Overfeeding...

[Emma-Leigh]

Posting a bunch of research on the topic.....


http://www.ajcn.org/cgi/content/full/74/6/737
American Journal of Clinical Nutrition, Vol. 74, No. 6, 737-746, December 2001
? 2001 American Society for Clinical Nutrition
Original Research Communication

De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women1,2,3

Regina M McDevitt, Sarah J Bott, Marilyn Harding, W Andrew Coward, Leslie J Bluck and Andrew M Prentice

Background: The results of previous studies suggest that de novo lipogenesis may play an important role in the etiology of obesity, particularly during overconsumption of different carbohydrates.

Objective: We hypothesized that de novo lipogenesis would increase during overfeeding, would vary depending on the type of carbohydrate consumed, and would be greater in obese than in lean women.

Design: De novo lipogenesis was measured during 96 h of overfeeding by 50% with either sucrose or glucose and during an energy balance treatment (control) in 8 lean and 5 obese women. De novo lipogenesis was determined by measuring the amount of deuterium incorporation into plasma triacylglycerols. Fat and carbohydrate balance were measured simultaneously by continuous whole-body calorimetry.

Results: De novo lipogenesis did not differ significantly between lean and obese subjects, except with the control treatment, for which de novo lipogenesis was greater in the obese subjects. De novo lipogenesis was 2- to 3-fold higher after overfeeding by 50% than after the control treatment in all subjects. The type of carbohydrate overfeeding (sucrose or glucose) had no significant effect on de novo lipogenesis in either subject group. Estimated amounts of absolute VLDL production ranged from a minimum of 2 g/d (control) to a maximum of 10 g/d after overfeeding. This compares with a mean fat balance of 275 g after 96 h of overfeeding. Individual subjects showed characteristic amounts of de novo lipogenesis, suggesting constitutive (possibly genetic) differences.

Conclusion: De novo lipogenesis increases after overfeeding with glucose and sucrose to the same extent in lean and obese women but does not contribute greatly to total fat balance.

Key Words: De novo lipogenesis ? deuterium ? overfeeding ? carbohydrate ? glucose ? sucrose ? lean women ? obese women ? calorimetry



http://www.ajcn.org/cgi/content/abstract/62/1/19

American Journal of Clinical Nutrition, Vol 62, 19-29, Copyright ? 1995 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

Fat and carbohydrate overfeeding in humans: different effects on energy storage

TJ Horton, H Drougas, A Brachey, GW Reed, JC Peters and JO Hill
Center for Human Nutrition, University of Colorado Health Sciences Center, Denver 80262, USA.

Both the amount and composition of food eaten influence body-weight regulation. The purpose of this study was to determine whether and by what mechanism excess dietary fat leads to greater fat accumulation than does excess dietary carbohydrate. We overfed isoenergetic amounts (50% above energy requirements) of fat and carbohydrate (for 14 d each) to nine lean and seven obese men. A whole-room calorimeter was used to measure energy expenditure and nutrient oxidation on days 0, 1, 7, and 14 of each overfeeding period. From energy and nutrient balances (intake-expenditure) we estimated the amount and composition of energy stored. Carbohydrate overfeeding produced progressive increases in carbohydrate oxidation and total energy expenditure resulting in 75-85% of excess energy being stored. Alternatively, fat overfeeding had minimal effects on fat oxidation and total energy expenditure, leading to storage of 90-95% of excess energy. Excess dietary fat leads to greater fat accumulation than does excess dietary carbohydrate, and the difference was greatest early in the overfeeding period.


http://www.ajcn.org/cgi/content/abstract/56/5/857

American Journal of Clinical Nutrition, Vol 56, 857-862, Copyright ? 1992 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

Overfeeding and energy expenditure in humans

A Tremblay, JP Despres, G Theriault, G Fournier and C Bouchard
Physical Activity Sciences Laboratory, Laval University, Ste-Foy, Quebec, Canada.

The effect of overfeeding on energy expenditure was investigated in 23 young men subjected to a 353-MJ energy intake surplus over 100 d. The major part of this excess (222 MJ) was stored as body energy. The increase in energy cost of weight maintenance amounted to 52 MJ and was proportional to body weight gain. When it was added to the obligatory cost of fat and fat-free mass gains, the overall increase in energy expenditure amounted to a mean of 100 MJ. Four months after overfeeding, subjects had lost 82%, 74%, and 100% of the overfeeding gain in body weight, fat mass, and fat-free mass, respectively. We conclude that 1) in response to overfeeding, two-thirds of the excess energy intake is stored as body energy; 2) overfeeding induces an increase in energy cost of weight maintenance proportional to body weight gain, and 3) preoverfeeding energy balance tends to be restored when nonobese individuals return to their normal daily-life habits.



http://www.ajcn.org/cgi/content/abstract/56/4/641

American Journal of Clinical Nutrition, Vol 56, 641-655, Copyright ? 1992 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

Metabolic response to experimental overfeeding in lean and overweight healthy volunteers

EO Diaz, AM Prentice, GR Goldberg, PR Murgatroyd and WA Coward
Dunn Clinical Nutrition Centre, Cambridge, UK.

Possible adaptive mechanisms that may defend against weight gain during periods of excessive energy intake were investigated by overfeeding six lean and three overweight young men by 50% above baseline requirements with a mixed diet for 42 d [6.2 +/- 1.9 MJ/d (mean +/- SD), or a total of 265 +/- 45 MJ]. Mean weight gain was 7.6 +/- 1.6 kg (58 +/- 18% fat). The energy cost of tissue deposition (28.7 +/- 4.4 MJ/kg) matched the theoretical cost (26.0 MJ/kg). Basal metabolic rate (BMR) increased by 0.9 +/- 0.4 MJ/d and daily energy expenditure assessed by whole-body calorimetry (CAL EE) increased by 1.8 +/- 0.5 MJ/d. Total free-living energy expenditure (TEE) measured by doubly labeled water increased by 1.4 +/- 2.0 MJ/d. Activity and thermogenesis (computed as CAL EE--BMR and TEE--BMR) increased by only 0.9 +/- 0.4 and 0.9 +/- 2.1 MJ/d, respectively. All outcomes were consistent with theoretical changes due to the increased fat-free mass, body weight, and energy intake. There was no evidence of any active energy-dissipating mechanisms.


http://www.ajcn.org/cgi/content/abstract/56/3/483

American Journal of Clinical Nutrition, Vol 56, 483-490, Copyright ? 1992 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

Massive overfeeding and energy balance in men: the Guru Walla model

P Pasquet, L Brigant, A Froment, GA Koppert, D Bard, I de Garine and M Apfelbaum
CNRS UPR263: Anthropologie de l'Alimentation, Paris, France.

To determine the magnitude of the thermogenic response to a massive long-term overfeeding, an energy-balance study was carried out in nine lean, young Cameroonian men participating in a traditional fattening session: the Guru Walla. Food intake, body weight, body composition, activity, and metabolic rates were recorded during a 10-d baseline period and over the 61-65 d of fattening. Total energy expenditure (TEE) was measured by using doubly labeled water during the baseline period and the final 10 d of Guru Walla. Cumulative overfeeding consisted of 955 +/- 252 MJ (chi +/- SD) mainly as carbohydrate. Body- weight increase was 17 +/- 4 kg, 64-75% as fat. Metabolic rates increased but TEE did not. However, when accounting for the reduction in physical activity, substantial thermogenesis was observed but its amplitude was not greater than that observed under less extreme carbohydrate-overfeeding conditions. If luxuskonsumption does exist, it is not related to the magnitude of the cumulative overfeeding.

[Emma-Leigh]

More....


http://www.ajcn.org/cgi/content/abstract/33/5/978

American Journal of Clinical Nutrition, Vol 33, 978-988, Copyright ? 1980 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

The effect of 6 weeks of overfeeding on the body weight, body composition, and energy metabolism of young men

NG Norgan and JV Durnin

The effect of overfeeding on the body weight, body fat, water content, energy expenditure, and digestibility of energy and nitrogen was investigated over 42 days in six young men. The metabolic rates in standard situations of work and rest were determined. Energy intakes were apparently increased by 6.2 MJ/day and energy expenditure fell slightly by 0.3 MG/day during overfeeding. Fecal and urinary losses of energy were a similar proportion of the gross energy intake in control and overfeeding periods (8%). Metabolizable energy intakes calculated from food tables agreed well with values derived from digestibility measurements in the control period (mean difference = +2%) but not in the overfeeding period (+8%). The implications of this are discussed. Mean body weight gain was 6.0 kg, 10% of initial weight; mean fat gain was 3.7 kg and water gain 1.8 liter. There were considerable interindividual differences in the weight and fat gain for a given excess energy intake. Metabolic rates in standard tasks were 10% higher at the end of overfeeding but expressed as kilojoules per kilogram per minute were similar to control values. Mean energy gain (144 MJ = fat gain X 39 kJ/g) was less than excess energy intake even allowing for overestimation of intakes using food tables and increases in metabolic rate. Such a discrepancy is unlikely to be due to unmeasured increases in metabolic rate but could have arisen from errors in the calculation of the variables involved. In this study where moderate weight gains were achieved by overfeeding mainly fat, increases in metabolic rate appear to be associated with increased body size and tissue gain rather than a luxuskonsumption mechanism.


http://jcem.endojournals.org/cgi/content/abstract/91/4/1462

Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2005-1598
The Journal of Clinical Endocrinology & Metabolism Vol. 91, No. 4 1462-1469
Copyright ? 2006 by The Endocrine Society

Fat Oxidation before and after a High Fat Load in the Obese Insulin-Resistant State

Ellen E. Blaak, Gabby Hul, Camilla Verdich, Vladimir Stich, Alfredo Martinez, Martin Petersen, Edith F. M. Feskens, Kishor Patel, Jean Michel Oppert, Pierre Barbe, S?ren Toubro, Ingalena Anderson, Jan Polak, Arne Astrup, Ian A. Macdonald, Dominique Langin, Claus Holst, Thorkild I. S?rensen, Wim H. M. Saris and the Consortium for Nutrient-Gene Interactions in Human Obesity?Implications for Dietary Guidelines
Department of Human Biology, Nutrition and Toxicology Research Centre NUTRIM (E.E.B., G.H., W.H.M.S.), Maastricht University, Maastricht, The Netherlands; Department of Health and Nutrition (E.F.M.F.), National Institute of Public Health and the Environment, Bilthoven, The Netherlands; Institute of Preventive Medicine (C.V., C.H., T.I.S.), Danish Epidemiology Science Centre, Copenhagen University Hospital, Copenhagen, Denmark; Department of Sports Medicine (V.S., J.P.), Centre of Preventive Medicine, Third Faculty of Medicine, Charles University, Prague, Czech Republic; Department of Physiology and Nutrition (A.M.), University of Navarra, Pamplona, Spain; Institute of Human Nutrition (M.P., S.T., A.A.), The Royal Veterinary and Agricultural University, Copenhagen, Denmark; School of Biomedical Sciences (K.P., I.A.M.), Queens Medical Centre, University of Nottingham Medical School, Nottingham, United Kingdom; Department of Nutrition (J.M.O.), H?tel-Dieu Hospital, Paris, France; Obesity Research Unit of the French Institute of Health and Medical Research U586 (P.B., D.L.), Louis Bugnard Institute and Clinical Investigation Centre, Toulouse University Hospitals, Paul Sabatier University, Toulouse, France; and Department of Medicine (I.A.), Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden

Address all correspondence and requests for reprints to: Dr. E. E. Blaak, Department of Human Biology, Nutrition Research Centre, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. E-mail: e.blaak@hb.unimaas.nl.

Background: Obesity may be associated with a lowered use of fat as a fuel, which may contribute to the enlarged adipose tissue stores.

Aim: The aim of the present study was to study fatty acid use in the fasting state and in response to a high fat load in a large cohort of obese subjects (n = 701) and a lean reference group (n = 113).

Methods: Subjects from eight European centers underwent a test meal challenge containing 95 en% fat [energy content 50% of estimated resting energy expenditure (EE)]. Fasting and postprandial fat oxidation and circulating metabolites and hormones were determined over a 3-h period.

Results: Postprandial fat oxidation (as percent of postprandial EE, adjusted for fat mass, age, gender, center, and energy content of the meal) decreased with increasing body mass index (BMI) category (P < 0.01), an effect present only in those obese subjects with a relatively low fasting fat oxidation (below median, interaction BMI category x fasting fat oxidation, P < 0.001). Fasting fat oxidation increased with increasing BMI category (P < 0.001), which was normalized after adjustment for fat-free mass and fat mass. Furthermore, insulin resistance was positively associated with postprandial fat oxidation (P < 0.05) and negatively associated with fasting fat oxidation (expressed as percent of EE), independent of body composition.

Conclusions: The present data indicate an impaired capacity to regulate fat oxidation in the obese insulin-resistant state, which is hypothesized to play a role in the etiology of both obesity and insulin resistance.



http://www.ajcn.org/cgi/content/abstract/73/2/253

American Journal of Clinical Nutrition, Vol. 73, No. 2, 253-261, February 2001
? 2001 American Society for Clinical Nutrition
Original Research Communication

Postprandial de novo lipogenesis and metabolic changes induced by a high-carbohydrate, low-fat meal in lean and overweight men1,2,3

Iva Marques-Lopes, Diana Ansorena, Iciar Astiasaran, Luis Forga and J Alfredo Mart?nez
1 From the Departments of Physiology and Nutrition and of Food Science, University of Navarra, Pamplona, Spain.

Background: Adjustments of carbohydrate intake and oxidation occur in both normal-weight and overweight individuals. Nevertheless, the contribution of carbohydrates to the accumulation of fat through either reduction of fat oxidation or stimulation of fat synthesis in obesity remains poorly investigated.

Objective: The objective of this study was to assess the postprandial metabolic changes and the fractional hepatic de novo lipogenesis (DNL) induced by a high-carbohydrate, low-fat meal in lean and overweight young men.

Design: A high-carbohydrate, low-fat meal was administered to 6 lean and 7 overweight men after a 17.5-h fast. During the fasting and postprandial periods, energy expenditure (EE), macronutrient oxidation, diet-induced thermogenesis, and serum insulin, glucose, triacylglycerol, and fatty acids were measured. To determine DNL, [1-13C]sodium acetate was infused and the mass isotopomer distribution analysis method was applied.

Results: After intake of the high-carbohydrate meal, the overweight men had hyperinsulinemia and higher fatty acid and triacylglycerol concentrations than did the lean men. The overweight group showed a greater EE, whereas there was no significant difference in carbohydrate oxidation between the groups. Nevertheless, the overweight men had a marginally higher protein oxidation and a lower lipid oxidation than did the lean men. DNL was significantly higher before and after meal intake in the overweight men and was positively associated with fasting serum glucose and insulin concentrations. Furthermore, postprandial DNL was positively correlated with body fat mass, EE, and triacylglycerol.

Conclusion: 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.



http://jap.physiology.org/cgi/content/abstract/90/1/155

J Appl Physiol 90: 155-163, 2001;
8750-7587/01
Vol. 90, Issue 1, 155-163, January 2001

Prolonged fasting significantly changes nutrient oxidation and glucose tolerance after a normal mixed meal

Tracy J. Horton and James O. Hill
Center for Human Nutrition and Department of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado 80262

The aim of this study was to establish the experimental paradigm of fasting, followed by refeeding, to investigate individual differences in nutrient partitioning. Eight nonobese men were fed a normal meal (25% of daily energy requirements) on two occasions, after an overnight (13-h) fast and after a prolonged (72-h) fast. During the entire fasting period, subjects were resident in a whole room indirect calorimeter, and blood samples were drawn periodically. Because no other food was consumed over the 12 h after either meal, negative energy balance was observed after the overnight and prolonged fast. Postprandial carbohydrate oxidation was significantly reduced after the 72- vs. 13-h fast (P < 0.0001), whereas fat oxidation was significantly increased (P < 0.0001). Interestingly, carbohydrate balance was positive after the prolonged fast but negative after the overnight fast (24 ? 17 vs. 57 ? 16 g/12 h, respectively; P < 0.001), whereas fat balance was negative under both conditions (78 ? 7 vs. 47 ? 8 g/12 h, respectively; P < 0.002). With 72 h of fasting, the glucose and insulin excursions in response to the mixed meal were significantly greater compared with the 13-h fast (P < 0.001). In conclusion, prolonged fasting resulted in a significant decrease in carbohydrate oxidation and an increase in fat oxidation, after a normal mixed meal, in healthy men. This was associated with a significant decrease in glucose tolerance. Because circulating free fatty acids were greatly elevated at all times after the prolonged fast, these may be mediating some of the changes in postprandial metabolism.

[Emma-Leigh]

and again....


http://ajpendo.physiology.org/cgi/content/abstract/294/2/E416

Am J Physiol Endocrinol Metab 294: E416-E424, 2008. First published November 27, 2007; doi:10.1152/ajpendo.00573.2007

Efficiency of autoregulatory homeostatic responses to imposed caloric excess in lean men

Mario Siervo,1 Gema Fr?hbeck,2 Adrian Dixon,3 Gail R. Goldberg,1 W. Andy Coward,1 Peter R. Murgatroyd,4 Andrew M. Prentice,5 and Susan A. Jebb1
1Medical Research Council Human Nutrition Research, Elsie Widdowson Laboratory, Cambridge, United Kingdom; 2Department of Endocrinology, Cl?nica Universitaria de Navarra, Pamplona, Spain; 3Department of Radiology and 4Wellcome Trust Clinical Research Facility, University of Cambridge, Addenbrooke's Hospital, Cambridge; and 5Medical Research Council International Nutrition Group, London School of Hygiene and Tropical Medicine, London, United Kingdom

Submitted 5 September 2007 ; accepted in final form 23 November 2007

Obesity implies a failure of autoregulatory homeostatic responses to caloric excess. We studied the mechanisms, effectiveness, and limits of such responses in six lean (21.9 ? 1.3 kg/m2), healthy men based in a metabolic suite for 17 wk of progressive intermittent overfeeding (OF) (3 wk, baseline; 3 wk, 20% OF; 1 wk, ad libitum; 3 wk, 40% OF; 1 wk, ad libitum; 3 wk, 60% OF; 3 wk, ad libitum). Body composition was assessed by a four-compartment model using dual X-ray absorptiometry, deuterium dilution, and plethysmography. Magnetic resonance imaging assessed subcutaneous/visceral fat at abdominal level at baseline and at the end of 60% OF. Energy intake was assessed throughout, energy expenditure (EE) and substrate oxidation rates were measured repeatedly by whole body calorimetry (calEE), and free-living EE (TEE) was measured by doubly labeled water at baseline and after 60% OF. At the end of 60% OF, calEE and TEE had increased by just 11.4% (P = 0.001) and 16.2% (P = 0.001), respectively. Weight and body fat (fat mass) had increased by 5.98 kg (8.8%, P = 0.001) and 3.31 kg (22.6%, P = 0.01), respectively. The relative increase in visceral fat (32.6%, P = 0.02) exceeded that of subcutaneous fat (13.3%, P = 0.002) in the abdominal region. The computed energy cost of tissue accretion differed from the excess ingested by only 13.1% (using calEE) and 11.6% (using TEE), indicating an absence of effective dissipative mechanisms. We conclude that elevations in EE provide very limited autoregulatory capacity in body weight regulation, and that regulation must be dominated by hypothalamic modulation of energy intake. This result supports present conclusions from genetic studies in which all known causes of human obesity are related to defects in the regulation of appetite.

[Emma-Leigh]

Last run....


http://www.ajcn.org/cgi/content/abstract/48/2/240

American Journal of Clinical Nutrition, Vol 48, 240-247, Copyright ? 1988 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man

KJ Acheson, Y Schutz, T Bessard, K Anantharaman, JP Flatt and E Jequier
Institute of Physiology, Faculty of Medicine, University of Lausanne, Switzerland.

The metabolic balance method was performed on three men to investigate the fate of large excesses of carbohydrate. Glycogen stores, which were first depleted by diet (3 d, 8.35 +/- 0.27 MJ [1994 +/- 65 kcal] decreasing to 5.70 +/- 1.03 MJ [1361 +/- 247 kcal], 15% protein, 75% fat, 10% carbohydrate) and exercise, were repleted during 7 d carbohydrate overfeeding (11% protein, 3% fat, and 86% carbohydrate) providing 15.25 +/- 1.10 MJ (3642 +/- 263 kcal) on the first day, increasing progressively to 20.64 +/- 1.30 MJ (4930 +/- 311 kcal) on the last day of overfeeding. Glycogen depletion was again accomplished with 2 d of carbohydrate restriction (2.52 MJ/d [602 kcal/d], 85% protein, and 15% fat). Glycogen storage capacity in man is approximately 15 g/kg body weight and can accommodate a gain of approximately 500 g before net lipid synthesis contributes to increasing body fat mass. When the glycogen stores are saturated, massive intakes of carbohydrate are disposed of by high carbohydrate- oxidation rates and substantial de novo lipid synthesis (150 g lipid/d using approximately 475 g CHO/d) without postabsorptive hyperglycemia.


http://www.ajcn.org/cgi/content/abstract/65/6/1774

American Journal of Clinical Nutrition, Vol 65, 1774-1782, Copyright ? 1997 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

Hepatic and whole-body fat synthesis in humans during carbohydrate overfeeding

A Aarsland, D Chinkes and RR Wolfe
Metabolism Unit, Shriners Burns Institute, Galveston, TX 77551, USA.

The magnitude of the capacity to convert carbohydrate to fat in the human body is still controversial, as is the extent to which it takes place in the liver as opposed to the adipose tissue. We calculated whole-body net fat synthesis from indirect calorimetry and substrate balance data from five healthy men in the basal state and after 1 and 4 d on a hyperenergetic carbohydrate diet (approximately 2.5 times energy expenditure). At the same time, the secretion of fatty acids synthesized in the liver was measured to determine the extent to which fat synthesis occurs in the liver in a lipogenic state. The respiratory exchange ratio (RER) was 0.81 +/- 0.01 in the basal state and 0.99 +/- 0.025 and 1.15 +/- 0.022 on days 1 and 4, respectively. Although there was net fat oxidation in the basal state (955 +/- 139 mg.kg-1.min-1), there was net fat synthesis at the whole-body level both during early (day 1; 481 +/- 205 mg.kg-1.min-1) and late (day 4; 2243 +/- 253 mg.kg- 1.min-1) carbohydrate overfeeding. Although hepatic secretion of fat synthesized de novo increased approximately 35-fold during the study (basal state, 1.0 +/- 0.3; day 1, 13.8 +/- 6.8; and day 4, 43.3 +/- 16.3 mg.kg-1.min-1) this could only account for a small portion of total fat synthesis. We conclude that the liver plays a quantitatively minor role when surplus carbohydrate energy is converted into fat in the human body. The main site for fat synthesis is likely to be the adipose tissue.


http://www.ajcn.org/cgi/content/abstract/35/4/678

American Journal of Clinical Nutrition, Vol 35, 678-682, Copyright ? 1982 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride

N Baba, EF Bracco and SA Hashim

The mechanism whereby overfeeding with diet containing medium chain triglyceride (MCT) results in diminished body weight and fat was studied. Fifteen male Sprague-Dawley rats were fitted under anesthesia with gastrostomy tubes and divided into two groups. One group was fed MCT diet, the other an isocaloric diet containing long chain triglyceride (LCT) in excess (150%) of spontaneous calorie intake. Both diets, fed for 6 wk, derived 50% of calories from fat. Basal and norepinephrine (25 micrograms/100 g) stimulated 02 consumption and CO2 production, as well as metabolic rate were measured. After the rats were killed, total dissectible fat and fat cell size and number were determined. MCT rats gained 15% less weight than LCT controls (p less than 0.001). Total dissectible fat was significantly lower (p less than 0.001) in MCT group, as was mean adipocyte size (p less than 0.001). Resting and maximal norepinephrine-stimulated 02 consumptions were 39.7 and 22.1% higher in MCT than in LCT group, respectively. Resting and norepinephrine-stimulated metabolic rates were 38.8 and 22.2% higher in MCT than LCT fed rats, respectively. Overfeeding MCT diet results in decreased body fat related to increased metabolic rate and thermogenesis.

[Confuzzl3dOn3]

Mmm...so according to the last article, even if in calorie excess (overfeeding) with MCTs this will result in fat loss because of increased metabolic rate and thermogenesis. That's just WOW! so basically when you 'cut' you can maintain the amount of cals you intake but just substitute in MCTs to achieve weight loss?

[soundcheck129]

Mmm...so according to the last article, even if in calorie excess (overfeeding) with MCTs this will result in fat loss because of increased metabolic rate and thermogenesis. That's just WOW! so basically when you 'cut' you can maintain the amount of cals you intake but just substitute in MCTs to achieve weight loss?

Um, no. Even in the MCT group, the rats nearly doubled in weight, it just said they accumulated less fat. And good luck trying to get 50% of your energy intake from MCTs.

[Emma-Leigh]

Mmm...so according to the last article, even if in calorie excess (overfeeding) with MCTs this will result in fat loss because of increased metabolic rate and thermogenesis. That's just WOW! so basically when you 'cut' you can maintain the amount of cals you intake but just substitute in MCTs to achieve weight loss?

errmmm....

Um, no. Even in the MCT group, the rats nearly doubled in weight, it just said they accumulated less fat. And good luck trying to get 50% of your energy intake from MCTs.
^^
this...

Plus:

Int J Obes Relat Metab Disord. 2001 Sep;25(9):1393-400. Links
Value of VLCD supplementation with medium chain triglycerides.

Krotkiewski M.
Department of Medical Rehabilitation, Sahlgrenska University Hospital, G?teborg, Sweden. mpab@algonet.se
BACKGROUND: Medium chain triglycerides (MCT) are energetically less dense, highly ketogenic, and more easily oxidised than long chain triglycerides (LCT). MCT also differ from LCT in their digestive and metabolic pathways. OBJECTIVE: To test the effects of MCT supplementation during a very low calorie diet (VLCD). SUBJECTS AND METHODS: Three groups of tightly matched obese women with body mass index (BMI)>30 kg/m(2) received an isoenergetic (578.5 kcal) VLCD (Adinax, Novo Vital, Sweden) enriched with MCT or LCT (8.0 and 9.9 g/100 g Adinax respectively) or a low-fat (3 g/100 g) and high-carbohydrate regimen. The diets were administered over 4 weeks. Body composition was measured with DEXA and appetite/satiety-according to Blundell. Beta hydroxybutyric acid concentration in plasma and nitrogen excretion in urine was measured during consecutive days of VLCD. The study was performed in a randomised double-blind manner. RESULTS: The MCT group showed a significantly greater decrease in body weight during the first 2 weeks. The contribution of body fat to the total weight loss was higher while the contribution of fat-free mass (FFM) was lower. The MCT group had a higher concentration of ketone bodies in plasma and a lower nitrogen excretion in urine. Hunger feelings were less intense while satiety was higher. These differences were observed during the first 2 weeks of treatment and gradually declined during the third and fourth weeks. CONCLUSIONS: Replacement of LCT by MCT in the VLCD increased the rate of decrease of body fat and body weight and has a sparing effect on FFM. The intensity of hunger feelings was lower and paralleled the higher increase of ketone bodies. These effects gradually declined, indicating subsequent metabolic adaptation. Further studies are required to confirm the protein-sparing and appetite-suppressing effects of MCT supplementation during the first 2 weeks of VLCD treatment.
^ your body adapts to the metabolic effect after a few weeks.... ;)

[Confuzzl3dOn3]

Oh well it was a blissful dream :D

[bodydropcris]

english please...

[Emma-Leigh]

english please...
eat too much - and eventually you get fat...
eat lots of carbs - you store glycogen first... but you eventually get fat...
eat lots of fat and you get fatter faster than if you ate carbs...
if you are lean - it takes longer to get fat than if you are fat.... but you still get fat eventually.

:p

[bodydropcris]

i wish i wasnt dumb!! they should put pictures in these fancy articles...

[Frankdaddy]

eat too much - and eventually you get fat...
eat lots of carbs - you store glycogen first... but you eventually get fat...
eat lots of fat and you get fatter faster than if you ate carbs...
if you are lean - it takes longer to get fat than if you are fat.... but you still get fat eventually.

:p

Reps for laymens terms :)

It i pretty awesome getting very lean for a show and eating like a pig after, even though feeling like a fat. bloated pig you eventually look at post pics and think MAN, I wish I Was still that "fat" as I felt at the time haha.

[Kruczynski]

eat too much - and eventually you get fat...
eat lots of carbs - you store glycogen first... but you eventually get fat...
eat lots of fat and you get fatter faster than if you ate carbs...
if you are lean - it takes longer to get fat than if you are fat.... but you still get fat eventually.

:p

And the solution is?

[dimasso69]

And the solution is?

Don't eat too much.

[Emma-Leigh]

And the solution is?


Don't eat too much.
^
this....
or steroids. :p

:o

[Kruczynski]

Thanks! Got it

[Emma-Leigh]

Thanks! Got it
ps - this doesn't mean you can't 'eat more than you need' in order to gain weight/ mass << just means that you don't 'stuff yourself stupid' day after day after day.... ;)

[lorinelise]

Great reads Emma! :)

[ilove2run]

Great reads Emma! :)

x2 :D

[soundcheck129]

The fact that in overfeeding scenarios, fat leads to higher storage rates than carbohydrates almost makes it seem like a high-fat diet would be ideal for bulking....interesting.

[Emma-Leigh]

The fact that in overfeeding scenarios, fat leads to higher storage rates than carbohydrates almost makes it seem like a high-fat diet would be ideal for bulking....interesting.
ermmm.... no.
More fat = more fat stored.
Less fat = less fat stored.
I don't know about you - but when I bulk my aim is not to store fat.... It's to store less fat and more muscle.
^
thus: unless insulin resistant, higher carbs / moderate fat when bulking = better than massively high fat intake. ;)

[soundcheck129]

My mistake :)

I was looking at it as more stored energy, which could then be used for growth.

[CashmereKermit]

I'd like to add:

"Excess calories build the same amount of muscle as the perfect number of calories."

[dimasso69]

^
this....
or steroids. :p

:o

ill go with the cheaper option and safer option:)

[Nefariousx1]

ermmm.... no.
More fat = more fat stored.
Less fat = less fat stored.
I don't know about you - but when I bulk my aim is not to store fat.... It's to store less fat and more muscle.
^
thus: unless insulin resistant, higher carbs / moderate fat when bulking = better than massively high fat intake. ;)

ehhh so more dietary fat can lead to more body fat?!?!?!?!?! mind = blown

[Confuzzl3dOn3]

So if ya gonna clear a buffet you're better off binging on carbs like SUSHI!!!