl/6 mice were fed a high-SFA diet or regular chow during gestation and lactation while their pups, both male and female, received either SFA or a chow diet after weaning. Male offspring obtained from mothers fed an SFA diet and those who continued on chow postweaning had higher plasma triglycerides and total cholesterol, whereas female offspring had higher plasma total and LDL cholesterol levels, lower hepatic LDL-r mRNA expression, and reduced aortic contractile responses compared with the offspring that were fed chow throughout the study. A comparison of the postweaning diet revealed significantly lower hepatic LDL-r expression along with significantly higher plasma LDL-cholesterol concentration in the female offspring that were obtained from mothers fed an SFA diet and who continued on an SFA diet postweaning, compared with the female offspring that were obtained from mothers fed an SFA diet but who continued on chow postweaning. In conclusion, we report a novel observation of hepatic LDL-r-mediated programming of altered lipid metabolism, along with aortic vascular dysfunction, in the female offspring of mothers fed a high-SFA diet. Male offspring only exhibited dyslipidemia, suggesting gender-mediated programming. This study further highlighted the role of postweaning diets in overriding the effects of maternal programming. fetal programming; plasma lipids; hepatic LDL-receptor; dietary fats; cardiovascular disease RECENT EVIDENCE BASED ON THE developmental origins of health and disease hypothesis suggests that early nutrition can be critical in determining the cardiovascular health of an individual (43, 44). According to this hypothesis, which was originally known as Barker's hypothesis, an adverse maternal nutrition during gestation can create a stressed environment for the developing fetus. The fetus responds to this nutritional stress by programming its own growth in a way that could increase its risk of developing metabolic disorders in later life (6 -8). Considering that a typical Western diet is rich in dietary fat content (17), especially saturated fatty acids (SFA), s...

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“…Elevations in LDL and VLDL occur commonly among mice fed high-fat diets (33)(34)(35)(36). In fact, the major lipoprotein increase is seen in ␤-VLDL (36), cholesterol-rich particles containing both apoB and apoE (24).…”

Section: Discussionmentioning

confidence: 99%

Mutation of the RIIβ Subunit of Protein Kinase A Prevents Diet-Induced Insulin Resistance and Dyslipidemia in Mice

et al. 2001

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The mechanisms by which obesity contributes to diabetic phenotypes remain unclear. We evaluated the role of protein kinase A (PKA) signaling events in mediating diabetes associated with obesity. PKA comprises two regulatory subunits and two catalytic subunits and is activated by cAMP. The RII␤ regulatory subunit is abundantly expressed in adipose tissue and brain. Knockout mice lacking this subunit are lean and display remarkable resistance to diet-induced obesity. We investigated whether these mice were also resistant to diet-induced diabetes and whether this effect was dependent on reduced adiposity. Mice were fed a high-fat, high-carbohydrate diet and weight gain and diabetes phenotypes were examined. RII␤ ؊/؊ mice displayed decreased body weights, reduced insulin levels, improved insulin sensitivity, and improved total-body glucose disposal as compared with wild-type controls. Plasma levels of VLDL and LDL cholesterol were also reduced in high fat-fed RII␤ ؊/؊ mice compared with wild-type mice. Taken together, these data demonstrate that loss of RII␤ protects mice from diet-induced obesity, insulin resistance, and dyslipidemia. Diabetes 50:2555-2562, 2001 R ecent reports indicate that obesity is rapidly increasing in industrialized nations. More than 35% of American adults are now considered overweight or obese (1), and obesity is an important contributing factor to the development of type 2 diabetes (2-4). Dyslipidemia is often observed in association with obesity and diabetes and is a significant contributor to the increased mortality observed in diabetic patients (5,6). Characteristics of type 2 diabetes include impaired glucose disposal, diminished insulin production, and increased hepatic glucose output. The mechanisms by which obesity contributes to these phenotypes remain unclear (7).Signaling via protein kinase A (PKA) plays an important role in regulating metabolism and body weight (8). PKA is activated by cAMP and comprises two regulatory and two catalytic subunits (8). Four regulatory isoforms (RI␣, RI␤, RII␣, and RII␤) and two catalytic isoforms (C␣ and C␤) are expressed in the mouse, and each is encoded by a separate gene. The RII␤ subunit is expressed principally in three tissues known to regulate energy homeostasis: brown adipose tissue, white adipose tissue, and brain (8,9). Recent studies suggest that the induction of PKA in certain tissues may decrease obesity. For example, activation of the adipose-specific ␤-adrenergic receptor (10), which signals via PKA, decreases obesity in both genetically obese (ob/ob) (11,12) and diet-induced obese mice (13), suggesting that signaling mechanisms through this pathway are important in preventing obesity.Studies in mice lacking a specific PKA subunit, RII␤, have revealed an unexpected role for this protein in regulating energy balance (9). RII␤ knockout mice (RII␤ Ϫ/Ϫ ) remain remarkably lean even when challenged with a high-fat diet (9). These animals have increased metabolic activity, manifested by increases in body temperature, uncoupling protein 1 ...

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In vivo regulation of low-density lipoprotein receptor and apolipoprotein B gene expressions by dietary fat and cholesterol in inbred strains of mice

Cited by 76 publications

References 38 publications

Effects of Dietary Fat on Cholesterol Metabolism: Regulation of Plasma LDL Concentrations

Effects of Dietary Fat on Cholesterol Metabolism: Regulation of Plasma LDL Concentrations

Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor

Mutation of the RIIβ Subunit of Protein Kinase A Prevents Diet-Induced Insulin Resistance and Dyslipidemia in Mice

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