Effect of dietary macronutrient composition on tissue-specific lipoprotein lipase activity and insulin action in normal-weight subjects

Yost, Trudy J.; Jensen, Dalan R.; Haugen, Bryan R.; Eckel, Robert H.

doi:10.1093/ajcn/68.2.296

Cited by 57 publications

(51 citation statements)

References 37 publications

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“…30 In the present study increased consumption of dietary fat did not lead to an increased insulin resistance index, which is consistent with findings in short term fat diet adaptation studies where peripheral insulin resistance was either unchanged 10,11 or only modestly increased. 12 In rodents there is evidence that inclusion of dietary n-3 fatty acids at least partly ameliorates the fat-diet-induced increase in insulin resistance.…”

Section: Discussionsupporting

confidence: 91%

“…5,7 In addition to physical inactivity epidemiological data indicate that an excess in dietary intake and particularly fat intake is considered one of the key factors in the development of glucose intolerance and insulin resistance. 8,9 Somewhat in contrast, shorter term fat adaptation studies in man have demonstrated either unchanged 10,11 or only modestly increased 12 peripheral insulin resistance. However, controlled long-term studies where dietary fat content and physical activity levels are manipulated are very sparse.…”

Section: Introductionmentioning

confidence: 99%

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Prolonged adaptation to fat-rich diet and training; effects on body fat stores and insulin resistance in man

Helge¹

2002

Int J Obes

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OBJECTIVE:To investigate the effect of prolonged adaptation to training and fat-or carbohydrate-rich diet on body composition and insulin resistance. DESIGN: Longitudinal study. Of three groups two consumed a fat-rich diet, of which one performed regular training (FAT-Train, n ¼ 17) and the other maintained normal habitual activity (Fat-Control, n ¼ 8). The third group trained and consumed a carbohydrate-rich diet (CHO-Train, n ¼ 16). SUBJECTS: Forty-one untrained, healthy male subjects. MEASUREMENTS: Before and after 7 weeks body composition was estimated from skinfold measurements. At rest the respiratory exchange ratio (RER) was determined by the Douglas bag technique. Glycogen was determined in m vastus lateralis and concentrations of insulin and triacylglycerol in serum and glucose, fatty acid and beta-hydroxy-butyrate in plasma was measured. The insulin resistance index was calculated from fasting plasma insulin and glucose values. RESULTS: Across the 7 weeks body weight was reduced (1.3 AE 0.3%) in all three groups, however body fat mass was decreased only in the CHO-Train (13%) and maintained in the two FAT-groups. RER at rest was similarly decreased (5%) in the three groups. Plasma insulin tended to decrease (16%) in CHO-Train (P ¼ 0.065) and remained unchanged in the two FAT-groups. In contrast plasma glucose (4.6 AE 0.1 mmol=l) and plasma FA (453 AE 27 mmol=l) remained unchanged across the 7 weeks. The calculated insulin resistance index HOMA-R mod was significantly decreased by 19% in CHO-train but remained unchanged in both of the FAT-groups, whereas the calculated insulin secretion index HOMA-ß mod was unchanged in all three groups. CONCLUSION: In the present study we demonstrate that despite of a mild energy deficit body fat mass was maintained after prolonged adaptation to fat-rich diet both when normal physical activity was maintained and when training was performed. In contrast a significant decrease in fat mass was observed when carbohydrate-rich diet and training was combined. Furthermore we observed that the insulin resistance index was significantly decreased only when training was combined with a carbohydraterich diet.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Prolonged adaptation to fat-rich diet and training; effects on body fat stores and insulin resistance in man

Helge¹

2002

Int J Obes

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“…(decreased), 2 weeks of a high-carbohydrate diet or highfat diet increased the LPL response to feeding in both adipose tissue and skeletal muscle (24). In adipose tissue only, there was a significant difference between the two diets in the LPL meal response (high-carbohydrate diet .…”

Section: Nutritional and Hormonal Regulation Of Lplmentioning

confidence: 96%

Regulation of fatty acid uptake into tissues: lipoprotein lipase- and CD36-mediated pathways

Goldberg

Eckel

Abumrad

2009

Journal of Lipid Research

349

276

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Cells obtain FAs either from LPL-catalyzed hydrolysis of lipoprotein triglyceride or from unesterified FFAs associated with albumin. LPL also influences uptake of esterified lipids such as cholesteryl and retinyl esters that are not hydrolyzed in the plasma. This process might not involve LPL enzymatic activity. LPL is regulated by feeding/ fasting, insulin, and exercise. Although a number of molecules may affect cellular uptake of FFAs, the best characterized is CD36. Genetic deletion of this multiligand receptor reduces FFA uptake into skeletal muscle, heart, and adipose tissue, and impairs intestinal chylomicron production and clearance of lipoproteins from the blood.CD36 is regulated by some of the same factors that regulate LPL, including insulin, muscle contraction, and fasting, in part, via ubiquitination. LPL and CD36 actions in various tissues coordinate biodistribution of fat-derived calories. There are several pathways that allow the uptake of circulating lipids into cells. Cell surface receptors mediate the uptake of whole lipoproteins. FA uptake is more similar to that of the other major blood nutrient, glucose. Unlike glucose, which is water soluble, FAs are either associated with albumin, so-called free (FFA), or are esterified as a component of triglycerides (TGs), phospholipids, and esterified cholesterol. Esterified FAs within VLDL and chylomicrons comprise .90% of blood FAs. Nonetheless, the rapid plasma turnover of FFA has the potential to supply large amounts of energy to tissues. LIPID UPTAKE VIA THE LIPOLYSIS PATHWAYThe importance of the lipolysis reaction in the catabolism of TG-rich lipoproteins was shown more than 50 years ago by the discovery that intravenous heparin injection leads to the release of LPL into the plasma and reduces postprandial lipemia. Subsequent studies established that LPL is robustly expressed in tissues like adipose and muscle that require large influxes of FAs for storage or energy and that LPL is the primary enzyme responsible for chylomicron-and VLDL-TG lipolysis. However, several questions on the role of this enzyme in fuel partitioning and tissue lipid uptake, its regulation, and its importance for vascular biology remained to be answered.Genetic modulation of LPL protein and its sites of expression have partially elucidated how LPL affects physiology and has confirmed prior in vitro studies. Although humans with LPL deficiency develop severe hypertriglyceridemia and are at risk for pancreatitis, mice with spontaneous or genetic loss of LPL die within 24 h of birth. Prior to death, LPL-deficient mice develop hypoglycemia, a process that is partially abrogated by ketone body production via LPL expression in the liver (1). In contrast, tissuespecific overexpression of LPL in skeletal muscle and liver increased cellular stores of TG and probably other lipids and led to insulin resistance (2). Loss of LPL in adipose tissue and its overexpression in skeletal muscle reduced adipose development when these mice were crossed onto the obesity ob/ob background ...

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“…This divergent response would serve to direct lipoprotein TG-derived fatty acids away from muscle to adipose tissue for storage. A high-carbohydrate diet for 16 d in normalweight subjects increased postprandial LPL activity in adipose tissue, with elevation of blood glucose and insulin concentrations after meals, relative to a high-fat diet (75). Therefore, increased insulin and glucose from a high-carbohydrate diet may promote obesity via activation of LPL in adipose tissues.…”

Section: An Increase In Lipoprotein Lipase (Lpl) Activity In Adipose mentioning

confidence: 95%

The Optimal Dietary Fat to Carbohydrate Ratio to Prevent Obesity in the Japanese Population: A Review of the Epidemiological, Physiological and Molecular Evidence

Ezaki¹

2011

J Nutr Sci Vitaminol

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Summary The prevention of obesity, which leads to diabetes and other diseases, is a major concern for public health. There might be an optimal dietary fat to carbohydrate ratio for prevention and treatment of obesity. According to the Japanese Dietary Reference Intakes (RDA) for 2010, the optimal fat intake is 20-30% of energy for ages 1-29 y and 20-25% for ages 30 y and over. Upper boundary values of this recommendation were the median of the percentage of energy from dietary fat in Japanese. In a systematic review to estimate the optimal dietary fat to carbohydrate ratio, it was found that obese subjects with hyperinsulinemia (or insulin resistance) lost more weight on a mild low-carbohydrate (LC) (or low-glycemic load diet; 40% carbohydrate, 30-35% fat) than on a low-fat (LF) diet (55-60% carbohydrate, 20% fat), whereas those without hyperinsulinemia showed the opposite. In non-obese primarily insulin-sensitive subjects, decreasing fat rather than carbohydrate intake is generally more effective to prevent obesity. Physiological and molecular evidence supports this conclusion. Increased carbohydrate intake, especially in high-glycemic food, leads to postprandial hyperglycemia and hyperinsulinemia, which are exaggerated in obese insulin-resistant subjects. Even in an insulin-resistant state, insulin is able to stimulate fatty acid synthesis in liver, activate lipoprotein lipase, and prevent lipolysis in adipose tissues, which all facilitate adipose tissue enlargement. Optimal dietary fat to carbohydrate ratio may differ in populations depending on their prevalence for obesity. Because the prevalence of overweight/obesity in Japanese is low, a LF diet is recommended in the general population. Key Words low-carbohydrate diet, low-fat diet, RDA, insulin resistance, obesity , as compared with women who had a BMI of less than 23.0 kg/m 2 ( 2 ). In Japan, the prevalence of overweight/obesity (BMI Ն 25 kg/m 2 ) in adults is very low compared with the United States: 30.4% in men and 20.2% in women in 2007, according to Japanese cross-sectional nationwide surveys ( 3 ). However, a strong positive association between baseline BMI and the incidence of diabetes in the follow-up period was observed similar to that in the United States. In a Japanese cohort of healthy men ( n ϭ 16,829) and women ( n ϭ 8,370) followed for 7.4 y, new cases of diabetes were documented in 869 men and 224 women ( 4 ). The relative risk of diabetes was 5.55 for men with a BMI of 25.2 to 26.3, compared with men who had a BMI of 15.0 to 19.7, and the relative risk of diabetes was 5.70 for women with a BMI of 24.4 to 25.9, compared with women who had a BMI of 14.9 to 19.1. Therefore, in Japan also, the prevention of overweight/obese subjects is a major public issue.The role of dietary fat and carbohydrate in the obesity epidemic has been a hotly debated topic for decades and remains unresolved. To reduce the incidence of obesity in general populations, public statements on optimal ratios of dietary fat to carbohydrate have been issued. Health organiz...

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Effect of dietary macronutrient composition on tissue-specific lipoprotein lipase activity and insulin action in normal-weight subjects

Cited by 57 publications

References 37 publications

Prolonged adaptation to fat-rich diet and training; effects on body fat stores and insulin resistance in man

Prolonged adaptation to fat-rich diet and training; effects on body fat stores and insulin resistance in man

Regulation of fatty acid uptake into tissues: lipoprotein lipase- and CD36-mediated pathways

The Optimal Dietary Fat to Carbohydrate Ratio to Prevent Obesity in the Japanese Population: A Review of the Epidemiological, Physiological and Molecular Evidence

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