Cholesterol absorption decreases after Roux-en-Y gastric bypass but not after gastric banding

Pihlajamäki, Jussi; Grönlund, Sari; Simonen, Marko; Moilanen, Leena; Pääkkönen, Matti; Pirinen, Elina; Kolehmainen, Marjukka; Kärjä, Vesa; Kainulainen, Sakari; Uusitupa, Matti; Alhava, Esko; Miettinen, Tatu A.; Gylling, Helena

doi:10.1016/j.metabol.2009.10.004

Cited by 83 publications

(72 citation statements)

References 27 publications

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“…All patients undergoing obesity surgery in Kuopio University Hospital are recruited into our ongoing study investigating metabolic consequences of obesity surgery (Kuopio Obesity Surgery Study) ( 14,15 …”

Section: Subjectsmentioning

confidence: 99%

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Lipoprotein subclass metabolism in nonalcoholic steatohepatitis

Männistö

Simonen

Soininen

et al. 2014

Journal of Lipid Research

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Section: Subjectsmentioning

confidence: 99%

“…Plasma glucose, insulin, serum total cholesterol, HDL cholesterol, and triglyceride levels were analyzed as described before ( 14,15 ).…”

Section: Laboratory Determinationsmentioning

confidence: 99%

Lipoprotein subclass metabolism in nonalcoholic steatohepatitis

Männistö

Simonen

Soininen

et al. 2014

Journal of Lipid Research

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“…Ninety-six consecutive subjects (32 men, 64 women, age 47.1 ± 9.1 years, BMI 45.2 ± 6.3 kg/m 2 ) from an ongoing study including all subjects undergoing bariatric surgery at Kuopio University Hospital were included (16). Every participant had a 1-day visit including an interview and evaluation of cardiovascular risk factors.…”

Section: Methodsmentioning

confidence: 99%

“…Expression of PRKCB, PRKCH, and PRKCI/L also showed trends toward increases, but these did not reach statistical significance (P = 0.06), possibly due to the small sample size ( Figure 3B). To further explore this relationship, we compared mRNA levels for PRKCD and other PKCs using liver samples from 96 obese patients included in the study by Pihlajamaki et al (16). These levels correlated with multiple physiological parameters including fasting insulin, glucose, age, circulating triglycerides, and homeostatic model assessment of insulin resistance (HOMA-IR) status.…”

Section: Figurementioning

confidence: 99%

PKCδ regulates hepatic insulin sensitivity and hepatosteatosis in mice and humans

Bézy¹,

Tran²,

et al. 2011

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C57BL/6J and 129S6/Sv (B6 and 129) mice differ dramatically in their susceptibility to developing diabetes in response to diet-or genetically induced insulin resistance. A major locus contributing to this difference has been mapped to a region on mouse chromosome 14 that contains the gene encoding PKCδ. Here, we found that PKCδ expression in liver was 2-fold higher in B6 versus 129 mice from birth and was further increased in B6 but not 129 mice in response to a high-fat diet. PRKCD gene expression was also elevated in obese humans and was positively correlated with fasting glucose and circulating triglycerides. Mice with global or liverspecific inactivation of the Prkcd gene displayed increased hepatic insulin signaling and reduced expression of gluconeogenic and lipogenic enzymes. This resulted in increased insulin-induced suppression of hepatic gluconeogenesis, improved glucose tolerance, and reduced hepatosteatosis with aging. Conversely, mice with liver-specific overexpression of PKCδ developed hepatic insulin resistance characterized by decreased insulin signaling, enhanced lipogenic gene expression, and hepatosteatosis. Therefore, changes in the expression and regulation of PKCδ between strains of mice and in obese humans play an important role in the genetic risk of hepatic insulin resistance, glucose intolerance, and hepatosteatosis; and thus PKCδ may be a potential target in the treatment of metabolic syndrome. IntroductionObesity and type 2 diabetes (T2D) are major health problems worldwide and are projected to further increase in prevalence over the next two decades. Likewise, the closely related metabolic syndrome, with all of its complications, is increasing at epidemic rates. Indeed, nonalcoholic hepatosteatosis is now the second most common cause of chronic liver failure (1). All these disorders are the result of interactions between inherited genetic factors and varying environmental exposures.Mouse models provide a powerful tool to investigate genetic and environmental components involved in the disease susceptibility. In mice, it has been shown that different genetic backgrounds strongly modify the susceptibility to diet-induced obesity, insulin resistance, hepatic steatosis, β cell failure, and T2D, in some cases in very dramatic ways (2-6). For example, we have previously shown that C57BL/6J and 129S6/Sv (B6 and 129) mice have remarkably different metabolic responses to high-fat diet-induced (HFD-induced) insulin resistance. On regular chow diet, B6 mice gain more weight, have higher levels of insulin and leptin, and show greater glucose intolerance than 129 mice, and these phenotypic differences are further exacerbated with high-fat feeding (6). Likewise, when stressed with genetically induced insulin resistance due to heterozygous deletion of both insulin receptor and insulin receptor substrate 1 (IRS-1), more than 90% of B6 mice develop diabetes, whereas less than 5% of 129 mice carrying this form of genetic insulin resistance become diabetic (5). This difference in development of diabete...

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“…This is especially the case for testing of agents or identifying conditions that interfere with cholesterol absorption. For example, Miettinen and colleagues ( 19 ) reported a reduction in plasma noncholesterol sterols in a variety of circumstances in which a reduction of cholesterol absorption was plausible or certain: during administration of plant stanols; after Roux-en-Y gastric bypass ( 20 ); in primary biliary cirrhosis ( 21 ); and in those with genetic forms of low cholesterol absorption ( 22 ). Reductions in absorption likewise have been reported by others during treatment with plant stanols ( 23 ), ezetimibe ( 24 -26 ), surfomer (AOMA) ( 10 ), sucrose polyester (olestra) ( 27 ), and Lactobacillus reuteri ( 28 ).…”

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Plasma noncholesterol sterols as indicators of cholesterol absorption

Grundy¹

2013

Journal of Lipid Research

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A publication by Jakulj et al. ( 1 ) in this issue of the Journal of Lipid Research calls into question the validity of plasma noncholesterol sterols for the evaluation of cholesterol absorption in humans. This method was fi rst proposed by Miettinen and coworkers ( 2 -5 ), who showed that either sitosterol/total cholesterol or campesterol/lathosterol ratios refl ect amounts of cholesterol absorbed by the intestine. Normally only small amounts of plant sterols (sitosterol and campesterol) are absorbed, but Miettinen and associates claimed that quantities absorbed are proportional to amounts of cholesterol absorbed. In turn, the greater the total of plant sterol absorbed, the higher will be the plasma level, normalized for plasma cholesterol levels. These investigators ( 4 , 6 , 7 ) further showed that plasma levels of a cholesterol synthesis precursor, lathosterol, refl ect the body's cholesterol synthesis rate. Because absorbed cholesterol returns to the liver and suppresses cholesterol synthesis, a low level of plasma lathosterol will denote reduced cholesterol synthesis because of more cholesterol absorption. Consequently, the campesterol/ lathosterol ratio should better indicate cholesterol absorption than the sitosterol/cholesterol ratio. Jakulj et al. ( 1 ) attempted to validate plant sterols in plasma as a marker of cholesterol absorption. To do so, they compared plasma campesterol/cholesterol ratios with cholesterol absorption in mildly hypercholesterolemic subjects. Fractional absorption of dietary cholesterol was determined by comparing isotope ratios of plasma cholesterol following oral and intravenous administration. They found no difference in fractional cholesterol absorption in those with the highest and lowest campesterol/ cholesterol ratios. Nor was there a correlation between these ratios and fractional absorption in the total population. The authors concluded that previous studies claiming a relationship between plasma sterol ratios and cholesterol absorption are of questionable validity.It might be noted that Jakulj et al.( 1 ) did not measure a marker of cholesterol synthesis, e.g., lathosterol. Because of the inverse relation between cholesterol absorption and synthesis, the addition of a synthesis precursor could have helped to validate the use of noncholesterol sterols as a marker for cholesterol absorption as well as synthesis.The overall design of the study of Jakulj et al.( 1 ) nonetheless is of interest. Testing whether subgroups with the highest and lowest plant sterol levels have a different fractional absorption of cholesterol is innovative and worthy of further evaluation. On the other hand, methodological issues raised by this study deserve consideration.The method for measuring fractional absorption of cholesterol employed a dual stable-isotope method ( 1 ). ]sitosterol in sunfl ower oil by gentle heating and stirring before adding it to stomach-soluble gelatin capsules. Cholesterol absorption was determined by differences in isotope ratios between oral administration and fecal...

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Cholesterol absorption decreases after Roux-en-Y gastric bypass but not after gastric banding

Cited by 83 publications

References 27 publications

Lipoprotein subclass metabolism in nonalcoholic steatohepatitis

Lipoprotein subclass metabolism in nonalcoholic steatohepatitis

PKCδ regulates hepatic insulin sensitivity and hepatosteatosis in mice and humans

Plasma noncholesterol sterols as indicators of cholesterol absorption

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