Carbohydrate- and lipid-enriched meals acutely disrupt glycemic homeostasis by inducing transient insulin resistance in rats

Chronic intake of high-carbohydrate or high-lipid diets is a well-known insulin resistance inducer. This study investigates the immediate effect (1-6 h) of a carbohydrate-or lipid-enriched meal on insulin sensitivity. Fasted rats were refed with standard, carbohydrate-enriched (C), or lipid-enriched (L) meal. Plasma insulin, glucose, and non-esterified fatty acids (NEFA) were measured at 1, 2, 4, and 6 h of refeeding. The glucose-insulin index showed that either carbohydrates or lipids decreased insulin sensitivity at 2 h of refeeding. At this time point, insulin tolerance tests (ITTs) and glucose tolerance tests (GTTs) detected insulin resistance in C rats, while GTT confirmed it in L rats. Reduced glycogen and phosphorylated AKT and GSK3 content revealed hepatic insulin resistance in C rats. Reduced glucose uptake in skeletal muscle subjected to the fatty acid concentration that mimics the high NEFA level of L rats suggests insulin resistance in these animals is mainly in muscle. In conclusion, carbohydrate-or lipid-enriched meals acutely disrupt glycemic homeostasis, inducing a transient insulin resistance, which seems to involve liver and skeletal muscle, respectively. Thus, the insulin resistance observed when those types of diets are chronically consumed may be an evolution of repeated episodes of this transient insulin resistance.

Avaliação da influência dos estímulos alimentares na actividade extracardíaca

Mestrado em Medicina Nuclear - Ramo de especialização: Radiofarmácia

Egg quality and yolk lipid composition of laying hens fed diets containing cashew nut meal

The objective of this study was to assess the effect of the addition of cashew nuts meal (0, 5, 10, 15, 20, and 25%) to laying hen diets on egg quality and yolk composition. The variables studied were: egg weight, specific gravity, Haugh Units, percentages of shell, albumen, and yolk, moisture, total solids, total lipids, fatty acids profile, and yolk cholesterol. The addition of up to 25% of cashew nuts meal to hen diets did not affect egg quality and freshness, moisture and total solids content. However, an increase in total lipid content and a decrease in yolk pigmentation was observed. Oleic acid level increased in the yolk, whereas palmitic, stearic, and linoleic acid levels decreased. The addition of cashew nuts meal increased the monounsaturated/saturated fatty acid ratio in the yolk and reduced the cholesterol content. Therefore, the use of cashew nuts meal in laying hen diets favorably modifies the fatty acid composition of egg yolk and contributes to a better acceptance of this food by consumers since it also reduces yolk cholesterol levels.

The effect of test meal monounsaturated fatty acid: saturated fatty acid ratio on postprandial lipid metabolism

Epidemiological evidence shows that a diet high in monounsaturated fatty acids (MUFA) but low in saturated fatty acids (SFA) is associated with reduced risk of CHD. The hypocholesterolaemic effect of MUFA is known but there has been little research on the effect of test meal MUFA and SFA composition on postprandial lipid metabolism. The present study investigated the effect of meals containing different proportions of MUFA and SFA on postprandial triacylglycerol and non-esterified fatty acid (NEFA) metabolism. Thirty healthy male volunteers consumed three meals containing equal amounts of fat (40 g), but different proportions of MUFA (12, 17 and 24% energy) in random order. Postprandial plasma triacylglycerol, apolipoprotein B-48, cholesterol, HDL-cholesterol, glucose and insulin concentrations and lipoprotein lipase (EC 3.1.1.34) activity were not significantly different following the three meals which varied in their levels of SFA and MUFA. There was a significant difference in the postprandial NEFA response between meals. The incremental area under the curve of postprandial plasma NEFA concentrations was significantly (P = 0.03) lower following the high-MUFA meal. Regression analysis showed that the non-significant difference in fasting NEFA concentrations was the most important factor determining difference between meals, and that the test meal MUFA content had only a minor effect. In conclusion, varying the levels of MUFA and SFA in test meals has little or no effect on postprandial lipid metabolism.

Meat Quality of Lambs Fed on Palm Kernel Meal, a By-product of Biodiesel Production

This study aimed to establish the optimum level of palm kernel meal in the diet of Santa Ines lambs based on the sensorial characteristics and fatty acid profile of the meat. We used 32 lambs with a starting age of 4 to 6 months and mean weight of 22 2.75 kg, kept in individual stalls. The animals were fed with Tifton-85 hay and a concentrate mixed with 0.0, 6.5, 13.0 or 19.5% of palm kernel meal based on the dry mass of the complete diet. These levels formed the treatments. Confinement lasted 80 days and on the last day the animals were fasted and slaughtered. After slaughter, carcasses were weighed and sectioned longitudinally, along the median line, into two antimeres. Half-carcasses were then sliced between the 12th and 13th ribs to collect the loin (longissimus dorsi), which was used to determine the sensorial characteristics and fatty acid profile of the meat. For sensorial evaluation, samples of meat were given to 54 judges who evaluated the tenderness, juiciness, appearance, aroma and flavor of the meat using a hedonic scale. Fatty acids were determined by gas chromatography. The addition of palm kernel meal to the diet had no effect on the sensorial characteristics of meat juiciness, appearance, aroma or flavor. However, tenderness showed a quadratic relationship with the addition of the meal to the diet. The concentration of fatty acids C12:0, C14:0 and C16:0 increased with the addition of palm kernel meal, as did the sum of medium-chain fatty acids and the atherogenicity index. Up to of 19.5% of the diet of Santa Ines lambs can be made up of palm kernel meal without causing significant changes in sensorial characteristics. However, the fatty acid profile of the meat was altered.

Optimum dietary protein requirement for Amazonian Tambaqui, Colossoma macropomum Cuvier, 1818, fed fish meal free diets

Fish meal free diets were formulated to contain graded protein levels as 25% (diet 1), 30% (diet 2), 35% (diet 3) and 40% (diet 4). The diets were fed to tambaqui juveniles (Colossoma macropomum) (46.4 ± 6.3g) in randomly designed recirculating systems for 60 days, to determine the optimum protein requirement for the fish. The final weight of the fish, weight gain (28.1, 28.5, 32.2, 28.0g) and specific growth rate increased (P>0.05) consistently with increasing dietary protein up to treatment with 35% protein diet and then showed a declining trend. Feed intake followed the same trend resulting in best feed efficiency (62.5%) in fish fed diet with 35% protein. Similarly, the protein intake increased significantly with increasing dietary protein levels and reduced after the fish fed with 35% protein; while protein efficiency ratio (2.28, 1.99, 1.87, 1.74) decreased with increasing dietary protein levels. Carcass ash and protein had linear relationship with dietary protein levels while the lipid showed a decreasing trend. Ammonia content (0.68, 0.73, 0.81, 1.21 mg L-1) of the experimental waters also increased (P<0.05) with increasing protein levels while pH, dissolved oxygen and temperature remained fairly constant without any clear pattern of inclination. Broken-line estimation of the weight gain indicated 30% protein as the optimum requirement for the fish.

Circulating antioxidant defences are decreased in healthy people after a high-fat meal.

The aim of this study was to examine the responses of uric acid, antioxidant defences and pro-oxidant variables after a high-fat meal. Twenty-five healthy persons without criteria for the metabolic syndrome, underwent a high-fat meal with Supracal (60 g fat). Measurements were made at baseline and 3 h after the meal of TAG, uric acid, HDL-cholesterol, total proteins and oxidative stress. Following the high-fat meal, we detected a significant increase in pro-oxidative variables and a decrease in antioxidative variables. The uric acid concentrations were significantly lower after the high-fat meal and the reduction correlated significantly with the oxidative stress variables. The inverse relation between reduced uric acid and increased carbonylated proteins remained in multiple regression analysis. We conclude that uric acid is a powerful antioxidant and its reduction following a high-fat meal may be related with its acute antioxidative action.

Contributions of fat and protein to the incretin effect of a mixed meal.

Background: The relative contributions of fat and protein to the incretin effect are still largely unknown.Objective: This study assessed the incretin effects elicited by a mixed meal, and by its fat and protein components alone, with the use of a hyperglycemic clamp combined with oral nutrients.Design: Eight healthy volunteers were studied over 6 h after ingestion of a sandwich containing 1) dried meat, butter, and white bread; 2) dried meat alone; 3) butter alone; or 4) no meal (fasting control). Meals were ingested during a hyperglycemic clamp, and the incretin effect was calculated as the increment in plasma insulin after food intake relative to the concentrations observed during the control study.Results: A significant augmentation of postprandial insulin secretion, independent of plasma glycemia, occurred after ingestion of the mixed nutrients and the lipid component of the mixed meal (203 +/- 20.7% and 167.4 +/- 22.9% of control, respectively; both P < 0.05), whereas the protein component did not induce a significant incretin effect (129.0 +/- 7.9% of control; P = 0.6)Conclusions: Fat ingestion, in an amount typical of a standard meal, increases insulin secretion during physiologic hyperglycemia and thus contributes to the incretin effect. In contrast, ingestion of protein typical of normal meals does not contribute to the augmentation of postprandial insulin secretion. This trial was registered at clinicaltrials.gov as NCT00869453.

Effects of dietary protein on lipid metabolism in high fructose fed humans.

BACKGROUND & AIMS: It has been reported that a high protein diet improves insulin sensitivity and reduces ectopic lipids in animals and humans with the metabolic syndrome. We therefore tested the hypothesis that a high dietary protein content may stimulate whole body lipid oxidation and alter post-prandial triglyceride (TG) after fructose ingestion. METHODS: The post-prandial metabolism of 8 young males was studied after two 6-day periods of hyper-energetic, high fructose diet (HiFruD), and after two 6-day periods of hyper-energetic high fructose high protein diet (HiFruHiProD). The order with which these periods were applied was randomized. At the end of each period, either a low protein, (13)C fructose test meal (Fru meal) or a high protein, (13)C fructose test meal (HiPro Fru meal) was administered. This resulted in the monitoring of metabolic parameters at 4 occasions in random order: a) with Fru meal ingested after HiFruD, b) with HiPro Fru meal ingested after HiFruD, c) with Fru meal ingested after HiFruHiProD or d) with HiPro Fru meal ingested after HiFruHiProD. On each occasion, post-prandial TG concentrations were monitored, energy expenditure and substrate metabolism were measured by indirect calorimetry, and fructose-induced gluconeogenesis was evaluated by measuring plasma (13)C-labeled glucose. RESULTS: TG responses to fructose ingestion were significantly higher after a hyper-energetic HiFruHiProD and after HiPro Fru meals than after a Fru meal ingested after a hyper-energetic HiFruD. Compared to low protein meals, high protein meals increased post-prandial energy expenditure, inhibited post-prandial lipid oxidation, and enhanced fructose-induced gluconeogenesis. These effects were similar with HiFruD and HiFruHiProD. CONCLUSIONS: Dietary proteins did not increase lipid oxidation and increased fructose-induced post-prandial TG in healthy humans fed an hyper-energetic, high fructose diet.

Nutritional influences on lipogenesis and thermogenesis after a carbohydrate meal.

In vivo lipogenesis and thermogenesis were studied for 24 h after ingestion of 500 g of carbohydrate (CHO) in subjects who had consumed either a high-fat, a mixed, or a high-CHO diet during the 3-6 days preceding the test. CHO oxidation and conversion to fat was significantly less in the high-fat diet group (222 +/- 5 g) than in the mixed (300 +/- 13 g) or high-CHO diet (331 +/- 7 g) groups, resulting in a greater glycogen storage in the high-fat (278 +/- 6 g) than in the other two groups (197 +/- 11 and 170 +/- 2 g). Net lipogenesis occurred sooner and lasted longer in the high-CHO group, amounting to 0.8 +/- 0.5, 3.4 +/- 0.6, and 9 +/- 1 g of lipid synthesized in the high-fat, mixed, and high-CHO groups, respectively. The thermic effect of the CHO load was 5.2 +/- 0.5% on the high-fat, 6.5 +/- 0.4% on the mixed diet, and 8.6 +/- 0.4% on the high-CHO diet. Significant relationships were demonstrated between the postabsorptive nonprotein respiratory quotient and net lipogenesis after the CHO load (r = 0.82) and between net lipogenesis and the increase in energy expenditure (r = 0.71). It is concluded that the antecedent diet influences the amount of net lipogenesis and the magnitude of thermogenesis after a large CHO test meal. However, lipogenesis remains too limited even after such large CHO intakes to cause an increase in the body's fat content.

Long-term effects of Roux-en-Y gastric bypass on postprandial plasma lipid and bile acids kinetics in female non diabetic subjects: A cross-sectional pilot study.

BACKGROUND AND AIMS: Formerly obese patients having undergone Roux-en-Y gastric bypass (RYGB) display both an accelerated digestion and absorption of carbohydrate and an increased plasma glucose clearance rate after meal ingestion. How RYGB effects postprandial kinetics of dietary lipids has yet not been investigated. METHODS: Plasma triglyceride (TG), apoB48, total apoB, bile acids (BA), fibroblast growth factor 19 (FGF19), and cholecystokinin (CCK) were measured in post-absorptive conditions and over 4-h following the ingestion of a mixed test meal in a cross-sectional, pilot study involving 11 formerly obese female patients 33.8 ± 16.4 months after RYGB surgery and in 11 weight- and age-matched female control participants. RESULTS: Compared to controls, RYGB patients had faster (254 ± 14 vs. 327 ± 7 min, p < 0.05) and lower (0.14 ± 0.04 vs. 0.35 ± 0.07 mM, p < 0.05) peak TG responses, but their peak apoB48 responses tended to be higher (2692 ± 336 vs. 1841 ± 228 ng/ml, p = 0.09). Their postprandial total BA concentrations were significantly increased and peaked earlier after meal ingestion than in controls. Their FGF19 and CCK concentrations also peaked earlier and to a higher value. CONCLUSIONS: The early postprandial apoB48 and BA responses indicate that RYGB accelerated the rate of dietary lipid absorption. The lower postprandial peak TG strongly suggests that the RYGB simultaneously increased the clearance of TG-rich lipoproteins. CLINICAL TRIAL REGISTRATION: NCT01891591.

Dietary, physiological, genetic and pathological influences on postprandial lipid metabolism

Most of diurnal time is spent in a postprandial state due to successive meal intakes during the day. As long as the meals contain enough fat, a transient increase in triacylglycerolaemia and a change in lipoprotein pattern occurs. The extent and kinetics of such postprandial changes are highly variable and are modulated by numerous factors. This review focuses on factors affecting postprandial lipoprotein metabolism and genes, their variability and their relationship with intermediate phenotypes and risk of CHD. Postprandial lipoprotein metabolism is modulated by background dietary pattern as well as meal composition (fat amount and type, carbohydrate, protein, fibre, alcohol) and several lifestyle conditions (physical activity, tobacco use), physiological factors (age, gender, menopausal status) and pathological conditions (obesity, insulin resistance, diabetes mellitus). The roles of many genes have been explored in order to establish the possible implications of their variability in lipid metabolism and CHD risk. The postprandial lipid response has been shown to be modified by polymorphisms within the genes for apo A-I, A-IV, AN, E, B, C-I and C-III, lipoprotein lipase, hepatic lipase, fatty acid binding and transport proteins, microsomal trigyceride transfer protein and scavenger receptor class B type I. Overall, the variability in postprandial response is important and complex, and the interactions between nutrients or dietary or meal compositions and gene variants need further investigation. The extent of present knowledge and needs for future studies are discussed in light of ongoing developments in nutrigenetics.

Methodology for studying postprandial lipid metabolism

Background: Postprandial lipid metabolism in humans has deserved much attention during the last two decades. Although fasting lipid and lipoprotein parameters reflect body homeostasis to some extent, the transient lipid and lipoprotein accumulation that occurs in the circulation after a fat-containing meal highlights the individual capacity to handle an acute fat input. An exacerbated postprandial accumulation of triglyceride-rich lipoproteins in the circulation has been associated with an increased cardiovascular risk. Methods: The important number of studies published in this field raises the question of the methodology used for such postprandial studies, as reviewed. Results: Based on our experiences, the present review reports and discuss the numerous methodological issues involved to serve as a basis for further works. These aspects include aims of the postprandial tests, size and nutrient composition of the test meals and background diets, pre-test conditions, characteristics of subjects involved, timing of sampling, suitable markers of postprandial lipid metabolism and calculations. Conclusion: In conclusion, we stress the need for standardization of postprandial tests.