Voihan se noin kyllä olla. Mutta esim bulkilla, kun ollaan plussalla ja jos vetää paljon hiilihydraattia, niin ylijäämä tuppaa menemään helpommin läskiksi. Luin tämän esimerkiksi kirjostosta lainaamastani "urheilijan ravitsemus" kirjasta. Kaikki hiilihydraatti muuttuu lopulta glukoosiksi, jonka määrä ja imeytymisen nopeus vaikuttaa suoraan verensokerin ja insuliinin tasoon. Suuret insuliinimäärät ottaa rasvaa vastaan ja pienet eivät. Jos insuliinia ei olisi ollenkaan, kukaan ei lihoisi.
Koska jos vetää paljon hiilihydraatteja tulee paljon kaloreita. Ja lihoo. Se mistä ne kalorit tulevat, on täysin merkityksetöntä. Rasva lihottaa vähintään yhtä paljon kuin hiilihydraatit samalla kalorimäärällä. Lue edellinen postaus jos olet eri mieltä. Tai heitä tieteellistä dataa joka osoittaa, että asia ei välttämättä olekaan näin
.
Sisälsikö ko. kirja muuten mitään lähteitä tästä aiheesta? Mainitsisitko ne jos niitä oli? Se, mitä joku kirja sanoo, on täysin merkityksetöntä. Kirjoissa kun ei aina puhuta totta. Painettu sana ei valitettavasty pysty kumoamaan termodynamiikan lakeja. Kuka vaan voi sanoa mitä vaan - mutta kaikki eivät voi todistaa sanomaansa.
Suuret insuliinimäärät ottaa rasvaa vastaan ja pienet eivät
No ei nyt aivan. Pelkät insuliinin lepotasot ehkäisevät rasvanpolttoa melko tehokkaasti. Syöminen lopettaa rasvanpolton sitten kokonaan. Ja pitkällä aikavälillä merkityksetöntä, koska kalorit ratkaisevat.
Jos insuliinia ei olisi ollenkaan, kukaan ei lihoisi.
No ei nyt aivan. Insuliini ei ole ainoa tekijä. Oletko kuullut ASP:stä? Nyt olisi korkea aika tutustua.
Metabolic response of Acylation Stimulating Protein to an oral fat load.
Acylation Stimulating Protein (ASP) is a small (mol wt 14,000), basic (pI 9.0) protein present in human plasma. When examined in vitro with normal human cultured skin fibroblasts and adipocytes, ASP appears to be the most potent stimulant of triglyceride synthesis yet described. In this study, a competitive ELISA assay for ASP has been developed using immunospecific polyclonal antibodies, and ASP levels have been measured in seven normal subjects. Following an oral fat load, a sustained significant increase in ASP occurs, whereas after an oral glucose load, ASP levels do not change significantly. These responses are entirely opposite to those of insulin, which rises sharply but transiently after an oral glucose load but is unchanged after an oral fat load. Both the fasting and peak ASP levels were significantly related to the postprandial lipemia. These data provide the first in vivo evidence that Acylation Stimulating Protein may play an important physiological role in the normal response to an oral fat load.
Coordinated release of acylation stimulating protein (ASP) and triacylglycerol clearance by human adipose tissue in vivo in the postprandial period.
The objective of this study was to determine whether Acylation Stimulating Protein (ASP) is generated in vivo by human adipose tissue during the postprandial period. After a fat meal, samples from 12 subjects were obtained (up to 6 h) from an arterialized hand vein and an anterior abdominal wall vein that drains adipose tissue. Veno-arterial (V-A) gradients across the subcutaneous adipose tissue bed were calculated. The data demonstrate that ASP is produced in vivo (positive V-A gradient) With maximal production at 3-5 h postprandially. The plasma triacylglycerol (TAG) clearance was evidenced by a negative V-A gradient. It increased substantially after 3 h and remained prominent until the final time point. There was, therefore, a close temporal coordination between ASP generation and TAG clearance. In contrast, plasma insulin and non-esterified fatty acid (NEFA) had an early (1-2 h) postprandial change. Fatty acid incorporation into adipose tissue (FIAT) was calculated from V-A glycerol and non-esterified fatty acid (NEFA) differences postprandially. FIAT was negative during the first hour, implying net fat mobilization. FIAT then became increasingly positive, implying net fat deposition, and overall followed the same time course as ASP and TAG clearance. There was a direct positive correlation between total ASP production and total FIAT (r = 0.566, P < 0.05). These data demonstrate that ASP is generated in vivo by human adipocytes and that this process is accentuated postprandially, supporting the concept that ASP plays an important role in clearance of TAG from plasma and fatty acid storage in adipose tissue.
Eli ASP on mukana rasvan kerääämisessä.
The effect of ASP on the adipocyte of the morbidly obese.
The control of triglyceride synthesis within the adipocyte is not fully understood. Insulin is considered to be the most potent stimulant of triglyceride synthesis. In this paper, we report on the effect of a small (14000 Da), basic (pI 9.0) protein isolated from human serum. This protein has been called acylation stimulating protein (ASP). It is a potent stimulant of triglyceride synthesis in adipocytes from both normal weight and morbidly obese subjects. Its stimulatory effect on adipocytes is both rapid, occurring between 15-30 min after the start of incubation, and prolonged, lasting for up to 3 hr. Compared to insulin, it is sixfold more potent in its effect on triglyceride synthesis. As well as acting on isolated cells, ASP also has a fourfold stimulatory effect on triglyceride synthesis in human adipose microsomes at a concentration of 25 micrograms/ml. This study indicates that ASP is a potent stimulant of triglyceride synthesis and therefore may play a role in the pathogenesis of morbid obesity.
Lipoprotein lipase deficiency is associated with elevated acylation stimulating protein plasma levels.
Acylation stimulating protein (ASP, C3adesArg) is an adipose tissue derived hormone that stimulates triglyceride (TG) synthesis. ASP stimulates lipoprotein lipase (LPL) activity by relieving feedback inhibition caused by fatty acids (FA). The present study examines plasma ASP and lipids in male and female LPL-deficient subjects primarily with the P207L mutation, common in the population of Quebec, Canada. We evaluated the fasting and postprandial states of LPL heterozygotes and fasting levels in LPL homozygotes. Homozygotes displayed increased ASP (58-175% increase, P < 0.05-0.01), reduced HDL-cholesterol (64-75% decrease, P < 0.0001), and elevated levels of TG (19-38-fold, P < 0.0001) versus control (CTL) subjects. LPL heterozygotes with normal fasting TG (1.3-1.9 mmol/l) displayed increased ASP (101-137% increase, P < 0.05-0.01) and delayed TG clearance after a fatload; glucose levels remained similar to controls. Hypertriglyceridemics with no known LPL mutation also had increased ASP levels (63-192% increase, P < 0.001). High-TG LPL heterozygotes were administered a fatload before and after fibrate treatment. The treatment reduced fasting and postprandial plasma ASP, TG, and FA levels without changing insulin or glucose levels. ASP enhances adipose tissue fatty-acid trapping following a meal; however in LPL deficiency, high ASP levels are coupled with delayed lipid clearance.
Of mice and men (and women) and the acylation-stimulating protein pathway.
The storage and release of energy by adipocytes is of fundamental biologic importance. Not surprisingly, therefore, the rate at which these processes occur can be modulated by a variety of physiologic molecules. A newly recognized participant is produced by adipocytes themselves: acylation-stimulating protein (ASP). This article focuses on the most recent in-vivo evidence regarding how the ASP pathway may influence energy storage and release. In brief, the rate at which triglycerides are cleared from plasma (i.e. the rate at which they are hydrolysed) is determined by lipoprotein lipase and insulin, which is the principal hormone that regulates lipoprotein lipase. By contrast, the ASP pathway modulates the rate at which fatty acids are taken up and converted to triglycerides by adipocytes. Under certain circumstances, however, reduction of activity of the ASP pathway may negatively impact on the first step of the process. ASP also influences the rate at which fatty acids are released by adipocytes, and it is clear that insulin and ASP interact in a variety of ways that involve energy storage and release. Accordingly, to understand the impact of any intervention on energy storage and release by adipocytes, the effects of both insulin and ASP must be taken into account.
Effects of an oral and intravenous fat load on adipose tissue and forearm lipid metabolism.
We have studied the fate of lipoprotein lipase (LPL)-derived fatty acids by measuring arteriovenous differences across subcutaneous adipose tissue and skeletal muscle in vivo. Six subjects were fasted overnight and were then given 40 g of triacylglycerol either orally or as an intravenous infusion over 4 h. Intracellular lipolysis (hormone-sensitive lipase action; HSL) was suppressed after both oral and intravenous fat loads (P < 0.001). Insulin, a major regulator of HSL activity, showed little change after either oral or intravenous fat load, suggesting that suppression of HSL action occurred independently of insulin. The rate of action of LPL (measured as triacylglycerol extraction) increased with both oral and intravenous fat loads in adipose tissue (P = 0.002) and skeletal muscle (P = 0.001). There was increased escape of LPL-derived fatty acids into the circulation from adipose tissue, shown by lack of reesterification of fatty acids. There was no release into the circulation of LPL-derived fatty acids from skeletal muscle. These results suggest that insulin is not essential for HSL suppression or increased triacylglycerol clearance but is important in reesterification of fatty acids in adipose tissue but not uptake by skeletal muscle, thus affecting fatty acid partitioning between adipose tissue and the circulation, postprandial nonesterified fatty acid concentrations, and hepatic very low density lipoprotein secretion.
Purification and characterization of acylation stimulating protein.
We have purified to homogeneity and analyzed the amino acid composition of a small (Mr 14,000), basic (pI 9.0) protein from human plasma. This has been named acylation stimulating protein (ASP) because it markedly stimulates triacylglycerol synthesis in human adipocytes. As well, it stimulates triacylglycerol synthesis in human skin fibroblasts cultured from normal individuals. Characteristic saturation curves for the cell metabolic responses to ASP were observed in both cell types with higher stimulation of oleate incorporation into triacylglycerol being observed in adipocytes. The stimulation of triacylglycerol synthesis was much greater with ASP than with insulin. Neither fatty acid binding protein nor albumin was able to mimic the ASP effect.
Control of fatty acid and glycerol release in adipose tissue lipolysis.
Adipose tissue lipolysis is the catabolic process leading to the breakdown of triglycerides stored in fat cells and the release of fatty acids and glycerol. Recent work has revealed that lipolysis is not a simple metabolic pathway stimulated by catecholamines and inhibited by insulin. New discoveries on the regulation of lipolysis by endocrine and paracrine factors and on the proteins involved in triglyceride hydrolysis have led to a reappraisal of the complexity of the various signal transduction pathways. The steps involved in the dysregulation of lipolysis observed in obesity have partly been identified.
Eli insuliini ei ole ainoa tekijä. Sen takia pelkkä insuliinin kontrolloiminen ei riitä.
Diet composition and energy balance in humans.
Inpatient metabolic studies of human subjects were performed to obtain data on important nutritional issues. It was shown that wide variations in the ratio of carbohydrate to fat do not alter total 24-h energy need. Studies of the fatty acid composition of plasma low-density lipoproteins during low-fat feeding indicated that there can be considerable lipogenesis from carbohydrate in humans during isoenergetic feeding. The energy cost of this conversion must be small or be counterbalanced by other changes in energy metabolism because measured energy need was unaltered by fat-to-carbohydrate ratios. Energy need was, however, markedly varied by changes in body weight. Subjects at their usual body weights who had experimentally induced increases in body weight became inefficient and required a higher energy.
Energetics of obesity and weight control: does diet composition matter?
Greater average weight losses (2.5 kg over 12 weeks) have been reported for low-carbohydrate diets (<90 g/day) compared with traditional low-fat (<25% of energy), hypocaloric diets, implying a 233 kcal/day greater energy deficit. It has therefore been suggested that a low-carbohydrate diet may provide a metabolic advantage (an increase in energy expenditure), resulting in a positive effect on weight loss and maintenance. However, a review of studies in which 24-hour energy expenditure was measured did not provide evidence to support a metabolic advantage of low-carbohydrate diets and showed little evidence of a metabolic advantage of high-protein (>25% of energy) diets. Nonetheless, diets high in protein, but either low or modest in carbohydrate, have resulted in greater weight losses than traditional low-fat diets. We speculate that it is the protein, and not carbohydrate, content that is important in promoting short-term weight loss and that this effect is likely due to increased satiety caused by increased dietary protein. It has been suggested that the increased satiety might help persons to be more compliant with a hypocaloric diet and achieve greater weight loss. The current evidence, combined with the need to meet all nutrient requirements, suggests that hypocaloric weight-loss diets should be moderate in carbohydrate (35% to 50% of energy), moderate in fat (25% to 35% of energy), and protein should contribute 25% to 30% of energy intake. More studies of the efficacy of weight-loss and weight-maintenance diets that address protein content are needed. In addition, controlled studies of total energy expenditure or physical activity measured under free-living conditions that directly compare high-protein diets with those containing low and moderate carbohydrate content should also be performed.
Benefit of low-fat over low-carbohydrate diet on endothelial health in obesity.
Obesity is associated with impaired endothelial-dependent flow-mediated dilation, a precursor to hypertension and atherosclerosis. Although dieting generally improves cardiovascular risk factors, the direct effect of different dietary strategies on vascular endothelial function is not known. The purpose of this study was to test the hypothesis that a low-fat (LF) diet improves endothelial function compared with an isocaloric low-carbohydrate (LC) diet. Obese (n=20; body mass index: 29 to 39; mean systolic blood pressure: 107 to 125 mm Hg) and otherwise healthy volunteers were randomly assigned to either the American Heart Association modeled LF (30% fat calories) diet or an isocaloric LC Atkins' style diet (20 g of carbohydrates) for 6 weeks (4-week weight loss and 2-week maintenance phase). Brachial flow-mediated dilation and dilation to nitroglycerin were measured with ultrasound using automated edge detection technology (baseline, week 2, and week 6). Blood pressure, weight loss, and cholesterol profiles were measured throughout the study. Weight loss was similar in LF (100+/-4 to 96.1+/-4 kg; P<0.001) and LC (95.4+/-4 to 89.7+/-4 kg; P<0.001) diets. Blood pressure decreased similarly in both groups (LF: 8/5 mm Hg; LC: 12/6 mm Hg) at 6 weeks. After 6 weeks, the percentage of flow-mediated dilation improved (1.9+/-0.8; P<0.05) in the LF diet but was reduced in the LC diet (-1.4+/-0.6; P<0.05) versus baseline. Dilation to nitroglycerin and lipid panels was similar at 0, 2, and 6 weeks. Despite similar degrees of weight loss and changes blood pressure, LF diets improved brachial artery flow-mediated dilation over LC diets. LF diets may confer greater cardiovascular protection than LC diets.
Kalorimäärät samat ja samanlainen painonpudotus. Ehkä kalorit ratkaisevat?
Low-fat versus low-carbohydrate weight reduction diets: effects on weight loss, insulin resistance, and cardiovascular risk: a randomized control trial.
OBJECTIVE: Low-fat hypocaloric diets reduce insulin resistance and prevent type 2 diabetes in those at risk. Low-carbohydrate, high-fat diets are advocated as an alternative, but reciprocal increases in dietary fat may have detrimental effects on insulin resistance and offset the benefits of weight reduction. RESEARCH DESIGN AND METHODS: We investigated a low-fat (20% fat, 60% carbohydrate) versus a low-carbohydrate (60% fat, 20% carbohydrate) weight reduction diet in 24 overweight/obese subjects ([mean +/- SD] BMI 33.6 +/- 3.7 kg/m(2), aged 39 +/- 10 years) in an 8-week randomized controlled trial. All food was weighed and distributed, and intake was calculated to produce a 500 kcal/day energy deficit. Insulin action was assessed by the euglycemic clamp and insulin secretion by meal tolerance test. Body composition, adipokine levels, and vascular compliance by pulse-wave analysis were also measured. RESULTS: Significant weight loss occurred in both groups (P < 0.01), with no difference between groups (P = 0.40). Peripheral glucose uptake increased, but there was no difference between groups (P = 0.28), and suppression of endogenous glucose production was also similar between groups. Meal tolerance-related insulin secretion decreased with weight loss with no difference between groups (P = 0.71). The change in overall systemic arterial stiffness was, however, significantly different between diets (P = 0.04); this reflected a significant decrease in augmentation index following the low-fat diet, compared with a nonsignificant increase within the low-carbohydrate group. CONCLUSIONS: This study demonstrates comparable effects on insulin resistance of low-fat and low-carbohydrate diets independent of macronutrient content. The difference in augmentation index may imply a negative effect of low-carbohydrate diets on vascular risk.
Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk.
BACKGROUND: It is speculated that high saturated fat very low carbohydrate diets (VLCARB) have adverse effects on cardiovascular risk but evidence for this in controlled studies is lacking. The objective of this study was to compare, under isocaloric conditions, the effects of a VLCARB to 2 low saturated fat high carbohydrate diets on body composition and cardiovascular risk. METHODS: Eighty three subjects, 48 +/- 8 y, total cholesterol 5.9 +/- 1.0 mmol/L, BMI 33 +/- 3 kg/m2 were randomly allocated to one of 3 isocaloric weight loss diets (6 MJ) for 8 weeks and on the same diets in energy balance for 4 weeks: Very Low Fat (VLF) (CHO:Fat:Protein; %SF = 70:10:20; 3%), High Unsaturated Fat (HUF) = (50:30:20; 6%), VLCARB (4:61:35; 20%) RESULTS:
VLCARB -4.5 +/- 0.5, VLF-4.0 +/- 0.5, HUF -4.4 +/- 0.6 kg). Lean mass loss was 32-31% on VLCARB and VLF compared to HUF (21%) (P < 0.05). LDL-C increased significantly only on VLCARB by 7% (p < 0.001 compared with the other diets) but apoB was unchanged on this diet and HDL-C increased relative to the other 2 diets. Triacylglycerol was lowered by 0.73 +/- 0.12 mmol/L on VLCARB compared to -0.15 +/- 0.07 mmol/L on HUF and -0.06 +/- 0.13 mmol/L on VLF (P < 0.001). Plasma homocysteine increased 6.6% only on VLCARB (P = 0.026). VLCARB lowered fasting insulin 33% compared to a 19% fall on HUF and no change on VLF (P < 0.001). The VLCARB meal also provoked significantly lower post prandial glucose and insulin responses than the VLF and HUF meals. All diets decreased fasting glucose, blood pressure and CRP (P < 0.05). CONCLUSION: Isocaloric VLCARB results in similar fat loss than diets low in saturated fat, but are more effective in improving triacylglycerols, HDL-C, fasting and post prandial glucose and insulin concentrations. VLCARB may be useful in the short-term management of subjects with insulin resistance and hypertriacylglycerolemia.
A randomized trial comparing low-fat and low-carbohydrate diets matched for energy and protein.
Several recent studies have found greater weight loss at 6 months among participants on a very-low-carbohydrate (VLC) weight-loss diet compared with a low-fat (LF) weight-loss diet. Because most of these studies were not matched for calories, it is not clear whether these results are caused by decreased energy intake or increased energy expenditure. It is hypothesized that several energy-consuming metabolic pathways are up-regulated during a VLC diet, leading to increased energy expenditure. The focus of this study was to investigate whether, when protein and energy are held constant, there is a significant difference in fat and weight loss when fat and carbohydrate are dramatically varied in the diet. The preliminary results presented in this paper are for the first four of six postmenopausal overweight or obese participants who followed, in random order, both a VLC and an LF diet for 6 weeks. Other outcome measures were serum lipids, glucose, and insulin, as well as dietary compliance and side effects. Our results showed no significant weight loss, lipid, serum insulin, or glucose differences between the two diets. Lipids were dramatically reduced on both diets, with a trend for greater triglyceride reduction on the VLC diet. Glucose levels were also reduced on both diets, with a trend for insulin reduction on the VLC diet. Compliance was excellent with both diets, and side effects were mild, although participants reported more food cravings and bad breath on the VLC diet and more burping and flatulence on the LF diet
Fat loss depends on energy deficit only, independently of the method for weight loss.
BACKGROUND: This study was designed to compare the effects of 2 different but isocaloric fat reduction programs with the same amount of energy deficit - diet alone or diet combined with aerobic training - on body composition, lipid profile and cardiorespiratory fitness in non- or moderately obese women. METHODS: Twenty non- or moderately obese (BMI 24.32 +/- 3.11) females (27.3 +/- 6.6 years) were tested at the beginning and after an 8-week period of a mild hypocaloric diet for the following parameters: (1) body mass and body fat; (2) total cholesterol, HDL-C, LDL-C and triglycerides; (3) lactate (millimol/liter) during submaximal exertion (100 W); (4) heart rate during submaximal exertion (100 W), and (5) maximum exercise performance (watt). Subjects were randomly divided into either a diet alone (D, -2,095 +/- 659 kJ/day) or a diet (-1,420 +/- 1,084 kJ/day) plus exercise (DE, three 60-min sessions per week at 60% of VO(2)max or -5,866 kJ/week) group. RESULTS: Body mass and body fat decreased significantly in D (-1.95 +/- 1.13 kg or -1.47 +/- 0.87%; p < 0.05) and DE (-2.23 +/- 1.28 kg or -1.59 +/- 0.87%; p < 0.05), but there was no significant difference observed between the groups. Statistical analysis revealed no significant changes of total cholesterol, HDL-C, LDL-C, triglycerides and heart rate during submaximal exertion (100 W). Lactic acid accumulation during submaximal exertion (100 W) decreased significantly (-0.8 +/- 1.4 mmol/l, p < 0.05) in DE and increased significantly (+0.4 +/- 0.5 mmol/l, p < 0.05) in D. Maximum exercise performance improved significantly (+12.2 +/- 8.8 W, p < 0.05) in DE and did not change significantly in D. CONCLUSIONS: This study showed that independently of the method for weight loss, the negative energy balance alone is responsible for weight reduction.
Ja minulle kaikista rakkain tutkimus.
Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets.
BACKGROUND: Low-carbohydrate diets may promote greater weight loss than does the conventional low-fat, high-carbohydrate diet. OBJECTIVE: We compared weight loss and biomarker change in adults adhering to a ketogenic low-carbohydrate (KLC) diet or a nonketogenic low-carbohydrate (NLC) diet. DESIGN: Twenty adults [body mass index (in kg/m(2)): 34.4 +/- 1.0] were randomly assigned to the KLC (60% of energy as fat, beginning with approximately 5% of energy as carbohydrate) or NLC (30% of energy as fat; approximately 40% of energy as carbohydrate) diet. During the 6-wk trial, participants were sedentary, and 24-h intakes were strictly controlled. RESULTS: Mean (+/-SE) weight losses (6.3 +/- 0.6 and 7.2 +/- 0.8 kg in KLC and NLC dieters, respectively; P = 0.324) and fat losses (3.4 and 5.5 kg in KLC and NLC dieters, respectively; P = 0.111) did not differ significantly by group after 6 wk. Blood beta-hydroxybutyrate in the KLC dieters was 3.6 times that in the NLC dieters at week 2 (P = 0.018), and LDL cholesterol was directly correlated with blood beta-hydroxybutyrate (r = 0.297, P = 0.025). Overall, insulin sensitivity and resting energy expenditure increased and serum gamma-glutamyltransferase concentrations decreased in both diet groups during the 6-wk trial (P < 0.05). However, inflammatory risk (arachidonic acid:eicosapentaenoic acid ratios in plasma phospholipids) and perceptions of vigor were more adversely affected by the KLC than by the NLC diet. CONCLUSIONS: KLC and NLC diets were equally effective in reducing body weight and insulin resistance, but the KLC diet was associated with several adverse metabolic and emotional effects. The use of ketogenic diets for weight loss is not warranted.
No niin. Staattisissa kalori ja proteiinitiloissa ei merkitystä syökö hillareita vai rasvaa. Insuliini on merkityksetön.
Ja insuliiniresistenssi on tila, jossa keho erittää enemmän insuliinia, koska insuliini ei tee tehtäviään kehossa kunnolla. Ja siitä on apua laihduttamiseen. Eli selkeästi pelkkä insuliini ei kerro kaikkea.
To study demographic, anthropometric and metabolic determinants of weight change, we divided a random sample of 1493 Mexican Americans and non-Hispanic whites into two groups: weight gainers and weight losers. This classification was based on the weight change during the eight-year follow-up of participants of the San Antonio Heart Study, a population-based longitudinal study of diabetes and cardiovascular disease. Men gained significantly less weight and lost more weight than women. The average gains for weight gainers were 6.1 kg and 6.8 kg for men and women respectively; and the average losses for weight losers were 4.4 and 3.4 kg for men and women respectively. There was no ethnic difference in either category of weight change. Weight gainers were significantly younger and leaner than weight losers. Fasting insulin was the only independent metabolic predictor of weight change and only among the most obese tertile of the population: the higher the baseline levels of fasting insulin, the less the likelihood of gaining and the greater the likelihood of losing weight. Our results support the hypothesis that insulin resistance is part of a negative feedback mechanism that attenuates further weight gain among the obese.
Loss of 50% of excess weight using a very low energy diet improves insulin-stimulated glucose disposal and skeletal muscle insulin signalling in obese insulin-treated type 2 diabetic patients.
AIMS/HYPOTHESIS: Both energy restriction (ER) per se and weight loss improve glucose metabolism in obese insulin-treated type 2 diabetic patients. Short-term ER decreases basal endogenous glucose production (EGP) but not glucose disposal. In contrast the blood glucose-lowering mechanism of long-term ER with substantial weight loss has not been fully elucidated. The aim of this study was to investigate the effect of loss of 50% of excess weight [50% excess weight reduction (EWR)] on EGP, whole-body insulin sensitivity and the disturbed myocellular insulin-signalling pathway in ten obese insulin-treated type 2 diabetic patients. METHODS: A euglycaemic-hyperinsulinaemic clamp with stable isotopes ([6,6-(2)H2]glucose and [2H5]glycerol) combined with skeletal muscle biopsies was performed during a very low energy diet (VLED; 1,883 kJ/day) on day 2 and again after 50% EWR. Oral blood glucose-lowering agents and insulin were discontinued 3 weeks prior to the VLED and at the start of the VLED, respectively. RESULTS: Loss of 50% EWR (20.3+/-2.2 kg from day 2 to day of 50% EWR) normalised basal EGP and improved insulin sensitivity, especially insulin-stimulated glucose disposal (18.8+/-2.0 to 39.1+/-2.8 micromol kg fat-free mass(-1) min(-1), p=0.001). The latter was accompanied by improved insulin signalling at the level of the recently discovered protein kinase B/Akt substrates AS160 and PRAS40 along with a decrease in intramyocellular lipid (IMCL) content. CONCLUSIONS/INTERPRETATION: Considerable weight loss in obese, insulin-treated type 2 diabetic patients normalises basal EGP and improves insulin sensitivity resulting from an improvement in insulin signal transduction in skeletal muscle. The decrease in IMCL might contribute to this effect.
Kappas vain. diabeetikoille annettiin dieetin aikana eksogeenista insuliinia ja mitä kävi? He laihtuivat. Miksi? Koska he söivät vähemmän kaloreita kun kuluttivat. Kalorit siis ratkaisevat eivät insuliini.
No effect of inhibition of insulin secretion by diazoxide on weight loss in hyperinsulinaemic obese subjects during an 8-week weight-loss diet.
AIM: Obesity is positively associated with hyperinsulinaemia, and it has been suggested that hyperinsulinaemia may contribute to maintain the obese state in insulin-resistant obese individuals. The aim of the present study was to investigate the effect of inhibition of insulin secretion by diazoxide on weight loss in obese, normoglycaemic (fasting plasma glucose of > or =6.1 mmol/l), hyperinsulinaemic (fasting plasma insulin of > or =100 pmol/l) adults during a 2.5 MJ/day energy-deficient diet. METHODS: In an 8-week, double-blind, placebo-controlled parallel design, 35 overweight and obese subjects (age: 23-54 years, body mass index: 27-66 kg/m(2)) were randomized either to 2 mg/kg/day (maximum 200 mg/day) of oral diazoxide or to placebo. Body composition and resting energy expenditure (REE) were measured before and after the intervention. Blood samples, and appetite sensations by visual analogue scales, were collected during fasting, during an oral glucose tolerance test (OGTT) and 4 h postprandially after a test meal. Subsequently, an ad libitum meal was given. RESULTS: Thirty-one subjects completed the protocol. Eight weeks of diazoxide decreased incremental area under the response curve (iAUC) for insulin (iAUC(insulin)) and for C-peptide (iAUC(C-peptide)) and increased iAUC for glucose (iAUC(glucose)) during the OGTT and the test meal compared with the use of placebo (p < 0.003). No differences in changes between the groups in body weight, body fat, REE or appetite were observed during the 8-week trial. CONCLUSION: These findings do not suggest that hyperinsulinaemia per se contributes to maintenance of the obese state, and insulin secretion inhibition seems not a promising drug target
.
Kappas vain. Insuliinin blokkaaminen ei tuonut mitään etuja rasvanpolton suhteen. Miksi? Koska insuliini ei ole ainoa tekijä. Kalorit ratkaisevat.
Insulin use and weight maintenance in well-controlled type 2 diabetes: a prospective cohort study.
Intensification of glycemic control is associated with weight gain, however, less is known about weight change during the maintenance phase of glycemic management. On the basis of current models of energy homeostasis, we hypothesize that insulin use will result in less weight gain than oral antidiabetic agents in patients with well-controlled diabetes. This is a prospective cohort nested within a randomized control trial at an academic clinic, with enrollment from June 2002 to January 2005. A total of 163 patients with type 2 diabetes were enrolled after obtaining glycemic control. Insulin use was assessed by self-report at baseline. Participants were weighed at baseline and five follow-up visits over 24 months. The weight change was compared between insulin users and noninsulin users. The average (s.d.) age was 55 (11), 44% are female and 21% are black. The median duration of diabetes was 5 (0.5-10) years. At baseline, 88 participants (54%) reported insulin use with an average of 69 (6) units/day. Baseline BMI in the insulin users was 35 (6) and 33 (6) in noninsulin patients. Over 24 months, noninsulin patients gained 2.3 additional kilograms compared with insulin users (2.8 kg (6.8) vs. 0.5 kg (6.5), P = 0.065). After adjusting for age, race, sex, baseline weight, intervention status, and change in A1C, insulin users had 2.5 kg less weight gain than noninsulin users (P = 0.033). Less weight gain was observed over 24 months in insulin-treated patients. Whether this effect may be due to central catabolic effects of insulin merits additional confirmatory study and mechanistic investigation.
Eli insuliinin käyttäjät lihoivat vähemmän. Ehkä kalorit ratkaisevat?
Is a failure to recognize an increase in food intake a key to understanding insulin-induced weight gain?
The present study aimed to assess the contribution of energy intake to positive energy balance and weight gain with insulin therapy. Changes in energy intake (self-report and weighed food intake), dietary behavior (auto-questionnaires), resting energy expenditure (REE) (indirect calorimetry), physical activity (accelerometry), and glucosuria were monitored over the first 6 months of insulin therapy in 46 diabetic adults. No change in REE, activity, or glucosuria could explain weight gain in the type 1 (4.1 +/- 0.6 kg, P < 0.0001) or type 2 (1.8 +/- 0.8 kg, P = 0.02) diabetic groups. An increase in energy intake provides the most likely explanation for weight gain with insulin. However, it is not being recognized because of significant underestimation of self-reported food intake, which appears to be associated with increased dietary restraint.
Lisää dataa.. Liiallinen energiansaanti lihottaa, ei insuliini.
Eli keho kerää rasvaa aterian jälkeen - nousi insuliinitasot paljon tai ei. Rasvan kerääntyminen/poistuminen määräytyy pitkällä aikavälillä energiatasapainon mukaan.
Jos vieläkin on vaikeuksia ymmärtää lue postaukseni uudestaan, myös nuo edelliset mitä quottasit. Kaloritaspaino ratkaisee, ei insuliini. Muuten hiilihhydraatit lihottaisivat eniten, proteiini toiseksi eniten ja rasva vähiten. Arvaa onko asia näin? Jos olet epävarma lue edelliset postaukseni niissä vähähiilihydraattinen dieetti EI ole parempi kuin hiilihydraattipitoinen, jos kalorit ovat kontrolloitu. Ja kalorikontrolloidussa tilassa rasva lihottaa vähintään yhtä paljon kuin hiilihydraatit. Olisko sen takia, että insuliini ei ole ainoa tekijä vai koska se ei ole? Vai sen takia että kalort ratkaisevat vai koska ne ratkaisevat?
