Comment: response of the hypothalamic-pituitary-adrenocortical axis to high-protein/fat and high-carbohydrate meals in women with different obesity phenotypes

Subjects with abdominal obesity are characterized by hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis. Food intake, particularly at noon, is a well-known inducer of HPA axis activation. Whether obese subjects present an abnormal response to meals containing different macronutrient proportions is at present unknown. Therefore, this study was carried out to investigate the effect of a high-lipid/protein meal (HLP-meal) and a high-carbohydrate meal (HCHO-meal) on the HPA axis activity in women with different obesity phenotypes. Nondepressed, noncomplicated obese (body mass index greater than 28 kg/m(2)) women with abdominal (A-BFD) (n = 10) and peripheral body fat distribution (P-BFD) (n = 9) and a group of 11 normal-weight controls were investigated in the follicular phase of the menstrual cycle. They were randomly given an 800-kcal HCHO-meal (containing 89% carbohydrates, 11% proteins, 0% lipids), and an 800-kcal HLP-meal (containing 53% lipids, 43% proteins, 4% carbohydrates), which were eaten within 15 min at noon, with an interval of 2 d between each meal. Blood samples for ACTH, cortisol, glucose, and insulin were obtained at 15-min intervals before and after each meal. Baseline hormone and glucose concentrations in the three groups were similar. After the HLP-meal, ACTH tended to similarly but insignificantly increase in all groups, whereas cortisol increased significantly (P < 0.05) in the P-BFD group and insignificantly in the other groups. Conversely, both ACTH and cortisol significantly (P < 0.05) increased only in the A-BFD group, without any significant changes in both controls and P-BFD women. The analysis of the interaction between meals and groups clearly indicated that the cortisol response to the HLP-meal and the HCHO-meal was significantly different (P < 0.025) between the two obese groups, the A-BFD group being characterized by a significantly lower response to the HLP-meal and a significantly higher response to the HCHO-meal, compared with the P-BFD group. Considering all groups together and after adjusting for body mass index, a highly significant relationship was found between cortisol-area under the curve and ACTH-area under the curve after each meal test. However, no relationships were found between changes in ACTH and cortisol and those of glucose, insulin, and the glucose:insulin ratio after each meal. Therefore, our data demonstrate that the response of the HPA axis to meals containing different macronutrient proportions may depend on the pattern of body fat distribution. We also suggest that the activation of the HPA axis following the ingestion of large amounts of carbohydrates may have some pathophysiological relevance, specifically in women with the abdominal obesity phenotype.     

Metabolic effects of infusion of cortisol and adrenocorticotrophin in the tammar wallaby (Macropus eugenii Desmarest).

Infusion of cortisol (1 mg/kg of body weight infused over 1 hr) into the tammar wallaby, Macropus eugenii Desmarest, was followed by an immediate increase in plasma corticosteroid concentration. Plasma glucose concentration began to rise 45 min later and remained above control levels for 3 hr. There were no changes in the concentrations of amino acids, free fatty acids, or urea in the plasma. It is concluded that cortisol affects plasma glucose concentration directly rather than via protein catabolism. Intravenous infusion of 0.45 IU of porcine ACTH/kg of body weight over 1 hr was followed by an immediate increase in plasma corticosteroid concentration and a rise in plasma glucose level 15 min later. The plasma glucose response to ACTH was advanced about 1 hr compared with that to cortisol. It is concluded that the effects of ACTH cannot be mediated wholly by an increase in plasma corticosteroid concentration. There were no changes in the concentration of amino acids or urea in the plasma, but the free fatty acid concentration was increased after ACTH infusion. This is consistent with the lipolytic effects of ACTH in other mammalian species.     

Metabolic and hormonal investigations in long-term streptozotocin diabetic rats on different dietary regimens

Summary Groups of diabetic rats (65 mg/kg streptozotocin SC) were fed ad lib on three different dietary regimens for 43 weeks: a standard control diet (68% of calories as carbohydrate, 20% as protein, and 12% as fat), a low carbohydrate high protein diet (6% carbohydrate, 63% protein, 31% fat) or a low carbohydrate-high fat diet (5% carbohydrate, 75% fat, 20% protein). The high fat diet resulted in a fall of blood glucose from 700 to 350 mg/100 ml. Rats fed the high protein diet showed a similar initial decrease in blood glucose concentration, and a further improvement was evident from the 28th week on. After 43 weeks blood glucose levels were below 180 mg/100 ml and glycosuria below 100 mg/24 h in all rats fed the high protein diet. When rats exhibiting blood glucose levels below 180 mg/dl were transferred temporarily to standard diet blood glucose levels increased and marked glycosuria was observed. Rats on the standard diet maintained blood glucose concentrations greater than 500 mg/100 ml and glycosuria of about 16 g/24 h throughout the experiment. The pancreatic insulin content at death of rats fed the standard diet or the high fat diet was 1% of normal rats, whereas the values for the rats on the high protein diet were increased to 9%. Animals fed the low carbohydrate diets showed greater weight gain. In the high fat diet group there was a marked rise after 43 weeks in plasma triglycerides, free fatty acids, 3-hydroxybutyrate and acetoacetate in the plasma. Urea excretion was raised in the animals on the high protein diet. Thus, treatment with low carbohydrate diets for 10 months regardless of fat and protein content markedly improved the diabetic state of rats.     

Suppression of insulin secretion by protein deprivation in obesity.

The effect of low protein diets on insulin levels was studied in 17 obese, nondiabetic hyperinsulinemic subjects. Their mean weight was 271% of ideal weight. Nine patients were fed a weight-maintaining 3700-calorie diet for 14 days; this diet contained 398 g carbohydrate and 170 g protein. The patients were then fed an isocaloric diet containing only 6 g protein and 587 g carbohydrate for 14 more days. Mean basal insulin levels decreased from 50.4 to 34.7 μU/ml. This decrease was accompanied by a significant decrease in mean plasma glucose. In seven patients who were fed the low-protein diet after a 4-day period of total fast, the low-protein diet prevented the recovery of basal insulin levels decreased during fasting. These findings were in contrast to the apparent recovery of basal insulin levels observed when the control rather than the low-protein diet was refed in 4 patients following a fast. The suppression of basal insulin levels by protein deprivation was not correlated with changes in plasma glucose, glucagon, urinary 17-hydroxycorticoids, or body weight. Although urinary 17-hydroxycorticoids and free cortisol decreased significantly on protein-restricted diets, treatment with cortisol did not prevent the effect of protein deprivation on basal insulin and glucose levels. Plasma levels of branched chain amino acids (valine, leucine, and isoleucine) decreased in parallel to insulin levels on the isocaloric low-protein diets. We conclude that protein-restricted diets can decrease basal plasma insulin levels in obesity even in the presence of sufficient calories to maintain weight and high carbohydrate content. Of the factors investigated that may account for this phenomenon, it is unlikely that glucagon, glucose, or cortisol play a direct role. It is possible that protein as well as carbohydrate plays a role in the development of hyperinsulinemia and insulin resistance in obesity.     

The satiating effect of dietary protein is unrelated to postprandial ghrelin secretion

CONTEXT: Increasing dietary protein relative to carbohydrate and fat enhances weight loss, at least in part by increasing satiety. The mechanism for this is unclear. OBJECTIVE: The objective of this study was to compare the effects of isocaloric test meals with differing protein to fat ratios on fasting and postprandial ghrelin, insulin, glucose, appetite, and energy expenditure before and after weight loss on the respective dietary patterns. DESIGN: The study design was a randomized parallel design of 12 wk of weight loss (6 MJ/d) and 4 wk of weight maintenance (7.3 MJ/d) with meals administered at wk 0 and 16. SETTING: The study was performed at an out-patient research clinic. PATIENTS AND OTHER PARTICIPANTS: Fifty-seven overweight (body mass index, 33.8 +/- 3.5 kg/m2) hyperinsulinemic men (n = 25) and women (n = 32) were studied. Interventions: High-protein/low-fat (34% protein/29% fat) or standard protein/high-fat (18% protein/45% fat) diets/meals were given. MAIN OUTCOME MEASURES: The main outcome measures were weight loss and fasting and postprandial ghrelin, insulin, glucose, appetite, and energy expenditure before and after weight loss. RESULTS: Weight loss (9.2 +/- 0.7 kg) and improvements in fasting and postprandial insulin and glucose occurred independently of diet composition. At wk 0 and 16, subjects wanted less to eat after the high-protein/low-fat than the standard protein/high-fat meal (P = 0.02). Fasting ghrelin increased (157.5 +/- 3.4 pg/ml or 46.6 +/- 1.0 pmol/liter; P < 0.001), and the postprandial ghrelin response improved with weight loss (P = 0.043) independently of diet composition. Postprandial hunger decreased with weight loss (P = 0.018) and was predicted by changes in fasting and postprandial ghrelin (r2 = 0.246; P = 0.004). Lean mass was the best predictor of fasting (r2 = 0.182; P = 0.003) and postprandial ghrelin (r2 = 0.096; P = 0.039) levels. CONCLUSIONS: Exchanging protein for fat produced similar weight loss and improvements in metabolic parameters and ghrelin homeostasis. The reduced appetite observed with increased dietary protein appears not to be mediated by ghrelin homeostasis.     

Influence of weight loss on plasma ghrelin responses to high-fat and high-carbohydrate test meals in obese women

BACKGROUND: Diet-induced weight loss is associated with an increase in fasting ghrelin. The influence of weight loss on postprandial ghrelin response remains discussed, but the specific response to macronutrients is not known. OBJECTIVE: The objective of the study was to assess the influence of weight loss in obese women on the plasma ghrelin response to a fat- or carbohydrate-rich meal. DESIGN: Seventeen obese women (mean body mass index 37.6 +/- 5 kg/m2) were given an energy-restricted diet (800 kcal/d) for 7 wk, followed by a maintenance diet for 1 wk. Before and after the weight reduction diet, each woman was given (in random order) two isoenergetic test meals, corresponding to 40% of daily energy needs. The test meals contained either 80% fat and 20% protein or 80% carbohydrate and 20% protein. Blood samples were collected over a 10-h period. Two-way ANOVA with repeated measures was used to assess the effect of the test meal on variables. RESULTS: Weight loss (-11.2 +/- 1.4 kg) was associated with a significant decrease in baseline plasma insulin (9.7 +/- 4.1 to 7.9 +/- 2.4 mU/ml; P < 0.0001) and leptin (25.9 +/- 8.3 to 17.2 +/- 7.8 ng/ml; P < 0.0001) and an increase in plasma ghrelin (1.86 +/- 1.05 to 2.28 +/- 1.48 ng/ml; P < 0.05). Before weight loss, there was no significant difference in postprandial ghrelin response between the test meals. After weight reduction, the ghrelin response was more pronounced after the carbohydrate test meal than after the fat test meal (P < 0.02). CONCLUSION: Weight loss is associated with an improved postprandial plasma ghrelin response to a carbohydrate meal, whereas the response to a fat meal is not modified.     

Delayed Pro-Opiomelanocortin Activation after Ethanol Intake in Man

To elucidate the effect of ethanol on the secretion of ACTH and β-endorphin (BE) as the representatives of the pro-opiomelanocortin (POMC) system, as well as cortisol as the hypophyseally regulated peripheral hormone, we measured concentrations of serum ethanol and plasma ACTH, BE, and cortisol at 1- to 4-hr intervals for 12 hr after administration of 0.5 and 1.0 g ethanol/kg of body weight and placebo drinks between 1900–1945 hr to nine healthy volunteers according to a double-blind, cross-over design.
Plasma ACTH, BE, and cortisol showed an expected diurnal rhythm with the highest levels at 0700 hr. Intake of ethanol had no statistically significant effects on plasma ACTH up to 0700 hr in the morning. The higher dose caused increased levels of BE at 0100 hr and both doses at 0200 hr. Plasma cortisol at 0400 hr was higher in subjects receiving 1.0 g ethanol/kg than in those receiving placebo ( p < 0.05). Our present observation that plasma ACTH was unchanged after ethanol intake, but plasma BE was increased at 0100-0200 hr may be due to the fact that our BE antiserum cross-reacts with β-lipotropin, which has a considerably longer half-life than ACTH or BE, and also to the long sampling interval. Thus, the POMC system may have been stimulated after ethanol intake. The nocturnal rise of plasma cortisol levels at 0400 hr, 2-3 hr after the peak in plasma BE, may be caused by the increased secretion of POMC. Because the ethanol dose of 1.0 g/kg body weight stimulated the POMC system but the 0.5 g/kg body weight did not, we conclude that higher ethanol doses induce increases in stress hormone secretion.     

Nutritional effects on the lifespan of Syrian hamsters

Syrian hamsters were fed one of nine semipurified diets composed of three casein levels (9, 18, and 36 g/385 Kcal), with each of three corn oil levels (4.5, 9.0, and 18.0 g/385 Kcal). These diets were given either for five weeks and were followed by control diet (18 g casein and 9 g corn oil/385 Kcal) or control diet was fed for the first five weeks and was followed by the nine diets. Calorie consumption, maximum body weight and length of growth period and of life are reported. Calorie consumption was directly related to dietary fat levels. Maximum body weights increased with increasing dietary fat and protein when the various diets were fed during weeks 1–5. This result was not due to a conditioning of the animals fed high-fat or high-protein levels during weeks 1–5 to consume more calories after week 5, since after this time consumption was the same in all groups fed the control diet. When diets were fed from week 6 body weight increased in both sexes with increased dietary fat; however, higher dietary protein increased female and decreased male maximum body weight. Males took longer to reach these maximum weights than females, and were not affected by receiving the various diets during weeks 1–5. However, when diets were fed from week 6 until death, the growth period increased with higher dietary fat or protein. Male hamsters survived longer than females with each experimental treatment. Animals fed low-fat, low-protein diet or high-fat, high-protein diet during the first 5 weeks of the study survived longest. When diets were fed from 6 weeks until death, survival increased as dietary fat rose for both sexes. In contrast, survival improved as dietary protein rose for females or decreased for males. These studies establish a basis for further investigations on the link between nutrition and longevity in the Syrian hamster.     

Consumption of diets with different type of fat influences triacylglycerols-rich lipoproteins particle number and size during the postprandial state

Background and aims

Previous evidence suggests that dietary fat could influence the composition and size of triacylglycerols-rich lipoproteins (TRL). In a controlled intervention study on healthy subjects, we evaluated the influence of 3 dietary interventions, with different types of fat on postprandial TRL particle size and number.

Methods and results

Volunteers followed three different diets for four weeks each, according to a randomized crossover design. Western diet: 15% protein, 47% carbohydrates (CHO), 38% fat (22% saturated fatty acid (SFA)); Mediterranean diet: 15% protein, 47% CHO, 38% fat (24% monounsaturated fatty acid (MUFA)); high CHO enriched with ALNA diet: 15% protein, 55% CHO, <30% fat (8% polyunsaturated fatty acid (PUFA)). After a 12-h fast, volunteers consumed a breakfast with 1 g fat and 7 mg cholesterol per kg body weight and a fat composition similar to that consumed in each of the diets: Butter meal: 35% SFA; Olive oil meal: 36% MUFA; Walnut meal: 16% PUFA, 4% α-linolenic acid. Tryglicerides (TG) in TRL (large and small TRL) were determined by ultracentrifugation and size and number of lipoprotein particles were measured with Nuclear Magnetic Resonance Spectroscopy at different time points. The olive oil meal reduced the number of total TRL postprandial particles compared with the other meals (P = 0.002). Moreover, the olive oil meal also increased the TRL particle size compared with the walnut meal (P = 0.001).

Conclusion

Our data showed that short-term intake of the Mediterranean diet and the acute intake of an olive oil meal lead to the formation of a reduced number and higher-size TRL particle compared with other fat sources. These novel findings have implications for understanding the postprandial lipoprotein mechanisms, and could favour the lower cardiovascular risk in Mediterranean countries.     

Dietary thermogenesis in obesity. Response to carbohydrate and protein meals: the effect of beta-adrenergic blockade and semistarvation

Four obese and four lean women were studied for 4 or 5 weeks in a metabolic unit to assess their short-term responses to carbohydrate- and protein-containing meals and the effects of beta-adrenergic blockade during both weight maintenance and semistarvation. The study was divided into four periods: a period of weight maintenance; a maintenance diet with propranolol; semistarvation; semistarvation plus propranolol. The low-energy diets contained half the amount of carbohydrate and fat but the protein intake was maintained. The metabolic rate was measured in the fasting state by indirect calorimetry prior to a test meal and then for prolonged periods up to 5.5 h after carbohydrate and 7.5 h after protein test meals. Three lean subjects also spent 23 h in a whole-body calorimeter in each period, when BMR and metabolic rate at different activity levels were measured. Propranolol causes a fall in BMR in both groups on a maintenance diet, but had little further effect on the lower BMR during semistarvation. The protein meal caused a peak increase of 30 percent in oxygen consumption (321 kJ in obese, 257 kJ in lean), two to three times that of the carbohydrate meal (91 kJ) despite the energy intake being 25 percent less in the protein meal. There was no consistent difference in postprandial thermogenesis in obese and lean subjects and the effect was not modified by propranolol or semistarvation. Propranolol caused reduced thermogenesis after a mixed meal in lean subjects.     

Administration of growth hormone to pigs alters the relative amount of insulin-like growth factor-I mRNA in liver and skeletal muscle

The relative amount of insulin-like growth factor-I (IGF-I) mRNA was determined in the liver and skeletal muscle of market weight crossbred barrows (castrated male pigs) using a solution hybridization-nuclease protection assay. Pigs were given either 50 micrograms recombinant porcine GH per kg body weight or vehicle daily for 24 days i.m. They were fed corn-soybean meal diets containing either 140 or 200 g crude protein/kg (low or high protein). The percentage of muscle in the carcasses of pigs given GH was greater (P less than 0.01) than that of controls. Relative to controls, GH increased (P less than 0.05) the amount of liver IGF-I mRNA by 2.7-fold in pigs fed the low protein diet and 3.0-fold in pigs fed the high protein diet. The amount of IGF-I mRNA in the muscles of GH-treated pigs was 77% and 84% of control pigs in those fed the low and high protein diets respectively (P less than 0.08). GH increased (P less than 0.001) the serum concentration of IGF-I 1.6-fold in pigs fed the low protein diet and 2.0-fold in those fed the high protein diet. These results indicate that the administration of GH to pigs influences the relative amount of liver IGF-I mRNA. The increased amount of liver IGF-I mRNA and the increased serum IGF-I concentrations suggest that IGF-I plays an endocrine role in mediating GH-induced muscle hypertrophy in pigs.     

Whole body leucine and lysine metabolism studied with [1-13C]leucine and [α-15N]lysine: Response in healthy young men given excess energy intake

An excess intake of dietary energy in adult subjects enhances body N balance but the mechanism(s) responsible remains unknown. Thus, dynamic aspects of metabolism of whole body leucine and lysine were explored in healthy young adult men, receiving adequate or excess energy intakes, using a primed, continuous intravenous infusion of a mixture of L-[¹³C]leucine and L-[α-¹⁵N]lysine to provide a constant enrichment of plasma free leucine and lysine over a period of 2 hr. Twelve subjects were studied with the labeled amino acids following an overnight fast (post-absorptive state) and 12 additional subjects while consuming small isocaloric, isonitrogenous horly meals (fed state). Preceding each infusion, subjects were adapted for 7 days to experimental diets, providing a constant and barely adequate protein intake of 0.6 g/kg body weight/day, at either a maintenance energy intake, determining from estimates of usual food intake that maintain body weight, or an energy intake 25% greater than the maintenance level. The excess non-protein energy intake was given as an isocaloric mixture of carbohydrate and fat (eight subjects) or entirely as either carbohydrate or fat (eight subjects each). Whole body leucine and lysine flux remained unchanged with excess energy intakes, regardless of the source of energy substrate. Based on the combined data with all energy intake sources, the rate of leucine oxidation was significantly reduced and the rate of leucine incorporation into body protein showed a small increase with excess energy intakes. Thus, when expressed as net protein gain (leucine incorporation into body protein minus leucine release from protein breakdown) a significantly greater rate of body protein retention occurred with excess energy intake and this was more marked for the high carbohydrate diets. Mean change in body leucine retention determined by ¹³C-leucine was in good agreement with that calculated from alterations in overall N balance. In addition, the rate of inflow of leucine and of lysine into the metabolic pool via tissue protein breakdown was reduced with ingestion of meals. These results indicate that excess energy intake improves overall body N balance by reducing amino acid oxidation and enhancing protein synthesis. Furthermore, these effects are particularly evident at a time when passage of amino acids to tissues is stimulated by ingestion and absorption of meals.     

Relations between dietary choline or lecithin intake, serum choline levels, and various metabolic indices

Choline administration increases blood choline, brain choline, and brain acetylcholine levels in rats. It also increases blood choline levels in humans and appears to be a useful treatment for some patients with tardive dyskinesia, a brain disease probably associated with deficient cholinergic tone. In order to characterize other possible metabolic and hormonal effects of choline-containing compounds, we measured changes in serum choline, glucose, insulin, cortisol, prolactin, cholesterol, and triglyceride levels resulting from ingestion of low- or high-choline meals in 16 normal human subjects. After the consumption of a single meal containing 3 g choline chloride, serum choline rose by 86% (p < 0.01), attaining peak values after 30 min. When the same subjects ate a meal containing an equivalent amount of choline in the form of lecithin, serum choline levels rose by 33% after 30 min, and continued to rise for at least 12 hr, to 265% over control values (p < 0.001). Serum choline concentrations were related to the amount of choline in the diet: they did not vary significantly during 24-hr periods when the subjects consumed a low-choline diet for two consecutive days, but rose substantially (p < 0.01) after each high-choline meal. Serum glucose, insulin, cortisol, and prolactin levels were not significantly modified by choline or lecithin ingestion. Lecithin consumption increased serum triglyceride levels and lowered serum cholesterol concentration.     

L-tryptophan does not increase weight loss in carbohydrate-craving obese subjects

Eight subjects, aged 26 to 50 years, who had long histories of carbohydrate (CHO) craving and were more than 45 kg above desirable body weight participated in a randomized, double-blind, crossover pilot study on the effects of L-tryptophan on weight loss and mood state. One g of tryptophan with 10 g of CHO was administered three times a day, 30 min before meals, as an adjunct to a weight-loss protocol that included nutritional consultation teaching low fat, high fiber diets ranging from 1200-1600 kcals/day, behavior modification, and supportive therapy. During the pretreatment period, body weight and plasma tryptophan levels were measured and the Beck Depression Inventory, SCL 90 rating, and Profile-of-Mood State (POMS) were used to assess mood. During the treatment periods, subjects kept daily records of food intake and the timing of medication. All patients were seen at least biweekly. After six weeks on medication, baseline measurements were repeated and the crossover between tryptophan and placebo was implemented. After an additional six weeks on placebo or tryptophan, the same measurements were repeated. For the eight patients who completed the three-month protocol, the mean weight loss for six weeks on placebo was 1.14 kg and for six weeks on tryptophan was 2.3 kg. Mean Beck scores were 8.8 during the control period, 8.3 on placebo, and 10.9 on tryptophan. Mean SCL 90 ratings were 69.2 during the control, 54.6 on placebo, and 64.2 on tryptophan. Mean scores for total mood disturbance on the POMS were 48 during the control period, 43 on placebo, and 52 on tryptophan.(ABSTRACT TRUNCATED AT 250 WORDS)     

Lipid metabolism in pregnancy. VIII. Effects of dietary fat versus carbohydrate on lipoprotein and hepatic lipids and tissue triglyceride lipases

We have asked, is hypertriglyceridemia in the fed state in pregnancy due to intolerance to exogenous fat, accumulation of endogenous triglycerides, or accumulation of remnants of d < 1.006 lipoprotein metabolism? To answer these questions, we fed rat-free diets high in starch or sucrose, or diets containing fat or fat plus cholesterol to pregnant and nonpregnant rats for 12 days until gestational day 21 (term = 22 days). Blood was obtained 0, 4, or 8 hr after removal of food from the cages. Lipid concentrations were determined in chylomicrons and very low, low, and high density lipoproteins. Hypertriglyceridemia in pregnancy exists on both starch and sucrose containing fat-free diets and is exaggerated 4 and 8 hr after food is removed from the cage. The triglyceride rise occurs in d < 1.006 lipoproteins. With fat feeding, chylomicron triglyceride concentrations are not significantly elevated in pregnant rats, 0 or 8 hr postabsorptively despite greater food intake in pregnancy. In contrast, very low density lipoprotein (VLDL) triglyceride concentrations are elevated at all times following fat feeding in pregnant compared to nonpregnant animals. A significant contribution of lipoprotein remnants to the triglyceride rise in d < 1.006 lipoproteins seems unlikely since an isolated increase in VLDL cholesterol is not observed. No statistically significant accumulation of hepatic triglycerides occurs on any diet in pregnancy. Diet induced shifts in adipose tissue and muscle lipoprotein lipase activity are exaggerated in pregnancy while hepase in unaffected. Fetal weight is similar on all diets except sucrose where weight is reduced. Conclusions: Hypertriglyceridemia in fed pregnant rats is due to an increase in endogenous triglycerides. Remnant lipid accumulation does not appear to contribute to the endogenous hypertriglyceridemia. There is no intolerance to exogenous (dietary) fat. The results are compatible with an unimpaired delivery of exogenous fat to fat oxidizing tissues thereby maximizing glucose availability for fetal growth.     

Effects of diet composition on glucose tolerance and plasma lipids of non insulin-dependent diabetics

Summary The possible influence of qualitative dietary changes on carbohydrate tolerance and plasma lipid levels of non insulin-dependent diabetics was studied in 5 maturity-onset diabetics of normal weight who remained stabilized with 5 to 10 mg glibenclamide. Each patient was submitted to 4 isocaloric qualitatively different diets: standard, high carbohydrate, high fat, and high protein. Each diet was administered for 30 consecutive days in random order. Apart from assessing metabolic control, an oral glucose tolerance test (40 g/m² body surface area) was performed in the morning, at the end of each period. Blood was collected at 0, 60, 120, and 180 min after starting glucose ingestion, for blood glucose and plasma FFA determinations. Fasting total lipids, triglycerides, lipoalbumins, and α- and β-lipoproteins, and 24-h urinary urea were also investigated. The findings did not disclose any differences in carbohydrate tolerance after the various diets. The drop in FFA levels following an oral glucose load was greatest after the high protein diet. Fasting total lipids were lowest after the high fat and high protein diets. Triglycerides fell after the high fat diet. The remaining parameters showed less significant variations. Although no differences were observed in carbohydrate tolerance, the conclusion is that relative carbohydrate restriction together with sufficient protein supply might be most beneficial for non insulin-dependent diabetics.     

A low glycaemic diet improves oral glucose tolerance but has no effect on β-cell function in C57BL/6J mice

Aim: Clinical studies have suggested a role for dietary glycaemic index (GI) in body weight regulation and diabetes risk. Here, we investigated the long‐term metabolic effects of low and high glycaemic diets using the C57BL/6J mouse model. Methods: Female C57BL/6J mice were fed low or high glycaemic starch in either low‐fat or medium‐fat diets for 22 weeks. Oral and intravenous glucose tolerance tests were performed to investigate the effect of the experimental diets on glucose tolerance and insulin resistance. Results: In this study, a high glycaemic diet resulted in impaired oral glucose tolerance compared to a low glycaemic diet. This effect was more pronounced in the group fed a medium‐fat diet, suggesting that a lower dietary fat content ameliorates the negative effect of a high glycaemic diet. No effect on body weight or body fat content was observed in either a low‐fat diet or a medium‐fat diet. Static incubation of isolated islets did not show any differences in basal (3.3 mM glucose) or glucose‐stimulated (8.6 and 16.7 mM glucose) insulin secretion between mice fed a low or high glycaemic diet. Conclusion: Together, our data suggest that the impaired glucose tolerance seen after a high glycaemic diet is not explained by altered β‐cell function.     

Hypothalamic-pituitary-adrenal axis and sympathetic nervous system activities in Pima Indians and Caucasians

It has been proposed that both hypercortisolism and low sympathetic nervous system (SNS) activity contribute to obesity. Because glucocorticoids inhibit SNS activity, we hypothesized that hypercortisolism and low SNS activity may be found in association in Pima Indians, a population with a high prevalence of obesity. We therefore measured indices of hypothalamic-pituitary-adrenal (HPA) axis and SNS activities in 39 nondiabetic men, 20 Pimas (age, 30+/-5 years; weight, 94+/-26 kg; 35%+/-8% body fat [mean +/- SD]) and 19 Caucasians (33+/-9 years, 91+/-23 kg, 28%+/-11% body fat). HPA axis activity was assessed by measurements of morning fasting plasma corticotropin (ACTH) and cortisol concentrations and 24-hour urinary free cortisol (UFC) excretion. SNS activity was assessed as muscle sympathetic nerve activity (MSNA) by microneurography and by measurement of catecholamines (fasting plasma concentration and 24-hour urinary excretion). Plasma ACTH and cortisol and UFC were similar in Pimas and Caucasians. MSNA was positively correlated with percent body fat (r = .49, P = .002) and was lower in Pimas compared with Caucasians after adjustment for percent body fat (24+/-9 v 31+/-10 bursts/min, P = .04). We conclude that Pima Indians, a population with a high prevalence of obesity, have lower SNS activity but normal HPA axis activity compared with Caucasians.     

The role of dietary fat in obesity

Current scientific evidence indicates that dietary fat plays a role in weight loss and maintenance. Meta-analyses of intervention trials find that fat-reduced diets cause a 3-4-kg larger weight loss than normal-fat diets. A 10% reduction in dietary fat can cause a 4-5-kg weight loss in individuals with initial body mass index of 30 kg m (-2). Short-term trials show that nonfat dietary components are equally important. Sugar-sweetened beverages promote weight gain, and replacement of energy from fat by sugar-sweetened beverages is counterproductive in diets aimed at weight loss. Protein has been shown to be more satiating than carbohydrate, and fat-reduced diets with a high protein content (20-25% of energy) may increase weight loss significantly. There is little evidence that low-glycemic index foods facilitate weight control. Evidence linking certain fatty acids to body fatness is weak. Monounsaturated fatty acids may even be more fattening than polyunsaturated and saturated fats. No ad libitum dietary intervention study has shown that a normal-fat, high-monounsaturated fatty acid diet is comparable to a low-fat diet in preventing weight gain. Current evidence indicates that the best diet for prevention of weight gain, obesity, type 2 diabetes, and cardiovascular disease is low in fat and sugar-rich beverages and high in carbohydrates, fiber, grains, and protein.     

Some metabolic effects of fat infusions in depleted patients

Severely depleted surgical patients were given total parenteral nutrition, providing an average of 34.6 kcal and 266 mg nitrogen/kg body weight. Two diets were used, one with glucose as sole source of nonprotein energy, the other with a fat emulsion, Liposyn 10%, substituted isocalorically for one-third of the glucose. The two diets were given alternately, for 1 wk at a time, to each patient. N balance, at zero energy balance, was estimated to average 50 mg nitrogen/kg, indicating that energy intake in excess of expenditure is not required to restore lean body mass in depleted patients. Nitrogen (N) balance was equally good with either diet. Respiratory quotients and carbohydrate oxidation were lower, and fat oxidation was higher with the fat-containing diet. Amino acids and glucose were infused continuously over each 24-hr period and fat was given for only 6--8 hr. During the period of fat infusion, fat oxidation was significantly higher, and carbohydrate oxidation and RQ were lower than at other times of day.