ellis
Nasycone kwasy tłuszczowe mogą osłabiać wrażliwość insulinową na podstawie dwóch mechanizmów:
-krótkoterminowego związanego z pojawieniem się ich w krwiobiegu tuż po posiłku.
-długoterminowego związanego z płynnością błon komórkowych.
Temat jest interesujący szczególnie pod kątem diety w której tłuszcz stanowi większą część zapotrzebowania kalorycznego i są cykliczne ładowania węglowodanów, czyli CKD, TKD, itd.
Szukałem badań w tym temacie i taki jest efekt:
Pierwsze badanie potwierdza możliwość niekorzystnego wpływu w krótkim terminie, posiłek obfitujący w tłuszcze nasycone miał negatywny wpływ na wrażliwość insulinową po posiłku i w kolejnym posiłku zawierającym węglowodany. Drugie badanie w dużym stopniu faworyzuje wielonienasycone kwasy tłuszczowe.
Acute effects of meal fatty acid composition on insulin sensitivity in healthy post-menopausal women.
Robertson MD, Jackson KG, Fielding BA, Williams CM, Frayn KN.
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, OX2 6HE. [email protected]
Postprandial plasma insulin concentrations after a single high-fat meal may be modified by the presence of specific fatty acids although the effects of sequential meal ingestion are unknown. The aim of the present study was to examine the effects of altering the fatty acid composition in a single mixed fat-carbohydrate meal on glucose metabolism and insulin sensitivity of a second meal eaten 5 h later. Insulin sensitivity was assessed using a minimal model approach. Ten healthy post-menopausal women underwent four two-meal studies in random order. A high-fat breakfast (40 g fat) where the fatty acid composition was predominantly saturated fatty acids (SFA), n-6 polyunsaturated fatty acids (PUFA), long-chain n-3 PUFA or monounsaturated fatty acids (MUFA) was followed 5 h later by a low-fat, high-carbohydrate lunch (5.7 g fat), which was identical in all four studies. The plasma insulin response was significantly higher following the SFA meal than the other meals after both breakfast and lunch (P<0.006) although there was no effect of breakfast fatty acid composition on plasma glucose concentrations. Postprandial insulin sensitivity (SI(Oral)) was assessed for 180 min after each meal. SI(Oral) was significantly lower after lunch than after breakfast for all four test meals (P=0.019) following the same rank order (SFA < n-6 PUFA < n-3 PUFA < MUFA) for each meal. The present study demonstrates that a single meal rich in SFA reduces postprandial insulin sensitivity with 'carry-over' effects for the next meal.
Differential effects of monounsaturated, polyunsaturated and saturated fat ingestion on glucose-stimulated insulin secretion, sensitivity and clearance in overweight and obese, non-diabetic humans.
Xiao C, Giacca A, Carpentier A, Lewis GF.
Departments of Medicine and Physiology, University of Toronto, Toronto, ON, Canada.
AIMS/HYPOTHESIS: Prolonged elevation of plasma specific fatty acids may exert differential effects on glucose-stimulated insulin secretion (GSIS), insulin sensitivity and clearance. SUBJECTS AND METHODS: We examined the effect of oral ingestion, at regular intervals for 24 h, of an emulsion containing either predominantly monounsaturated (MUFA), polyunsaturated (PUFA) or saturated (SFA) fat or water (control) on GSIS, insulin sensitivity and insulin clearance in seven overweight or obese, non-diabetic humans. Four studies were conducted in each individual in random order, 4-6 weeks apart. Twenty-four hours after initiation of oral ingestion, subjects underwent a 2 h, 20 mmol/l hyperglycaemic clamp to assess GSIS, insulin sensitivity and insulin clearance. RESULTS: Following oral ingestion of any of the three fat emulsions over 24 h, plasma NEFAs were elevated by approximately 1.5- to 2-fold over the basal level. Ingestion of any of the three fat emulsions resulted in reduction in insulin clearance, and SFA ingestion reduced insulin sensitivity. PUFA ingestion was associated with an absolute reduction in GSIS, whereas insulin secretion failed to compensate for insulin resistance in subjects who ingested SFA. CONCLUSIONS/INTERPRETATION: Oral ingestion of fats with differing degrees of saturation resulted in different effects on insulin secretion and action. PUFA ingestion resulted in an absolute reduction in insulin secretion and SFA ingestion induced insulin resistance. Failure of insulin secretion to compensate for insulin resistance implies impaired beta cell function in the SFA study.
Odnośnie długoterminowego wpływu znalazłem bardzo ciekawe badanie. Końcowy wniosek jest taki: zamiana nasyconych kwasów tłuszczowych na jednonienasycone może mieć korzystny wpływ na wrażliwość insulinową, ale gdy ilość tłuszczu przekracza 37% zapotrzebowania kalorycznego ta zamiana nie daje dodatkowych korzyści pod tym względem.
Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study.
Vessby B, Unsitupa M, Hermansen K, Riccardi G, Rivellese AA, Tapsell LC, Nalsen C, Berglund L, Louheranta A, Rasmussen BM, Calvert GD, Maffetone A, Pedersen E, Gustafsson IB, Storlien LH; KANWU Study.
Unit for Clinical Nutrition Research, Department of Public Health and Caring Sciences/Geriatrics, University of Uppsala, Uppsala, Sweden.
AIMS/HYPOTHESIS: The amount and quality of fat in the diet could be of importance for development of insulin resistance and related metabolic disorders. Our aim was to determine whether a change in dietary fat quality alone could alter insulin action in humans. METHODS: The KANWU study included 162 healthy subjects chosen at random to receive a controlled, isoenergetic diet for 3 months containing either a high proportion of saturated (SAFA diet) or monounsaturated (MUFA diet) fatty acids. Within each group there was a second assignment at random to supplements with fish oil (3.6 g n-3 fatty acids/d) or placebo. RESULTS: Insulin sensitivity was significantly impaired on the saturated fatty acid diet (-10%, p = 0.03) but did not change on the monounsaturated fatty acid diet (+2%, NS) (p = 0.05 for difference between diets). Insulin secretion was not affected. The addition of n-3 fatty acids influenced neither insulin sensitivity nor insulin secretion. The favourable effects of substituting a monounsaturated fatty acid diet for a saturated fatty acid diet on insulin sensitivity were only seen at a total fat intake below median (37E%). Here, insulin sensitivity was 12.5% lower and 8.8% higher on the saturated fatty acid diet and monounsaturated fatty acid diet respectively (p = 0.03). Low density lipoprotein cholesterol (LDL) increased on the saturated fatty acid diet (+4.1%, p < 0.01) but decreased on the monounsaturated fatty acid diet (MUFA) (-5.2, p < 0.001), whereas lipoprotein (a) [Lp(a)] increased on a monounsaturated fatty acid diet by 12% (p < 0.001). CONCLUSIONS/INTERPRETATION: A change of the proportions of dietary fatty acids, decreasing saturated fatty acid and increasing monounsaturated fatty acid, improves insulin sensitivity but has no effect on insulin secretion. A beneficial impact of the fat quality on insulin sensitivity is not seen in individuals with a high fat intake (> 37E%).
Nie wszystkie kwasy tłuszczowe działają w ten sposób, kwas stearynowy obecny w dużych ilościach w czerwonym mięsie jest bezpieczny i nie wpływa na oporność insulinową:
A high-stearic acid diet does not impair glucose tolerance and insulin sensitivity in healthy women.
Louheranta AM, Turpeinen AK, Schwab US, Vidgren HM, Parviainen MT, Uusitupa MI.
Department of Clinical Nutrition, University of Kuopio, Finland.
Results in epidemiological and experimental studies suggest that a diet rich in saturated fat may affect insulin sensitivity. However, no published data are available on the effect of stearic acid in this respect. Therefore, we examined the effects of a high-stearic acid diet and a high-oleic acid diet on glucose metabolism, serum lipids and lipoproteins, and blood coagulation factors in 15 healthy female subjects. Subjects followed the two experimental diets for 4 weeks according to a randomized crossover design. Both experimental diet periods were preceded by consumption of a baseline diet for 2 weeks. The diets provided 36% of energy (E%) as fat. In the experimental diets, 5 E% stearic or oleic acid was substituted for 5 E% of saturated fatty acids in the baseline diet. After the experimental diets, no differences were found in the insulin sensitivity index (mean+/-SEM, 5.4+/-1.9 v 5.2+/-1.6 x 10(-4) min(-1) x microU(-1) x mL(-1), nonsignificant [NS]), glucose effectiveness (0.026+/-0.006 v 0.026+/-0.003 min(-1), NS), or first-phase insulin reaction ([FPIR] 368+/-57 v 374+/-66 mU/L x min, NS). The concentration of serum lipids and lipoproteins and blood coagulation factors did not differ after the diet periods. In conclusion, a diet rich in stearic acid did not deteriorate glucose tolerance or insulin action in young healthy female subjects as compared with a diet rich in oleic acid.
Znalazłem, również badanie nie potwierdzające tego negatywnego wpływu nasyconych tłuszczy u nieotyłych osób, otyłe osoby są dużo bardziej podatne na osłabienie wrażliwości insulinowej wynikające z kompozycji kwasów tłuszczowych w diecie. Kolejne badanie sugeruje, że tydzień to zbyt krotko by zaszła znacząca zmiana we wrażliwości insulinowej w odpowiedzi na kompozycję kwasów tłuszczowych w diecie.
Effects of diets enriched in saturated (palmitic), monounsaturated (oleic), or trans (elaidic) fatty acids on insulin sensitivity and substrate oxidation in healthy adults.
Lovejoy JC, Smith SR, Champagne CM, Most MM, Lefevre M, DeLany JP, Denkins YM, Rood JC, Veldhuis J, Bray GA.
Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana 70808, USA.
OBJECTIVE: Diets high in total and saturated fat are associated with insulin resistance. This study examined the effects of feeding monounsaturated, saturated, and trans fatty acids on insulin action in healthy adults. RESEARCH DESIGN AND METHODS: A randomized, double-blind, crossover study was conducted comparing three controlled 4-week diets (57% carbohydrate, 28% fat, and 15% protein) enriched with different fatty acids in 25 healthy men and women. The monounsaturated fat diet (M) had 9% of energy as C18:1cis (oleic acid). The saturated fat diet (S) had 9% of energy as palmitic acid, and the trans fatty acid diet (T) had 9% as C18:1trans. Body weight was kept constant throughout the study. After each diet period, insulin pulsatile secretion, insulin sensitivity index (S(I)) by the minimal model method, serum lipids, and fat oxidation by indirect calorimetry were measured. RESULTS: Mean S(I) for the M, S, and T diets was 3.44 +/- 0.26, 3.20 +/- 0.26, and 3.40 +/- 0.26 x 10(-4) min(-1). microU(-1). ml(-1), respectively (NS). S(I) decreased by 24% on the S versus M diet in overweight subjects but was unchanged in lean subjects (NS). Insulin secretion was unaffected by diet, whereas total and HDL cholesterol increased significantly on the S diet. Subjects oxidized the least fat on the M diet (26.0 +/- 1.5 g/day) and the most fat on the T diet (31.4 +/- 1.5 g/day) (P = 0.02). CONCLUSIONS: Dietary fatty acid composition significantly influenced fat oxidation but did not impact insulin sensitivity or secretion in lean individuals. Overweight individuals were more susceptible to developing insulin resistance on high-saturated fat diets.
Całość: http://care.diabetesjournals.org/cgi/content/full/25/8/1283
No effect of short-term dietary supplementation of saturated and poly- and monounsaturated fatty acids on insulin secretion and sensitivity in healthy men.
Fasching P, Ratheiser K, Schneeweiss B, Rohac M, Nowotny P, Waldhausl W.
Department of Medicine III, University of Vienna, Austria.
To evaluate the short-term influence of fatty acids with different grades of saturation on insulin secretion and sensitivity, 8 healthy males (age 26 +/- 3.5 years, body mass index 22.4 +/- 1.8 kg/m2) were provided with 800 kcal daily of either carbohydrates (CH; 200 g), or fat (90 g) enriched either with saturated fatty acids (SAFA; 72%) or (omega-6) polyunsaturated fatty acids (PUFA; 60%) or cis-monounsaturated fatty acids (MUFA; 40%; n = 5) in addition to a standard diet (2,000 kcal/ day; 50% CH, 15% protein, and 35% fat; 33% SAFA, MUFA, and PUFA each) for 1 week in a randomized order (washout period 2 weeks). The stimulated insulin secretion was quantified by the frequently sampled intravenous glucose tolerance test (FSIGT; 0.3 g glucose/kg body weight), while the insulin sensitivity was determined by an euglycemic-hyperinsulinemic 5-mU clamp. In parallel, basal and stimulated carbohydrate and fat oxidation rates were estimated by indirect calorimetry. One week of defined fat exposure failed to significantly affect the glucose-induced insulin secretion during FSIGT and insulin-dependent glucose disposal during an euglycemic clamp (M values: CH 9.6 +/- 1.6 mg/kg.min, SAFA 9.7 +/- 2.2, PUFA 9.8 +/- 2.5, and MUFA 11.5 +/- 3.2 mg/kg.min; NS). In addition, oxidation rates for fat and glucose in the postabsorptive state and during hyperinsulinemia did not differ between the different diets. We conclude that short-term (1-week) isocaloric supplementation of a standard diet with fatty acids of varying degree of saturation does not affect either insulin secretion or insulin sensitivity in healthy men, due to the compensatory metabolic capacity of healthy subjects.
Na koniec jeszcze dosyć ciekawa opinia Lyla McDonalda o lepszej adaptacji do low carb przy oporności na insulinę, ale niestety nie w sytuacji, gdy okresowo ładujemy węglowodany:
In the absence of a high glycemic load (a technical way of saying you're on a low-carb diet) it's fairly questionable whether insulin resistance is any big deal. Quite in fact, the insulin resistance that develops on a low-carb diet appears to be adaptive/beneficial. By limiting the muscle's use of glucose (in lieu of using fatty acids), what glucose is available is spared for the brain. Basically, insulin resistance during low-carbs is a very different animal that insulin resistance as occurs on a high-carb diet (due to chronically high insulin levels).
Of course, one question is what happens during an anabolic diet/bodyopus type of carb-load (or even the carb-load of my Ultimate Diet 2.0; note that the low-carb phase of my UD2 is also low-fat). Folks are insulin resistant going into the carb-load and lots of people get badly fluctuation energy levels/blood glucose from the combination of hyperinsulinemia/ insulin resistance. Is this a problem in the short or even long-term? Hard to say. But this is part of why I like to see full body workouts prior to carb-loads, it improves whole body muscular insulin sensitivity (via glycogen depletion and muscular contraction), which helps to limit the problems.
Podsumowanie:
1) Nasycone kwasy tłuszczowe mogą w niewielkim stopniu osłabiać wrażliwość insulinową z posiłku na posiłek.
2) Zamiana nasyconych kwasów tłuszczowych na jednonienasycone w dłuższym terminie może dać wyrażną poprawę wrażliwości insulinowej, taki zabieg może nie mieć znaczenia, gdy tłuszcz stanowi więcej niż 37% zapotrzebowania kalorycznego.
3) Tydzień to zbyt krótko by zaszły niekorzystne zmiany odnośnie mechanizmu długoterminowego.
5) Stearynowy kwas tłuszczowy nie powoduje oporności insulinowej.
6) Nieotyłe osoby nie są tak narażone na wywołanie oporności na insulinę pod wpływem kompozycji kwasów tłuszczowych w diecie.
7) Podczas low carb wrażliwość insulinowa nie ma takiego znaczenia, dodatkowo możemy liczyć na lepszą adaptację przy oporności insulinowej, lepsze wykorzystanie kwasów tłuszczowych w mieśniach i glukozy przez mózg. Sytuacja dramatycznie zmienia się, gdy w naszym planie mamy ładowania węglowodanów, wtedy możemy liczyć, że trening całego ciała, opróżnienie glikogenu tuż przed ładowaniem może rozwiązać problem.
Badań w tym temacie jest naprawdę sporo, te wydawały mi się najciekawsze, ale może ktoś ma coś jeszcze do powiedzenia, na co liczę
i nie jest to post informacyjny dla początkujących, więc przetłumaczyłem tylko główne wnioski
-krótkoterminowego związanego z pojawieniem się ich w krwiobiegu tuż po posiłku.
-długoterminowego związanego z płynnością błon komórkowych.
Temat jest interesujący szczególnie pod kątem diety w której tłuszcz stanowi większą część zapotrzebowania kalorycznego i są cykliczne ładowania węglowodanów, czyli CKD, TKD, itd.
Szukałem badań w tym temacie i taki jest efekt:
Pierwsze badanie potwierdza możliwość niekorzystnego wpływu w krótkim terminie, posiłek obfitujący w tłuszcze nasycone miał negatywny wpływ na wrażliwość insulinową po posiłku i w kolejnym posiłku zawierającym węglowodany. Drugie badanie w dużym stopniu faworyzuje wielonienasycone kwasy tłuszczowe.
Acute effects of meal fatty acid composition on insulin sensitivity in healthy post-menopausal women.
Robertson MD, Jackson KG, Fielding BA, Williams CM, Frayn KN.
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, OX2 6HE. [email protected]
Postprandial plasma insulin concentrations after a single high-fat meal may be modified by the presence of specific fatty acids although the effects of sequential meal ingestion are unknown. The aim of the present study was to examine the effects of altering the fatty acid composition in a single mixed fat-carbohydrate meal on glucose metabolism and insulin sensitivity of a second meal eaten 5 h later. Insulin sensitivity was assessed using a minimal model approach. Ten healthy post-menopausal women underwent four two-meal studies in random order. A high-fat breakfast (40 g fat) where the fatty acid composition was predominantly saturated fatty acids (SFA), n-6 polyunsaturated fatty acids (PUFA), long-chain n-3 PUFA or monounsaturated fatty acids (MUFA) was followed 5 h later by a low-fat, high-carbohydrate lunch (5.7 g fat), which was identical in all four studies. The plasma insulin response was significantly higher following the SFA meal than the other meals after both breakfast and lunch (P<0.006) although there was no effect of breakfast fatty acid composition on plasma glucose concentrations. Postprandial insulin sensitivity (SI(Oral)) was assessed for 180 min after each meal. SI(Oral) was significantly lower after lunch than after breakfast for all four test meals (P=0.019) following the same rank order (SFA < n-6 PUFA < n-3 PUFA < MUFA) for each meal. The present study demonstrates that a single meal rich in SFA reduces postprandial insulin sensitivity with 'carry-over' effects for the next meal.
Differential effects of monounsaturated, polyunsaturated and saturated fat ingestion on glucose-stimulated insulin secretion, sensitivity and clearance in overweight and obese, non-diabetic humans.
Xiao C, Giacca A, Carpentier A, Lewis GF.
Departments of Medicine and Physiology, University of Toronto, Toronto, ON, Canada.
AIMS/HYPOTHESIS: Prolonged elevation of plasma specific fatty acids may exert differential effects on glucose-stimulated insulin secretion (GSIS), insulin sensitivity and clearance. SUBJECTS AND METHODS: We examined the effect of oral ingestion, at regular intervals for 24 h, of an emulsion containing either predominantly monounsaturated (MUFA), polyunsaturated (PUFA) or saturated (SFA) fat or water (control) on GSIS, insulin sensitivity and insulin clearance in seven overweight or obese, non-diabetic humans. Four studies were conducted in each individual in random order, 4-6 weeks apart. Twenty-four hours after initiation of oral ingestion, subjects underwent a 2 h, 20 mmol/l hyperglycaemic clamp to assess GSIS, insulin sensitivity and insulin clearance. RESULTS: Following oral ingestion of any of the three fat emulsions over 24 h, plasma NEFAs were elevated by approximately 1.5- to 2-fold over the basal level. Ingestion of any of the three fat emulsions resulted in reduction in insulin clearance, and SFA ingestion reduced insulin sensitivity. PUFA ingestion was associated with an absolute reduction in GSIS, whereas insulin secretion failed to compensate for insulin resistance in subjects who ingested SFA. CONCLUSIONS/INTERPRETATION: Oral ingestion of fats with differing degrees of saturation resulted in different effects on insulin secretion and action. PUFA ingestion resulted in an absolute reduction in insulin secretion and SFA ingestion induced insulin resistance. Failure of insulin secretion to compensate for insulin resistance implies impaired beta cell function in the SFA study.
Odnośnie długoterminowego wpływu znalazłem bardzo ciekawe badanie. Końcowy wniosek jest taki: zamiana nasyconych kwasów tłuszczowych na jednonienasycone może mieć korzystny wpływ na wrażliwość insulinową, ale gdy ilość tłuszczu przekracza 37% zapotrzebowania kalorycznego ta zamiana nie daje dodatkowych korzyści pod tym względem.
Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study.
Vessby B, Unsitupa M, Hermansen K, Riccardi G, Rivellese AA, Tapsell LC, Nalsen C, Berglund L, Louheranta A, Rasmussen BM, Calvert GD, Maffetone A, Pedersen E, Gustafsson IB, Storlien LH; KANWU Study.
Unit for Clinical Nutrition Research, Department of Public Health and Caring Sciences/Geriatrics, University of Uppsala, Uppsala, Sweden.
AIMS/HYPOTHESIS: The amount and quality of fat in the diet could be of importance for development of insulin resistance and related metabolic disorders. Our aim was to determine whether a change in dietary fat quality alone could alter insulin action in humans. METHODS: The KANWU study included 162 healthy subjects chosen at random to receive a controlled, isoenergetic diet for 3 months containing either a high proportion of saturated (SAFA diet) or monounsaturated (MUFA diet) fatty acids. Within each group there was a second assignment at random to supplements with fish oil (3.6 g n-3 fatty acids/d) or placebo. RESULTS: Insulin sensitivity was significantly impaired on the saturated fatty acid diet (-10%, p = 0.03) but did not change on the monounsaturated fatty acid diet (+2%, NS) (p = 0.05 for difference between diets). Insulin secretion was not affected. The addition of n-3 fatty acids influenced neither insulin sensitivity nor insulin secretion. The favourable effects of substituting a monounsaturated fatty acid diet for a saturated fatty acid diet on insulin sensitivity were only seen at a total fat intake below median (37E%). Here, insulin sensitivity was 12.5% lower and 8.8% higher on the saturated fatty acid diet and monounsaturated fatty acid diet respectively (p = 0.03). Low density lipoprotein cholesterol (LDL) increased on the saturated fatty acid diet (+4.1%, p < 0.01) but decreased on the monounsaturated fatty acid diet (MUFA) (-5.2, p < 0.001), whereas lipoprotein (a) [Lp(a)] increased on a monounsaturated fatty acid diet by 12% (p < 0.001). CONCLUSIONS/INTERPRETATION: A change of the proportions of dietary fatty acids, decreasing saturated fatty acid and increasing monounsaturated fatty acid, improves insulin sensitivity but has no effect on insulin secretion. A beneficial impact of the fat quality on insulin sensitivity is not seen in individuals with a high fat intake (> 37E%).
Nie wszystkie kwasy tłuszczowe działają w ten sposób, kwas stearynowy obecny w dużych ilościach w czerwonym mięsie jest bezpieczny i nie wpływa na oporność insulinową:
A high-stearic acid diet does not impair glucose tolerance and insulin sensitivity in healthy women.
Louheranta AM, Turpeinen AK, Schwab US, Vidgren HM, Parviainen MT, Uusitupa MI.
Department of Clinical Nutrition, University of Kuopio, Finland.
Results in epidemiological and experimental studies suggest that a diet rich in saturated fat may affect insulin sensitivity. However, no published data are available on the effect of stearic acid in this respect. Therefore, we examined the effects of a high-stearic acid diet and a high-oleic acid diet on glucose metabolism, serum lipids and lipoproteins, and blood coagulation factors in 15 healthy female subjects. Subjects followed the two experimental diets for 4 weeks according to a randomized crossover design. Both experimental diet periods were preceded by consumption of a baseline diet for 2 weeks. The diets provided 36% of energy (E%) as fat. In the experimental diets, 5 E% stearic or oleic acid was substituted for 5 E% of saturated fatty acids in the baseline diet. After the experimental diets, no differences were found in the insulin sensitivity index (mean+/-SEM, 5.4+/-1.9 v 5.2+/-1.6 x 10(-4) min(-1) x microU(-1) x mL(-1), nonsignificant [NS]), glucose effectiveness (0.026+/-0.006 v 0.026+/-0.003 min(-1), NS), or first-phase insulin reaction ([FPIR] 368+/-57 v 374+/-66 mU/L x min, NS). The concentration of serum lipids and lipoproteins and blood coagulation factors did not differ after the diet periods. In conclusion, a diet rich in stearic acid did not deteriorate glucose tolerance or insulin action in young healthy female subjects as compared with a diet rich in oleic acid.
Znalazłem, również badanie nie potwierdzające tego negatywnego wpływu nasyconych tłuszczy u nieotyłych osób, otyłe osoby są dużo bardziej podatne na osłabienie wrażliwości insulinowej wynikające z kompozycji kwasów tłuszczowych w diecie. Kolejne badanie sugeruje, że tydzień to zbyt krotko by zaszła znacząca zmiana we wrażliwości insulinowej w odpowiedzi na kompozycję kwasów tłuszczowych w diecie.
Effects of diets enriched in saturated (palmitic), monounsaturated (oleic), or trans (elaidic) fatty acids on insulin sensitivity and substrate oxidation in healthy adults.
Lovejoy JC, Smith SR, Champagne CM, Most MM, Lefevre M, DeLany JP, Denkins YM, Rood JC, Veldhuis J, Bray GA.
Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana 70808, USA.
OBJECTIVE: Diets high in total and saturated fat are associated with insulin resistance. This study examined the effects of feeding monounsaturated, saturated, and trans fatty acids on insulin action in healthy adults. RESEARCH DESIGN AND METHODS: A randomized, double-blind, crossover study was conducted comparing three controlled 4-week diets (57% carbohydrate, 28% fat, and 15% protein) enriched with different fatty acids in 25 healthy men and women. The monounsaturated fat diet (M) had 9% of energy as C18:1cis (oleic acid). The saturated fat diet (S) had 9% of energy as palmitic acid, and the trans fatty acid diet (T) had 9% as C18:1trans. Body weight was kept constant throughout the study. After each diet period, insulin pulsatile secretion, insulin sensitivity index (S(I)) by the minimal model method, serum lipids, and fat oxidation by indirect calorimetry were measured. RESULTS: Mean S(I) for the M, S, and T diets was 3.44 +/- 0.26, 3.20 +/- 0.26, and 3.40 +/- 0.26 x 10(-4) min(-1). microU(-1). ml(-1), respectively (NS). S(I) decreased by 24% on the S versus M diet in overweight subjects but was unchanged in lean subjects (NS). Insulin secretion was unaffected by diet, whereas total and HDL cholesterol increased significantly on the S diet. Subjects oxidized the least fat on the M diet (26.0 +/- 1.5 g/day) and the most fat on the T diet (31.4 +/- 1.5 g/day) (P = 0.02). CONCLUSIONS: Dietary fatty acid composition significantly influenced fat oxidation but did not impact insulin sensitivity or secretion in lean individuals. Overweight individuals were more susceptible to developing insulin resistance on high-saturated fat diets.
Całość: http://care.diabetesjournals.org/cgi/content/full/25/8/1283
No effect of short-term dietary supplementation of saturated and poly- and monounsaturated fatty acids on insulin secretion and sensitivity in healthy men.
Fasching P, Ratheiser K, Schneeweiss B, Rohac M, Nowotny P, Waldhausl W.
Department of Medicine III, University of Vienna, Austria.
To evaluate the short-term influence of fatty acids with different grades of saturation on insulin secretion and sensitivity, 8 healthy males (age 26 +/- 3.5 years, body mass index 22.4 +/- 1.8 kg/m2) were provided with 800 kcal daily of either carbohydrates (CH; 200 g), or fat (90 g) enriched either with saturated fatty acids (SAFA; 72%) or (omega-6) polyunsaturated fatty acids (PUFA; 60%) or cis-monounsaturated fatty acids (MUFA; 40%; n = 5) in addition to a standard diet (2,000 kcal/ day; 50% CH, 15% protein, and 35% fat; 33% SAFA, MUFA, and PUFA each) for 1 week in a randomized order (washout period 2 weeks). The stimulated insulin secretion was quantified by the frequently sampled intravenous glucose tolerance test (FSIGT; 0.3 g glucose/kg body weight), while the insulin sensitivity was determined by an euglycemic-hyperinsulinemic 5-mU clamp. In parallel, basal and stimulated carbohydrate and fat oxidation rates were estimated by indirect calorimetry. One week of defined fat exposure failed to significantly affect the glucose-induced insulin secretion during FSIGT and insulin-dependent glucose disposal during an euglycemic clamp (M values: CH 9.6 +/- 1.6 mg/kg.min, SAFA 9.7 +/- 2.2, PUFA 9.8 +/- 2.5, and MUFA 11.5 +/- 3.2 mg/kg.min; NS). In addition, oxidation rates for fat and glucose in the postabsorptive state and during hyperinsulinemia did not differ between the different diets. We conclude that short-term (1-week) isocaloric supplementation of a standard diet with fatty acids of varying degree of saturation does not affect either insulin secretion or insulin sensitivity in healthy men, due to the compensatory metabolic capacity of healthy subjects.
Na koniec jeszcze dosyć ciekawa opinia Lyla McDonalda o lepszej adaptacji do low carb przy oporności na insulinę, ale niestety nie w sytuacji, gdy okresowo ładujemy węglowodany:
In the absence of a high glycemic load (a technical way of saying you're on a low-carb diet) it's fairly questionable whether insulin resistance is any big deal. Quite in fact, the insulin resistance that develops on a low-carb diet appears to be adaptive/beneficial. By limiting the muscle's use of glucose (in lieu of using fatty acids), what glucose is available is spared for the brain. Basically, insulin resistance during low-carbs is a very different animal that insulin resistance as occurs on a high-carb diet (due to chronically high insulin levels).
Of course, one question is what happens during an anabolic diet/bodyopus type of carb-load (or even the carb-load of my Ultimate Diet 2.0; note that the low-carb phase of my UD2 is also low-fat). Folks are insulin resistant going into the carb-load and lots of people get badly fluctuation energy levels/blood glucose from the combination of hyperinsulinemia/ insulin resistance. Is this a problem in the short or even long-term? Hard to say. But this is part of why I like to see full body workouts prior to carb-loads, it improves whole body muscular insulin sensitivity (via glycogen depletion and muscular contraction), which helps to limit the problems.
Podsumowanie:
1) Nasycone kwasy tłuszczowe mogą w niewielkim stopniu osłabiać wrażliwość insulinową z posiłku na posiłek.
2) Zamiana nasyconych kwasów tłuszczowych na jednonienasycone w dłuższym terminie może dać wyrażną poprawę wrażliwości insulinowej, taki zabieg może nie mieć znaczenia, gdy tłuszcz stanowi więcej niż 37% zapotrzebowania kalorycznego.
3) Tydzień to zbyt krótko by zaszły niekorzystne zmiany odnośnie mechanizmu długoterminowego.
5) Stearynowy kwas tłuszczowy nie powoduje oporności insulinowej.
6) Nieotyłe osoby nie są tak narażone na wywołanie oporności na insulinę pod wpływem kompozycji kwasów tłuszczowych w diecie.
7) Podczas low carb wrażliwość insulinowa nie ma takiego znaczenia, dodatkowo możemy liczyć na lepszą adaptację przy oporności insulinowej, lepsze wykorzystanie kwasów tłuszczowych w mieśniach i glukozy przez mózg. Sytuacja dramatycznie zmienia się, gdy w naszym planie mamy ładowania węglowodanów, wtedy możemy liczyć, że trening całego ciała, opróżnienie glikogenu tuż przed ładowaniem może rozwiązać problem.
Badań w tym temacie jest naprawdę sporo, te wydawały mi się najciekawsze, ale może ktoś ma coś jeszcze do powiedzenia, na co liczę
i nie jest to post informacyjny dla początkujących, więc przetłumaczyłem tylko główne wnioski
Krzysztof Piekarz
qazar
buby77
wylliam
