Triglyceride recrystallized phytosterols in fat-free milk improve lipoprotein profiles more than unmodified free phytosterols in hypercholesterolemic men and women.

OBJECTIVE: Foods incorporating plant sterols (PS) consistently decrease serum low-density lipoprotein cholesterol (LDL-C), although results vary depending on the PS form and food matrix. The objective was to study the effect of a novel triglyceride-recrystallized phystosterol (TRP) incorporated into fat-free milk on markers of cardiovascular risk compared to unmodified free sterols alone in the same fat-free milk. METHODS: Hypercholesterolemic men and women (n = 13 males/7 females; 56 ± 10 years; body mass index 27.3 ± 5.9 kg/m(2)) participated in 3 sequential 4-week phases of 480 mL milk consumption. During phase 1 (control) all subjects consumed 2% milk containing no PS, followed by phase 2 with fat-free milk containing free PS (2 g/d fPS) and phase 3 with fat-free milk with TRP (2 g/d). After each phase, determinations of lipoprotein cholesterol distribution, particle concentration via nuclear magnetic resonance (NMR), apolipoproteins, inflammatory markers, and fat-soluble dietary antioxidants were made. RESULTS: Body mass, body composition, dietary energy and macronutrients, and physical activity were unaffected throughout the study. Compared to the control 2% milk, LDL-C was significantly (p < 0.05) decreased by fPS (-9.1%) and was further decreased by TRP (-15.4%); reductions with TRP were significantly greater. Total LDL particle concentration was decreased to a greater extent after TRP (-8.8%) than fPS (-4.8%; p < 0.05). Only TRP significantly decreased serum levels of apolipoprotein B (apoB; -6%), interleukin-8 (IL-8; -11%) and monocyte chemotactic protein-1 (MCP-1; -19%). Plasma α- and γ-tocopherols and carotenoids, normalized to cholesterol, remained unchanged throughout the study with the exception that ß-carotene was lowered by 18%. CONCLUSION: In summary, TRP in fat-free milk may provide cardiovascular benefits beyond that of fPS by inducing more substantial decreases in LDL cholesterol and particle concentration, associated with declines in markers of vascular inflammation.

An animal model of spontaneous metabolic syndrome: Nile grass rat.

Metabolic syndrome (MetS) is a prevalent and complex disease, characterized by the variable coexistence of obesity, dyslipidemia, hyperinsulinaemia, and hypertension. The alarming rise in the prevalence of metabolic disorders makes it imperative to innovate preventive or therapeutic measures for MetS and its complications. However, the elucidation of the pathogenesis of MetS has been hampered by the lack of realistic models. For example, the existing animal models of MetS, i.e., genetically engineered rodents, imitate certain aspects of the disease, while lacking other important components. Defining the natural course of MetS in a spontaneous animal model of the disease would be desirable. Here, we introduce the Nile grass rat (NGR), Arvicanthis niloticus, as a novel model of MetS. Studies of over 1100 NGRs in captivity, fed normal chow, revealed that most of these animals spontaneously develop dyslipidemia (P<0.01), and hyperglycemia (P<0.01) by 1 yr of age. Further characterization showed that the diabetic rats develop liver steatosis, abdominal fat accumulation, nephropathy, atrophy of pancreatic islets of Langerhans, fatty streaks in the aorta, and hypertension (P<0.01). Diabetic NGRs in the early phase of the disease develop hyperinsulinemia, and show a strong inverse correlation between plasma adiponectin and HbA1c levels (P<0.01). These data indicate that the NGR is a valuable, spontaneous model for exploring the etiology and pathophysiology of MetS as well as its various complications.

Replacing trans fat: the argument for palm oil with a cautionary note on interesterification.

To replace dietary trans fatty acids (TFA), two practical options exist: revert to a natural saturated fat without cholesterol (most likely palm oil or its fractions) or move to a newer model of modified fat hardened by interesterification (IE). This review summarizes the relative risks for cardiovascular disease inherent in these options. Interestingly, both types of fat have been the subject of nutritional scrutiny for approximately the last 40 years, and both have positive and negative attributes. Only during that period has palm oil production developed to the point where it has become the major edible oil in world markets, making clinical studies of it an important objective. On the other hand, approximately 25 human studies have fed interesterified fat in one form or another over this period, some for weeks, some as a single meal. Two types of diet designs exist. Several fed a small amount of interesterified fat, usually incorporated within a margarine, and stayed below the radar of biological detection of any abnormal metabolism. A few fed interesterified fat that incorporated stearic acid, as interesterified 18:0 (IE-18:0), even comparing it to trans fat and saturated fat, as a major part of total daily calories to assess its metabolic impact per se. These latter 5 to 6 studies clearly reveal negative biological effects on lipoproteins, blood glucose, insulin, immune function, or liver enzymes when relatively high intake of IE-18:0 or palmitic acid (IE-16:0) were fed in fats with sn2-saturated fatty acids. High intake of 18:0 in natural fats can depress total lipoproteins, while IE-18:0 and IE-16:0 at high levels adversely affect lipoprotein metabolism. Still other studies have supplied interesterified fat as a single meal or fed such fat daily only in a single snack, as opposed to incorporating the fat into the entire fat pool consumed at all meals in association with most foods (which is the more physiological approach and more apt to elicit effects). Even in meal studies, IE-18:0 typically delayed fat absorption postprandially, indicating its effect on fat metabolism originating, in part, in the intestine. Mainly 2 saturated fatty acids (18:0 or 16:0) have been interesterified to harden oils, using the 16:0 from fully hydrogenated palm oil or 18:0 from fully hydrogenated soybean oil as the source material. It is not clear that IE-16:0 is as problematic as IE-18:0, but IE-16:0 has been studied less. Levels between 8% energy (%E) and 12%E from 18:0 as interesterified fat (the typical diet provides about 2%E-4%E as 18:0 from natural fats) show the most effect. Detection of adverse effects would seem to start around 7%E-8%E as IE-18:0, but one can assume that effects are initiated, even if undetected, at a lower intake, similar to the situation with TFA. Thus, although an intake of 1%E to 4%E from IE-18:0 does not appear to influence lipoproteins, it is not necessarily the only system affected. The negative effects of IE-18:0 may be alleviated or masked by dilution with other fats, especially by adding 18:2-rich polyunsaturated oils to the diet. This is similar to the trans fat story, i.e., if a limited intake of TFA is heavily diluted with other oils, the consumption of TFA fails to be detected as an adverse effect. Accordingly, more research is warranted to determine the appropriateness of interesterified fat consumption, particularly before it becomes insidiously embedded in the food supply similar to TFA and intake levels are achieved that compromise long-term health.

Low glycemic load diets protect against metabolic syndrome and Type 2 diabetes mellitus in the male Nile rat.

BACKGROUND: Dietary modification helps prevent and manage Metabolic Syndrome (MetS) and Type 2 Diabetes Mellitus (T2DM) in humans and Nile rats. Specifically fibrous legumes, like lentils, benefit humans, but whether this reflects a specific change in the Glycemic Load (GLoad) remains controversial. Accordingly, low-GLoad foods were tested in the glucose-sensitive Nile rat. METHODS: 131 male Nile rats aged 3 weeks to 15 months were challenged during four experiments with 15 dietary exposures that varied Glycemic Index (GI, 36-88), GLoad (102-305/2000 kcal), and cumulative GLoad (Cum GLoad=days×GLoad, 181-537g total glucose). RESULTS: Lentil diets with low GLoads (102, 202) prevented, delayed, reduced, even reversed the progress of MetS and T2DM as measured by blood glucose (fasting, random, and oral glucose tolerance test) and plasma lipid parameters (plasma cholesterol and triglycerides) plus necropsy findings (liver and kidney pathology plus adipose reserves). The benefit from lentils exceeded dietary factors such as macronutrient composition (%Energy from carbohydrate:fat:protein, between 70:10:20 to 40:40:20), total fiber (0-24%), or dietary caloric density (2.9-4.7 kcal/g). The benefit of a low GLoad applied equally to rats inherently susceptible or resistant to T2DM, based on random glucose above or below 75 mg/dl, respectively, during interventions of 7-17 weeks. CONCLUSIONS: Measuring total food intake and the novel concept of Cum GLoad during growth generated strong correlations (up to r=0.93) between Cum GLoad and parameters of MetS and T2DM, especially during sexual maturation. The present experiments confirm the applicability of male Nile rats to diet-induced human T2DM, and suggest dietary compositions to deter MetS and T2DM in humans.

Hepatic transcriptome implications for palm fruit juice deterrence of type 2 diabetes mellitus in young male Nile rats.

BACKGROUND: The Nile rat (NR, Arvicanthis niloticus) is a model of carbohydrate-induced type 2 diabetes mellitus (T2DM) and the metabolic syndrome. A previous study found that palm fruit juice (PFJ) delayed or prevented diabetes and in some cases even reversed its early stages in young NRs. However, the molecular mechanisms by which PFJ exerts these anti-diabetic effects are unknown. In this study, the transcriptomic effects of PFJ were studied in young male NRs, using microarray gene expression analysis. METHODS: Three-week-old weanling NRs were fed either a high-carbohydrate diet (%En from carbohydrate/fat/protein = 70:10:20, 16.7 kJ/g; n = 8) or the same high-carbohydrate diet supplemented with PFJ (415 ml of 13,000-ppm gallic acid equivalent (GAE) for a final concentration of 5.4 g GAE per kg diet or 2.7 g per 2000 kcal; n = 8). Livers were obtained from these NRs for microarray gene expression analysis using Illumina MouseRef-8 Version 2 Expression BeadChips. Microarray data were analysed along with the physiological parameters of diabetes. RESULTS: Compared to the control group, 71 genes were up-regulated while 108 were down-regulated in the group supplemented with PFJ. Among hepatic genes up-regulated were apolipoproteins related to high-density lipoproteins (HDL) and genes involved in hepatic detoxification, while those down-regulated were related to insulin signalling and fibrosis. CONCLUSION: The results obtained suggest that the anti-diabetic effects of PFJ may be due to mechanisms other than an increase in insulin secretion.

Free phytosterols facilitate excretion of endogenous cholesterol in gerbils.

To determine whether phytosterols (PST) facilitate excretion of whole body cholesterol and whether dietary fat or enhancing gallbladder contraction with curcumin might influence this process, four experiments were conducted in gerbils. In Experiment 1, naive gerbils received cholesterol-free purified diets with 30% energy from fat and 0% or 0.75% free PST from tall oil for 4 weeks. In Experiment 2, body cholesterol pools were expanded by feeding a diet containing 0.3% cholesterol for 3 weeks. Subsequently, PST was provided in either fat-free or normal-fat diets without cholesterol for only 2 h each morning, followed by a low-fat diet for the rest of the day and food restriction overnight. In Experiment 3, gerbils were preloaded with cholesterol, followed by either PST alone or PST+curcumin to enhance gallbladder contraction. In Experiment 4, curcumin or curcumin+PST were fed with 30% as fat and 0.15% cholesterol throughout the study. Because of the small whole body cholesterol pool in Experiment 1, the impact of PST was limited. When whole body cholesterol was expanded in Experiments 2 and 3, subsequent reductions of liver esterified cholesterol by PST were significant. In the presence of dietary fat, PST caused a greater reduction (23%) than in a fat-free diet (8%) compared to respective controls. Curcumin (Experiments 3 and 4) proved ineffective in reducing liver or plasma cholesterol pools, and the 3:1 ratio between PST/diet cholesterol was less effective at blocking cholesterol absorption than a 5:1 ratio previously employed. Thus, free PST removed whole body cholesterol, which was enhanced by concomitant fat intake, but was unaffected by a gallbladder contracting agent.

Dietary trans-18:1 raises plasma triglycerides and VLDL cholesterol when replacing either 16:0 or 18:0 in gerbils.

To compare the relative impact of trans-18:1 with the two main dietary saturated fatty acids it replaces, plasma lipid response was assessed in Mongolian gerbils fed diets rich in 16:0 (24%en),18:0 (10%en), or trans-18:1 (4 or 6%en). The diets were designed such that the 18:0-rich diet substituted 7%en as 18:0 for 16:0, whereas 4%en and 6%en from trans-18:1 was substituted for 16:0 in the two trans diets. The control group was fed a diet formulated according to the fatty acid balance of American Heart Association (AHA), but provided 40%en as fat. Gerbils (n = 10 per dietary group) were fed one of the five diets for 8 weeks. The control diet, with 4 times the polyunsaturated fatty acids (PUFA) content and a P:S ratio about 10 times greater than the test diets, resulted in the lowest plasma TC, LDL cholesterol (LDL-C) and VLDL cholesterol (VLDL-C). Among the test diets, plasma TC and TG were lowest with the 18:0-rich diet. TC in gerbils fed the 16:0-rich diet and 4%en-trans were 20% higher than the 18:0-rich diet, while the 6%en-trans diet was 35% higher. VLDL-C was significantly higher in the 6%en-trans diet compared to all other groups at 8 weeks. Both trans fatty acid diets elevated plasma TG approximately 2- and 3-fold, respectively, compared to the 16:0-rich and 18:0-rich diets at 8 weeks. Further, plasma TG continued to rise over time with trans fatty acids compared to 16:0 or 18:0. Thus, in the fatty acid-sensitive gerbil, impaired TG metabolism represents a major aspect of the hyperlipemia caused by trans fatty acid substitution for major saturated fatty acids.

Betaine in sub-acute and sub-chronic rat studies.

To evaluate the sub-acute and sub-chronic effect of large doses of betaine, this trimethyl glycine compound was fed to rats. Initial studies at BIBRA in the UK evaluated intakes of 0, 1, 2, and 5% betaine added to a maintenance chow designed for use in toxicology studies. Male and female Sprague-Dawley rats were followed for up to 90 days. No toxicity occurred, but at higher betaine intakes several serum chemistries were altered slightly, the MCV, MCH, and MCHC of red cells were reduced, and hepatocytes developed fatty droplets in direct proportion to betaine intake. Females were more affected than males. In a second study to assess reversibility in females, betaine effects were induced for 28 days, followed by a 28 day betaine-free period. All perturbations, except the reduced MCV and MCH, were reversed. As a follow up to BIBRA investigations, both 28 and 90 day feeding trials were conducted at Brandeis University using a rat chow with higher levels of energy, protein, and fat, with betaine added at 0, 0.5, 0.75, 1.0 and 5.0% of the diet. A similar broad range of clinical chemistries and physiological parameters were monitored, and hepatic lipid droplets were investigated in more detail. Liver lipid was actually reduced by betaine, and no significant adverse effects of clinical importance resulted from any dose. However, the MCV was again reduced at 5% betaine in the 28 day study. By 90 days all parameters were normal and comparable to controls. Based on these collective data, it was concluded that even at these high doses, betaine is nontoxic. Differences observed between the BIBRA and Brandeis studies were attributed to differences in the dietary formulations. Significant betainexdietxgrowth interactions were thought to reflect primary disparities in protein and energy concentrations, more than the addition of betaine per se.

Anti-diabetic effects of palm fruit juice in the Nile rat (Arvicanthis niloticus).

With the increasing incidence of metabolic diseases, numerous bioactive phytochemicals have been proffered in the dietary prevention of these conditions. Palm fruit juice (PFJ) possesses bioactive phenolic compounds (referred to as oil palm phenolics; OPP) that may deter diabetes. The objective of the present experiments was to document the degree to which PFJ reduces diabetes symptoms in a variety of circumstances in the Nile rat (Arvicanthis niloticus), a novel model for carbohydrate-induced type 2 diabetes (type 2 diabetes mellitus; T2DM) and the metabolic syndrome. Wild-type male Nile rats (n 100) were fed laboratory chow or semi-purified diabetogenic diets in five experiments lasting 4-36 weeks. PFJ was provided as a drink or mixed into the diet to provide OPP intakes from 170 to 720 mg gallic acid equivalents/kg body weight per d. Body weight and random and fasting blood glucose were assessed at different time points, and were analysed along with terminal fasting organ weights, insulin, plasma and liver lipids as measures of diabetes progression. PFJ proved to be anti-hyperglycaemic and anti-lipaemic in all experiments relative to untreated controls, delaying T2DM onset and even reversing advancing diabetes. Protection by PFJ was directly related to its OPP content, and no negative effects on energy intake or growth were observed. PFJ was effective both as a drink and mixed into the diet. Results suggest that PFJ may slow the rate of glucose absorption, reduce insulin resistance and/or enhance insulin secretion.

Dietary carbohydrate dictates development of Type 2 diabetes in the Nile rat.

Amount and type of dietary carbohydrate (CHO), as well as the CHO:fat ratio, are thought to be critical for both the rate of development and severity of Type 2 diabetes mellitus. Thus, these nutritional considerations were examined in the previously described "spontaneous" model of diabetes and metabolic syndrome, the Nile rat. Weanling male Nile rats (n=92) were fed semipurified diets, modifying glycemic index and load by changing the amount of fiber or altering the CHO:fat ratio. Random and fasting blood glucose and body weight were assessed, and diabetes was characterized in terms of blood glucose, relevant plasma and liver parameters, food and water intake and terminal organ weights. Nile rats fed with hiCHO became more hyperglycemic than rats fed with modCHO (P<.05), while loCHO and hiCHO+hiFiber rats remained essentially normoglycemic. Liver lipid and glycogen accumulation was associated with severe hyperlipemia in diabetic rats, analogous to metabolic syndrome in humans. Advanced diabetes was linked to liver and kidney damage and elevated blood urea nitrogen with weight loss. Dispersing dietary CHO by fiber or replacing it by moderate fat (reducing the glycemic index and load) delayed the onset of diabetes but did not prevent signs of insulin resistance. A very low content of dietary CHO (high fat) seemed to prevent even these early indicators of insulin resistance. Thus, the Nile rat represents a novel CHO-sensitive model for study of Type 2 diabetes that reliably follows the course of disease in humans.

Nutritional correlates and dynamics of diabetes in the Nile rat (Arvicanthis niloticus): a novel model for diet-induced type 2 diabetes and the metabolic syndrome.

BACKGROUND: The prevalence of Metabolic Syndrome and related chronic diseases, among them non-insulin-dependent (type 2) diabetes mellitus, are on the rise in the United States and throughout the world. Animal models that respond to environmental stressors, such as diet, are useful for investigating the outcome and development of these related diseases. OBJECTIVE: Within this context, growth and energy relationships were characterized in the Nile rat, an exotic African rodent, as a potential animal model for diet-induced type 2 diabetes mellitus and Metabolic Syndrome. METHODS: Compiled data from several studies established the relationship between age, body weight gain (including abdominal adiposity), food and water consumption, and blood glucose levels as determinants of diabetes in male and female Nile rats. Glucose Tolerance Testing, insulin, HbA1c, blood pressure measurements and plasma lipids further characterized the diabetes in relation to criteria of the Metabolic Syndrome, while diet modification with high-fat, low-fiber or food restriction attempted to modulate the disease. RESULTS: The Nile rat fed lab chow demonstrates signs of the Metabolic Syndrome that evolve into diet-induced non-insulin-dependent (type 2) diabetes mellitus characterized by hyperinsulinemia with rising blood glucose (insulin resistance), abdominal adiposity, and impaired glucose clearance that precedes increased food and water intake, as well as elevated HbA1c, marked elevation in plasma triglycerides and cholesterol, microalbuminuria, and hypertension. Males are more prone than females with rapid progression to diabetes depending on the challenge diet. In males diabetes segregated into early-onset and late-onset groups, the former related to more rapid growth and greater growth efficiency for the calories consumed. Interestingly, no correlation was found between blood glucose and body mass index (overall adiposity) in older male Nile rats in long term studies, whereas blood glucose and the perirenal fat pad, as well as liver and kidney weight, were positively related to early-onset diabetes. Rats weaned early (4-5 wks) and challenged with a high-fat Western-type diet developed diabetes faster, and body fat accumulation was more apparent, whereas food restriction curtailed it. CONCLUSION: The Nile rat fed typical rodent diets develops hyperinsulinemia that precedes hyperglycemia (insulin resistance) leading to diet-induced type 2 diabetes associated with hypertriglyceridemia, hypercholesterolemia, and hypertension. Dietary modulation affected growth rate (weight gain and central adiposity) to impact disease progression. This rodent model represents a novel system of gene-diet interactions affecting energy utilization that can provide insight into the prevention and treatment of the type 2 diabetes and Metabolic Syndrome.

Hyperlipidemic effects of trans fatty acids are accentuated by dietary cholesterol in gerbils.

Trans isomers of dietary fatty acids, generated during the commercial hydrogenation of unsaturated fats, may contribute to coronary heart disease (CHD) in humans by interfering with lipid metabolism. To examine this possibility in a fat-sensitive model, the Mongolian gerbil (Meriones unguiculatus) was used to compare the cholesterolemic and triglyceridemic potential of modest increments of trans fatty acids from partially hydrogenated soybean oil with other saturated fatty acids in the presence and absence of dietary cholesterol. Age-, dose-, and time-dependent effects were examined in weanling, 6-month-old, and 1-year-old gerbils. Although lipoprotein metabolism in weanling gerbils was initially refractory to trans fat, even as perturbations by saturated fatty acids were demonstrable, these gerbils eventually (after 16 weeks) developed a trans-induced hypercholesterolemia that was intermediate between the response to 16:0 and 12:0 + 14:0. The hepatic and plasma 18:1/18:2 cholesteryl ester (CE) ratio was depressed by trans in a manner similar to saturated fatty acids. The 6-month-old gerbils readily developed hypertriglyceridemia but not hypercholesterolemia, again revealing a decrease in the plasma 18:1/18:2 CE ratio. The 1-year-old gerbils revealed a dose-related (0, 5, 10%en as trans) elevation in total cholesterol (TC), and especially triglycerides (TG), that was accentuated by 0.04% dietary cholesterol. Increases in plasma lipids were again accompanied by a significant decrease in the mass of hepatic esterified cholesterol, particularly 18:1-cholesteryl esters. Thus, dietary trans-fatty acids induce age-, time-, and dose-dependent modulations in gerbil plasma lipids associated with decreased 18:1 cholesteryl esters. Further investigation with gerbils may reveal mechanisms by which trans fat consumption disturbs lipoprotein metabolism.

Dietary conjugated linoleic acid lowers plasma cholesterol during cholesterol supplementation, but accentuates the atherogenic lipid profile during the acute phase response in hamsters.

Conjugated linoleic acid (CLA) reportedly exerts anticarcinogenic and antiatherosclerotic effects in animals. To test the hypothesis that the putative antiatherosclerotic effect of CLA might derive from an anti-inflammatory or antioxidant action on lipoprotein metabolism, an acute phase response (APR) was elicited in hamsters while varying dietary cholesterol and vitamin E intakes in two experiments. The effect of CLA intake (to 1%) was examined with 0% (Experiment 1, 7 wk) and 0 or 0.3% (Experiment 2, 12 wk) cholesterol, at which point APR was induced. In hamsters not fed dietary cholesterol (Experiment 1), CLA exaggerated the rise in plasma and LDL cholesterol observed during the APR. When CLA was fed concurrently with cholesterol (Experiment 2), plasma and liver cholesterol were reduced up to 40% independent of the APR. In addition, CLA decreased body weight gain and adipose reserves in Experiment 1, but not in Experiment 2. Because CLA failed to attenuate APR and was not influenced by vitamin E status, an antioxidant/anti-inflammatory role was not apparent. However, the reduced burden on liver and lipoprotein cholesterol induced by CLA during cholesterol feeding, suggests that CLA curtailed cholesterol absorption, whereas the rise during APR suggests that CLA exaggerated the impaired clearance of plasma cholesterol associated with acute inflammation.

Glyceride stearic acid content and structure affect the energy available to growing rats.

To better understand the relative absorption of 18:0, specific structured triglycerides (STG) with varied ratios of 18:0 and short-chain organic acids (2:0, 3:0, 4:0) were compared with naturally occurring 18:0 in cocoa butter and to other mono- and diglycerides (DGs) containing 18:0. A bioassay for available fat energy was developed for growing Sprague-Dawley rats fed reduced energy from a control diet containing an American Heart Association (AHA) fat blend to generate 60 or 80% normal growth. The resulting standard growth curve was applied to the test fats, including cocoa butter and six glycerides, which were blended 3:1 with the AHA blend (to ensure EFA sufficiency) and pair-fed to match intake of control rats (AHA diet, 80% normal growth). Available energy from test fats ranged from 30 to 12 kJ/g (7.1 to 2.9 kcal/g) for cocoa butter to 18:0-DG, respectively, with the mean of the four different STG being 22 kJ/g (5.2 kcal/g). Energy available from test fats was negatively related to total 18:0 in the STG (r = -0.90; P < 0.001) and fecal dry weight (r = -0.92; P < 0.001); the effect was greater for monoglyceride (monolong-18:0) than for DG (dilong-18:0) but was not related to fecal 18:0. Compared with monoglyceride-18:0, available energy was increased or decreased when short-chain organic acids (SCOA) were added to form triglycerides, depending on the addition of butyrate or acetate, respectively. The different fat sources altered the available energy without apparent changes in lipoproteins or body composition. Thus, the reduced energy available from a glyceride containing 18:0 is determined by its total 18:0 and reflects the mono- or dilong chain character of the glyceride, its content of SCOA and triglyceride structure or organization per se.

Free phytosterols effectively reduce plasma and liver cholesterol in gerbils fed cholesterol.

The potential of free phytosterols (including 20% stanols) to lower plasma and liver lipids was assessed in three experiments with gerbils fed diets containing cholesterol. The first explored the ability of phytosterols (0.5%) to block absorption of 0.05, 0.10, and 0.5% cholesterol. The second assessed the importance of consuming phytosterols (0.75%) simultaneously with cholesterol (0.15%). The third compared free phytosterols (0.75%) with similar levels of esterified sterols or stanols using diets containing 0.15% cholesterol. A 5:1 ratio of phytosterols:cholesterol effectively blocked cholesterol absorption when the dietary cholesterol load was moderate. Consuming a 5:1 ratio with every meal was more effective than receiving equal phytosterols in a 10:1 ratio every other day. Finally, free phytosterols dissolved in fat were as effective as esterified sterols and stanols in lowering plasma and liver cholesterol, and all were equally effective at blocking cholesterol absorption as shown by increased fecal cholesterol output. Plant sterol accumulation in the liver was minimal for all test groups.