Postprandial de novo lipogenesis and metabolic changes induced by a high-carbohydrate, low-fat meal in lean and overweight men

Marques-Lopes, Iva; Ansorena, Diana; Astiasarán, Icíar; Forga, Luis; Martínez, J. Alfredo

doi:10.1093/ajcn/73.2.253

Cited by 130 publications

(109 citation statements)

References 34 publications

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“…The level of hepatic DNL in the obese has been found to be either unchanged 26,30 or increased. 31 The major confounding factor seems to be the degree of insulin resistance.…”

Section: Do Obese Women Convert More Cho To Fat Than Lean Women?mentioning

confidence: 99%

Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis

Schütz

2004

Int J Obes

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The measurement of fat balance (fat input minus fat output) involves the accurate estimation of both metabolizable fat intake and total fat oxidation. This is possible mostly under laboratory conditions and not yet in free-living conditions. In the latter situation, net fat retention/mobilization can be estimated based on precise and accurate sequential body composition measurements. In case of positive balance, lipids stored in adipose tissue can originate from dietary (exogenous) lipids or from nonlipid precursors, mainly from carbohydrates (CHOs) but also from ethanol, through a process known as de novo lipogenesis (DNL). Basic equations are provided in this review to facilitate the interpretation of the different subcomponents of fat balance (endogenous vs exogenous) under different nutritional circumstances. One difficulty is methodological: total DNL is difficult to measure quantitatively in man; for example, indirect calorimetry only tracks net DNL, not total DNL. Although the numerous factors (mostly exogenous) influencing DNL have been studied, in particular the effect of CHO overfeeding, there is little information on the rate of DNL in habitual conditions of life, that is, large day-to-day fluctuations of CHO intakes, different types of CHO ingested with different glycemic indexes, alcohol combined with excess CHO intakes, etc. Three issues, which are still controversial today, will be addressed: (1) Is the increase of fat mass induced by CHO overfeeding explained by DNL only, or by decreased endogenous fat oxidation, or both? (2) Is DNL different in overweight and obese individuals as compared to their lean counterparts? (3) Does DNL occur both in the liver and in adipose tissue? Recent studies have demonstrated that acute CHO overfeeding influences adipose tissue lipogenic gene expression and that CHO may stimulate DNL in skeletal muscles, at least in vitro. The role of DNL and its importance in health and disease remain to be further clarified, in particular the putative effect of DNL on the control of energy intake and energy expenditure, as well as the occurrence of DNL in other tissues (such as in myocytes) in addition to hepatocytes and adipocytes.

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“…The level of hepatic DNL in the obese has been found to be either unchanged 26,30 or increased. 31 The major confounding factor seems to be the degree of insulin resistance.…”

Section: Do Obese Women Convert More Cho To Fat Than Lean Women?mentioning

confidence: 99%

Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis

Schütz

2004

Int J Obes

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“…35 For carbohydrate oxidation, the glycogen formula was employed as roughly three-quarters of plasma glucose turnover is derived from liver glycogenolysis after an overnight fast. 35,36 The 24 h recall food intake was analyzed with a computerized program by a trained nutritionist on a computerized program (Medisystem, SanoCare, Madrid, Spain). 37 Analytical methods Plasma glucose, triglycerides, glycerol, FFA, D-3-hydroxybutyrate and urine urea were determined with a Cobas Mira S apparatus, by spectrophotometric methods.…”

Section: Analysis Of Pcr-rflpmentioning

confidence: 99%

Gln27Glu polymorphism in the beta2 adrenergic receptor gene and lipid metabolism during exercise in obese women

Macho-Azcarate

Martí

González³

et al. 2002

Int J Obes

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BACKGROUND:The Glu27Glu genotype in the beta-2-adrenergic receptor (ADRB2) is associated with fat mass, body mass index and obesity in females. In our population, we previously found an association of higher body mass index (BMI) among women who reported more physical activity and carried the Glu27 allele as compared to non carriers with the same level of activity. OBJECTIVE: To examine the lipid metabolism differences, both at rest and during submaximal exercise in ADRB2 Glu27Glu vs Gln27Gln obese women. SUBJECTS: Eight obese women with the Glu27Glu genotype (age, 43 AE 5 y; body mass index (BMI), 31.7 AE 0.9 kg=m 2 ; percentage fat mass, 42.0 AE 1.3; WHR, 0.83 AE 0.02; and VO 2max , 21.6 AE 0.9 ml=kg=min) were compared with seven obese women with the Gln27Gln genotype (age, 43 AE 5 y; BMI, 33.9 AE 1.3 kg=m 2 ; percentage fat mass, 41.6 AE 1.2; WHR, 0.83 AE 0.02; and VO 2max , 20.6 AE 0.8 ml=kg=min). MEASUREMENTS: The ADRB2 polymorphism was identified by PCR-RFLP. Respiratory quotient was determined by indirect calorimetry at baseline, during 1 h of walking on a treadmill and 1 h after the exercise. Plasma triglycerides, glycerol, FFA, hydroxybutyrate, glucose and lactate were assayed by spectrophotometric methods. Insulin, leptin and progesterone were measured by radioimmunoassay. Adrenaline and noradrenaline were quantified by high performance liquid chromatography. RESULTS: The ADRB2 Glu27Glu subjects had lower plasma glycerol (P ¼ 0.047) and lower hydroxybutyrate (P ¼ 0.001) throughout the study than the Gln27Gln group. Plasma triglycerides (P ¼ 0.001), lactate (P < 0.05) and serum insulin (P < 0.05) remained higher in the Glu27Glu group vs the Gln27Gln group. The respiratory quotient (RQ) was higher in the Glu27Glu obese women along the study (P ¼ 0.046), and fat oxidation was significantly lower in this group during the recovery (P ¼ 0.048). The other variables did not differ statistically between groups. CONCLUSION: These data suggest that both lipolysis and fat oxidation promoted by an acute submaximal exercise intervention could be blunted in the polymorphic ADRB2 Glu27Glu group of our female obese population.

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“…3 In obese insulin-resistant patients, hepatic DNL is increased, and appears to be stimulated by hyperinsulinemia. 4,5 Interestingly, insulin has a dual signaling pathway in hepatocytes: it suppresses gluconeogenesis and glucose production but this effect is blunted in insulin-resistant individuals; in contrast, it stimulates hepatic glucose uptake and DNL through activation of SREBP-1c, a pathway that remains fully responsive in insulin-resistant subjects. 6 This probably explains the impaired suppression of glucose production together with increased DNL observed in hyperinsulinemic insulin-resistant patients.…”

Section: Introductionmentioning

confidence: 99%

“…6 This probably explains the impaired suppression of glucose production together with increased DNL observed in hyperinsulinemic insulin-resistant patients. 4,5,7,8 Adipose tissue has been shown to synthesize lipids de novo when studied in vitro. Furthermore, it was observed that DNL was more active in adipose tissue obtained from obese than lean subjects.…”

Section: Introductionmentioning

confidence: 99%

Effect of carbohydrate overfeeding on whole body macronutrient metabolism and expression of lipogenic enzymes in adipose tissue of lean and overweight humans

et al. 2004

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OBJECTIVE: Lipids stored in adipose tissue can originate from dietary lipids or from de novo lipogenesis (DNL) from carbohydrates. Whether DNL is abnormal in adipose tissue of overweight individuals remains unknown. The present study was undertaken to assess the effect of carbohydrate overfeeding on glucose-induced whole body DNL and adipose tissue lipogenic gene expression in lean and overweight humans. DESIGN: Prospective, cross-over study. SUBJECTS AND METHODS: A total of 11 lean (five male, six female, mean BMI 21.070.5 kg/m 2 ) and eight overweight (four males, four females, mean BMI 30.170.6 kg/m 2 ) volunteers were studied on two occasions. On one occasion, they received an isoenergetic diet containing 50% carbohydrate for 4 days prior to testing; on the other, they received a hyperenergetic diet (175% energy requirements) containing 71% carbohydrates. After each period of 4 days of controlled diet, they were studied over 6 h after having received 3.25 g glucose/kg fat free mass. Whole body glucose oxidation and net DNL were monitored by means of indirect calorimetry. An adipose tissue biopsy was obtained at the end of this 6-h period and the levels of SREBP-1c, acetyl CoA carboxylase, and fatty acid synthase mRNA were measured by real-time PCR. RESULTS: After isocaloric feeding, whole body net DNL amounted to 3579 mg/kg fat free mass/5 h in lean subiects and to 4973 mg/kg fat free mass/5 h in overweight subjects over the 5 h following glucose ingestion. These figures increased (Po0.001) to 156721 mg/kg fat free mass/5 h in lean and 64711 mg/kg fat free mass/5 h (Po0.05 vs lean) in overweight subjects after carbohydrate overfeeding. Whole body DNL after overfeeding was lower (Po0.001) and glycogen synthesis was higher (Po0.001) in overweight than in normal subjects. Adipose tissue SREBP-1c mRNA increased by 25% in overweight and by 43% in lean subjects (Po0.05) after carbohydrate overfeeding, whereas fatty acid synthase mRNA increased by 66 and 84% (Po0.05). CONCLUSION: Whole body net DNL is not increased during carbohydrate overfeeding in overweight individuals. Stimulation of adipose lipogenic enzymes is also not higher in overweight subjects. Carbohydrate overfeeding does not stimulate whole body net DNL nor expression of lipogenic enzymes in adipose tissue to a larger extent in overweight than lean subjects.

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Postprandial de novo lipogenesis and metabolic changes induced by a high-carbohydrate, low-fat meal in lean and overweight men

Abstract: After a high-carbohydrate, low-fat meal, overweight men had a lower fat oxidation and a higher fractional hepatic fat synthesis than did lean men.

Cited by 130 publications

References 34 publications

Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis

Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis

Gln27Glu polymorphism in the beta2 adrenergic receptor gene and lipid metabolism during exercise in obese women

Effect of carbohydrate overfeeding on whole body macronutrient metabolism and expression of lipogenic enzymes in adipose tissue of lean and overweight humans

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