Enhanced dietary fat clearance in postobese women

The objective of this study was to examine the postprandial response toan exogenous fat source in eight weight-stable postobese subjects (2–3years after gastric bypass) and eight matched control women, using a stableisotope, [13C]oleate. After a high fat breakfast meal (1,062 cal, 67%fat), [13C]oleate in triglyceride (TG)-rich lipoproteins(Sf >400 and Sf 20–400) andnonesterified fatty acids (NEFA), and 13C in breath CO2,were monitored over 8 h. There were no differences in resting energyexpenditure, thermic effect of food, carbohydrate/fat oxidation ratio, breath13CO2 enrichment, or fecal fat content betweenpostobese and control subjects. Postprandially, there was no difference inSf 20–400 TG or NEFA, but postobese subjects had lowerSf >400 incremental area under the curve (AUC)(−33%, P < 0.0025) and glucose[P < 0.01 by repeated measures analysis of variance(RM ANOVA)]. Postprandial 13C in Sf >400 TGreturned to fasting levels 4 h earlier in postobese subjects and was lower thanin control subjects at 4 and 6 h (P < 0.05 by RMANOVA). The greatest difference was in the [13C]NEFA profiles. Incontrol subjects [13C]NEFA increased markedly over 8 h; postobesesubject [13C]NEFA remained close to fasting nonenriched values, andwas strikingly lower than in control subjects (72% lower by AUC,P < 0.0001 by RM ANOVA). Finally, postobesesubjects tended to have lower postprandial insulin (P <0.01, 4 h), lower postprandial acylation-stimulating protein, and lower fastingleptin (−46%, P < 0.02). This studydemonstrates clear metabolic differences in exogenous dietary fat partitioningin postobese women. These findings are compatible with an increased efficiencyof dietary fat storage and suggest one possible mechanism for promotion ofweight regain in postobese individuals. —Faraj, M., P. Jones, A. D. Sniderman, and K. Cianflone. Enhanceddietary fat clearance in postobese women. J. Lipid Res. 2001.42: 571–580. The objective of this study was to examine the postprandial response toan exogenous fat source in eight weight-stable postobese subjects (2–3years after gastric bypass) and eight matched control women, using a stableisotope, [13C]oleate. After a high fat breakfast meal (1,062 cal, 67%fat), [13C]oleate in triglyceride (TG)-rich lipoproteins(Sf >400 and Sf 20–400) andnonesterified fatty acids (NEFA), and 13C in breath CO2,were monitored over 8 h. There were no differences in resting energyexpenditure, thermic effect of food, carbohydrate/fat oxidation ratio, breath13CO2 enrichment, or fecal fat content betweenpostobese and control subjects. Postprandially, there was no difference inSf 20–400 TG or NEFA, but postobese subjects had lowerSf >400 incremental area under the curve (AUC)(−33%, P < 0.0025) and glucose[P < 0.01 by repeated measures analysis of variance(RM ANOVA)]. Postprandial 13C in Sf >400 TGreturned to fasting levels 4 h earlier in postobese subjects and was lower thanin control subjects at 4 and 6 h (P < 0.05 by RMANOVA). The greatest difference was in the [13C]NEFA profiles. Incontrol subjects [13C]NEFA increased markedly over 8 h; postobesesubject [13C]NEFA remained close to fasting nonenriched values, andwas strikingly lower than in control subjects (72% lower by AUC,P < 0.0001 by RM ANOVA). Finally, postobesesubjects tended to have lower postprandial insulin (P <0.01, 4 h), lower postprandial acylation-stimulating protein, and lower fastingleptin (−46%, P < 0.02). This studydemonstrates clear metabolic differences in exogenous dietary fat partitioningin postobese women. These findings are compatible with an increased efficiencyof dietary fat storage and suggest one possible mechanism for promotion ofweight regain in postobese individuals. —Faraj, M., P. Jones, A. D. Sniderman, and K. Cianflone. Enhanceddietary fat clearance in postobese women. J. Lipid Res. 2001.42: 571–580. Obesity, defined as a body mass index (BMI, weight divided by height squared)exceeding 30 kg/m2, is common in Western countries and is associated withdecreased longevity and increased morbidity (1Hodge A.M. Zimmet P.Z. The epidemiology of obesity.Baillieres Clin. Endocrinol. Metab. 1994; 8: 577-599Google Scholar).Weight loss decreases morbidity and mortality in the obese (2Williamson D.F. Pamuk E. Thun M. Flanders D. Byers T. Heath C. Prospective study of intentional weightloss and mortality in never-smoking overweight US white women aged40–64 years.Am. J.Epidemiol. 1995; 141 ([published erratum appears in Am. J. Epidemiol. 1995;142: 369]): 1128-1141Google Scholar), but most obese individuals who lose a significant amount ofweight tend to regain it (3Prentice A.M. Obesity—the inevitable penalty ofcivilisation.Br. MedBull. 1997; 53: 229-237Google Scholar). There are twoschools of thought regarding weight regain. On the one hand, there are those who proposethat genetically determined lower setpoints in basal metabolic rate (BMR), thermiceffect of food (TEF), decreased fat/carbohydrate oxidation rate, or increased insulinsensitivity predispose postobese individuals to regain weight (4Astrup A. Dietary composition, substrate balances andbody fat in subjects with a predisposition to obesity.Int. J. Obes. Relat. Metab. Disord. 1993; 17: S32-S36Google Scholar, 5Astrup A. Buemann B. Christensen N.J. Toubro S. Failure to increase lipid oxidation inresponse to increasing dietary fat content in formerly obesewomen.Am. J. Physiol. 1994; 266: E592-E599Google Scholar, 6Franssila-Kallunki A. Rissanen A. Ekstrand A. Ollus A. Groop L. Effects of weight loss on substrateoxidation, energy expenditure, and insulin sensitivity in obeseindividuals.Am. J. Clin.Nutr. 1992; 55: 356-361Google Scholar, 7Ranneries C. Bulow J. Buemann B. Christensen N.J. Madsen J. Astrup A. Fat metabolism in formerly obesewomen.Am. J. Physiol. 1998; 274: E155-E161Google Scholar, 8Shah M. Miller D.S. Geissler C.A. Lower metabolic rates of post-obese versus lean women:thermogenesis, basal metabolic rate and genetics.Eur. J. Clin. Nutr. 1988; 42: 741-752Google Scholar). On the other hand, there are those who believe that obesity and regaining lostweight result, quite simply, from overeating and decreased physical activity (9Hervey G.R. Regulation of energy balance.Nature. 1969; 222: 629-631Google Scholar, 10Weinsier R.L. Nelson K.M. Hensrud D.D. Darnell B.E. Hunter G.R. Schutz Y. Metabolic predictors of obesity.Contribution of resting energy expenditure, thermic effect of food, and fuelutilization to four-year weight gain of post-obese and never-obesewomen.J. Clin. Invest. 1995; 95: 980-985Google Scholar). In aprospective study of premenopausal obese women, mean BMR, TEF, and fasting andpostprandial substrate oxidation decreased after weight loss to normal BMI.Nevertheless, the subjects were not significantly different from matched never-obesesubjects (10Weinsier R.L. Nelson K.M. Hensrud D.D. Darnell B.E. Hunter G.R. Schutz Y. Metabolic predictors of obesity.Contribution of resting energy expenditure, thermic effect of food, and fuelutilization to four-year weight gain of post-obese and never-obesewomen.J. Clin. Invest. 1995; 95: 980-985Google Scholar). In other studies, neither the 24-henergy expenditure, carbohydrate/fat oxidation rate (11Burstein R. Prentice A.M. Goldberg G. Murgatroyd P.R. Harding M. Coward W.A. Metabolic fuel utilisation in obese women before and afterweight loss.Int. J. Obes. Relat. Metab.Disord. 1995; 20: 253-259Google Scholar), TEF, nor energy expenditure during various controlled daily activitieswas different from those of matched never-obese subjects (12dePeuter R. Withers R.T. Brinkman M. Tomas F.M. Clark D.G. No differences in rates of energy expenditure betweenpost-obese women and their matched, lean controls.Int. J. Obes. Relat. Metab. Disord. 1992; 16: 801-808Google Scholar). Discrepancies among studies may be attributed to differencesin body composition, meal size and composition, and length of study (13Raben A. Christensen N.J. Astrup A. Postprandial responses in substrateoxidation and appetite in post-obese subjects.Int. J. Obes. Relat. Metab. Disord. 1993; 17: S37-S40Google Scholar, 14Reed G.W. Hill J.O. Measuring the thermic effect of food.Am. J. Clin. Nutr. 1996; 63: 164-169Google Scholar). Clearly, there are opposing beliefs regarding the causes underlying thepronounced tendency of the postobese to regain weight. We have investigated thisquestion from the perspective of postprandial fat metabolism and three specific hormonesthat influence this process: acylation-stimulating protein (ASP), insulin, andleptin. ASP is a 76-amino acid basic protein, with a mass of 8,933 Da, which has beenidentified in human plasma. ASP markedly increases triglyceride (TG) synthesis throughenhanced fatty acid esterification and glucose transport in human adipocytes and skinfibroblasts (15Baldo A. Sniderman A.D. St-Luce S. Avramoglu R.K. Maslowska M. Hoang B. Monge J.C. Bell A. Mulay S. Cianflone K. The adipsin-acylation stimulating proteinsystem and regulation of intracellular triglyceridesynthesis.J. Clin.Invest. 1993; 92: 1543-1547Google Scholar, 16Cianflone K. Kwiterovich Jr., P.O. Walsh M. Forse M. Rodriguez M.A. Sniderman A.D. Stimulation of fatty acid uptake and triglyceride synthesisin human cultured skin fibroblasts and adipocytes by a serumprotein.Biochem. Biophys. Res.Commun. 1987; 144: 94-100Google Scholar, 17Cianflone K. Sniderman A.D. Walsh M.J. Vu H. Gagnon J. Rodriguez M.A. Purification and characterization of acylation stimulatingprotein.J. Biol. Chem. 1989; 264: 426-430Google Scholar, 18Cianflone K. Maslowska M. Sniderman A.D. Acylation stimulating protein (ASP), an adipocyte autocrine:new directions.Semin. Cell Dev.Biol. 1999; 10: 31-41Google Scholar, 19Germinario R. Sniderman A.D. Manuel S. Pratt S. Baldo A. Cianflone K. Coordinate regulation of triacylglycerolsynthesis and glucose transport by acylation stimulatingprotein.Metabolism. 1993; 42: 574-580Google Scholar, 20Tao Y. Cianflone K. Sniderman A.D. Colby-Germinario S.P. Germinario R.J. Acylation-stimulating protein (ASP) regulates glucosetransport in the rat L6 muscle cell line.Biochim. Biophys. Acta. 1997; 1344: 221-229Google Scholar). ASP is identical to complement C3-derived activation and is the of complement and with of which are and by K. Maslowska M. Baldo A. J. Sniderman A.D. The acylation stimulating protein in regulation of 1994; Scholar, K. Maslowska M. of human J. Clin.Invest. 1995; ASP levels in the tend to S. T. The influence of lipid stimulating protein (ASP) in J. Obes. Relat. Metab. Disord. 1998; Scholar, J. Cianflone K. Sniderman A.D. of acylation stimulating protein clearance by human in the postprandial Lipid Res. 1998; Scholar), ASP increases in the at h J. Cianflone K. Sniderman A.D. of acylation stimulating protein clearance by human in the postprandial Lipid Res. 1998; Scholar). a ASP difference and fatty acid uptake J. Cianflone K. Sniderman A.D. of acylation stimulating protein clearance by human in the postprandial Lipid Res. 1998; Scholar). On fasting ASP is in obesity than with weight loss K. Sniderman A.D. D. R. of ASP to a J. Obes. 1995; Scholar, M. Vu H. S. Sniderman A.D. D. Cianflone K. acylation stimulating and in and obese J. Clin. Invest. 1999; Scholar, A.D. Cianflone K. of acylation stimulating protein in obese women after weight loss.Int. Scholar). insulin increases and fasting insulin levels increase in has that in postobese sensitivity may be but the are and C. Bulow J. Buemann B. Christensen N.J. Madsen J. Astrup A. Fat metabolism in formerly obesewomen.Am. J. Physiol. 1998; 274: E155-E161Google a sensitivity in postobese women as never-obese control the in earlier studies significant difference (4Astrup A. Dietary composition, substrate balances andbody fat in subjects with a predisposition to obesity.Int. J. Obes. Relat. Metab. Disord. 1993; 17: S32-S36Google Scholar, S. Western P. Bulow J. A. Christensen N.J. Madsen J. Astrup A. sensitivity in 1994; Scholar). The objective of the study was to examine postobese weight with never-obese differences in postprandial fat resting TEF, carbohydrate/fat oxidation rate, and metabolic in the of for the control and postobese were to the women, with and normal of NEFA, high glucose as defined and no of or or not that metabolism 6 of the and for 6 before the study loss or gain the never-obese subjects had no of obesity or and the obese subjects had no for at 6 before the subjects were the of subjects had obese and had gastric before the study and were weight subjects subjects an and the study was by the The control subjects were to for body area body ratio, and of physical were the was of the control fat was by be by the of the body K.M. M.J. S. Hunter G.R. R.L. in human body J. Clin.Nutr. 1988; Scholar). as not to an to subjects were not to in or for before of body the subjects were and after this as and at their and energy expenditure is at M.A. in energy expenditure during the J. Nutr. 1989; Scholar, P. energy expenditure and the J. Clin. Nutr. Scholar). this was to of in on and energy expenditure in On the study the subjects in at 8 after fasting and substrate oxidation rate were were the subjects were the to of the daily This energy meal was to an fat and energy meal of daily fat is A. E. The of dietary fat J. Obes. Relat. Metab.Disord. 1997; Scholar). The high fat breakfast meal of an with and white meal weight was and the analysis was on the of the on the food with a for a The high fat meal of energy was protein and fat that was other The high fat meal was of [13C]oleate was as the dietary fat it most fatty acid in dietary fat M. in and Scholar), TG and The of from other human Scholar), and metabolism is other fatty acids M. The of and in lipid Nutr. 1994; 53: Scholar). was over the of were to the the breakfast meal was of and of with no during food or after in gastric in the postobese and of gastric 1994; Scholar, S. P. after J. 1988; Scholar). the subjects were to but to a and to on a after the subjects from were monitored during and After the the subjects were to of physical activity on postprandial increase in be attributed to the After the of food postprandial energy expenditure, and substrate oxidation rate at and 8 in to the fasting the study the subjects were not to or food or for and one of with no or fat were at a from postobese women and fat content body fat was determined at fasting with analysis was as the and the the was at the over the P.R. M.J. and to in Nutr. Clin.Nutr. Scholar). The was by over was on the ofweight and using the Y. J. R. of body Clin. 1992; Scholar). was for using a and After a over at and 8 h. The was of energy expenditure of the Scholar). was to be an of Y. A. R.L. Nelson K.M. of fat oxidation in the of in obese J. Clin.Nutr. 1992; 55: Scholar). oxidation of and protein were by as the carbohydrate/fat oxidation The of the of and substrate oxidation was as the area under the curve of with the basal were at and 8 was at for were at for insulin, The was for the and and ASP was by a as and a as in J. Cianflone K. Sniderman A.D. of acylation stimulating protein clearance by human in the postprandial Lipid Res. 1998; Scholar, M. Vu H. S. Sniderman A.D. D. Cianflone K. acylation stimulating and in and obese J. Clin. Invest. 1999; Scholar), with of of was in for human insulin was by was in by a >400 and Sf 20–400) by at for 30 and at for h R. H. J. The and in human Clin. Invest. Scholar). The was for and Sf 20–400 TG were by was by a and in fasting by a was to Miller M. S. and of of human by a Lipid Res. by was to as by and G. M. in and Chem. 1996; 42: Scholar). by after the were was a of body oxidation of dietary fatty J. Clin.Nutr. 42: Scholar). were for of 13C was by of of acid of in a body oxidation of dietary fatty J. Clin.Nutr. 42: Scholar). were to a mass for 13C In is with a The is defined to be and and of Scholar). The was with of of 13C was to the C. M. C. M. of to study triglyceride metabolism 1995; the at in breath was as a of 13C in breath was to T. Jr., 13C of and of in 13C of for breath J. Clin. Nutr. [13C]oleate is the mass of is the [13C]oleate P is 13C is the of the and is to for the uptake of the for the R.J. in Scholar). 13C was in >400 and Sf 20–400 were with The was and in and and TG by on using acid as were with and were were and and and were were under at a of than TG were at for 4 h. The and were by a was a in a body oxidation of dietary fatty J. Clin.Nutr. 42: Scholar). were in h. was for breath C. M. C. M. of to study triglyceride metabolism 1995; in of the three Sf 20–400 and was as of TG or in that were from postobese women on a and for fecal fat content by the acid acid is a and to fecal fat with a sensitivity of and of with the fecal fat a 1997; 92: Scholar). In the were by and with acid The was and the fatty and The normal is a 1997; 92: Scholar, M. P. A. J. B. R. The acid a 1994; Scholar, A. J. M. of 1997; Scholar). are as were by by repeated measures analysis of RM using analysis was with the or to the and the mean difference was fasting and was by was at P < of the postobese and control subjects are had gastric the and had for at 6 before the of the fasting were significantly different the which was significantly in the < 0.02). The fat meal was the postobese women nor the control subjects or which are associated with or and of gastric 1994; Scholar, S. P. after J. 1988; of the control and postobese body mass < postobese versus were for control and postobese acylation-stimulating body mass fatty high are as P < postobese versus in a were for control and postobese acylation-stimulating body mass fatty high are as metabolism was in the there was in basal or the 8 postobese and The carbohydrate/fat oxidation is in were to the carbohydrate/fat oxidation as the There was difference in the mean of the carbohydrate/fat oxidation the postobese subjects and the control We at in of and glucose over the of the fat in there was an increase TG by h increase of postobese which decreased to fasting was the of Sf >400 the greatest differences the in the Sf >400 there was no mean >400 TG to earlier in 8 with significantly lower Sf >400 6 h (P 0.02). Sf >400 incremental was lower in h in control h in P < The Sf 20–400 were the in and glucose are in In postobese and control a in at h (P < 0.05 fasting for increases over the but there was difference postobese and control subjects. On the other was a difference in postprandial glucose postobese subjects over the of the study (P the post-obese had lower glucose as in at and 4 h The for in the and breath in 4 and In the 13C there was of postprandial TG to fasting nonenriched levels in women 8 4 control with the postobese at 4 and 6 h (P < RM ANOVA). there was difference in the 13C postobese and control to a at 4 h and decreased basal with a lower in the and 13C in in control and postobese subjects. After the fat [13C]oleate in and 13C in were at for subjects and eight postobese women are as the at P < 0.0001 for postobese subjects and at 6 and 8 h for [13C]NEFA RM P < 0.01 for control subjects at 8 h for 13C in The most difference was in the of in the in the [13C]oleate increased control a at there was in the of [13C]oleate in the of the dietary TG the (P < RM postobese [13C]NEFA was by in the postobese versus subjects h in postobese h in P This that the by activity are a for storage or the breath is a of as in a increase in breath in over the 8 there was no difference the at 8 at which in breath was lower in women (P < The analysis of the TG mass and the was no difference in of the fat the the fat analysis in the postobese that had normal acid values, with an of the normal is This normal in the postobese women. The is by to which the or The with other acid that has the by has not by In this the are and and uptake is 6 for and [13C]NEFA in the control and postobese subjects. The for the In the control the [13C]NEFA of the in the postobese it is (P The differences to a the and the of the postobese with the Finally, postprandial responses of to in TG insulin and ASP levels of were not different the Postprandially, ASP levels decreased over the to a at 8 h in postobese h in was a for a lower postprandial ASP in the postobese the difference significant the to insulin, there was in insulin at h in (P < there was an earlier to basal levels at 4 h in at which it was significantly lower than in the control ASP and insulin and fasting fasting and postprandial and the significant in with fasting and [13C]NEFA with fasting TG as as with TG Sf >400 and but not with glucose not with ASP as with fasting >400 NEFA, and and Sf >400 TG and with postprandial of ASP and insulin to postprandial >400 20–400 and are for under the curve insulin and fasting for control and eight postobese in a and are for under the curve insulin and fasting for control and eight postobese divided as to obesity to of energy expenditure and fatty acid oxidation (4Astrup A. Dietary composition, substrate balances andbody fat in subjects with a predisposition to obesity.Int. J. Obes. Relat. Metab. Disord. 1993; 17: S32-S36Google Scholar, 5Astrup A. Buemann B. Christensen N.J. Toubro S. Failure to increase lipid oxidation inresponse to increasing dietary fat content in formerly obesewomen.Am. J. Physiol. 1994; 266: E592-E599Google Scholar, 6Franssila-Kallunki A. Rissanen A. Ekstrand A. Ollus A. Groop L. Effects of weight loss on substrateoxidation, energy expenditure, and insulin sensitivity in obeseindividuals.Am. J. Clin.Nutr. 1992; 55: 356-361Google Scholar, 7Ranneries C. Bulow J. Buemann B. Christensen N.J. Madsen J. Astrup A. Fat metabolism in formerly obesewomen.Am. J. Physiol. 1998; 274: E155-E161Google Scholar, 8Shah M. Miller D.S. Geissler C.A. Lower metabolic rates of post-obese versus lean women:thermogenesis, basal metabolic rate and genetics.Eur. J. Clin. Nutr. 1988; 42: 741-752Google Scholar, G.R. Regulation of energy balance.Nature. 1969; 222: 629-631Google Scholar, R. Prentice A.M. Goldberg G. Murgatroyd P.R. Harding M. Coward W.A. Metabolic fuel utilisation in obese women before and afterweight loss.Int. J. Obes. Relat. Metab.Disord. 1995; 20: 253-259Google Scholar, Y. R. M. M. L. of the obese and 1994; Scholar). has to the obesity may be the of fatty acid The study suggest at in this may and may mechanism in the of the This from in the there was clearance TG from the of the postobese women as with the and [13C]oleate in the postobese than in the control findings with fatty acid by in the with the control women. The subjects in postobese had gastric than before the weight had the normal and were weight for at 6 at of this The control subjects were to there were in body ratio, and the the difference the that the of one had a of obesity and gastric those of the other the of the the on fat be In and in not Metabolic of obesity J. Clin.Nutr. 1992; 55: Scholar, study of Scholar, for Scholar, rate after gastric 1987; Scholar), most of the of the On the other hand, after may from and of gastric 1994; Scholar, M. Harding M.J. Walsh of gastric after gastric Scholar). This after high with M. Harding after gastric J. Obes. 10: was of subjects had of and after the meal in this which to this and of gastric 1994; Scholar). the had normal fecal fat content and differences in fat for The is that over the of the study no of significant difference in energy expenditure the fatty acid was not in the postobese there was no difference in fasting TG the differences in clearance and of dietary be attributed to this and believe that is a There were differences in postprandial clearance of TG the but were not postprandial TG not the postprandial Sf >400 to fasting levels earlier in the postobese the control This was for the Sf >400 levels 4 h earlier in the postobese there was no in the the of TG is a suggest that of by may be increased and it has that increases after weight loss B. J. The of weight loss on the of in J. Scholar, of activity Clin.Invest. Scholar, in in J. Obes. 1995; Scholar). The the of the fatty acids that are from the which be or the or The with to the of dietary fatty the the postobese with the control was three in the postobese than control subjects. the [13C]oleate was three in the control subjects with the with those by C. C. M. M. R. M. Metabolic of an in 1996; Scholar, C. C. M. D. J. P. M. of human obesity on of dietary and J. Clin.Nutr. 1998; their study of postprandial fatty acid metabolism in obese women weight women. the On the other hand, no differences in the metabolism of levels of insulin, and were in this insulin and ASP there was a lower fasting and in the postobese subjects with the control subjects. the glucose levels and of fatty acid in it is possible that lower levels to as is the in are not is of that the levels were lower in the postobese subjects than in the this to regain weight to In to fatty acid by in postobese subjects and the that an be in the of studies are to a This was by the of and Cianflone is from the of of

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