Anthropometric evaluations of body composition of undergraduate students at the University of La Reunion

A positive correlation is well established between obesity and the susceptibility to develop metabolic syndrome, a multifactorial disease dramatically associated with an enhanced mortality risk in the developed world. A high prevalence of obesity has recently been described at La Réunion Island, a French department in the Indian Ocean. Anthropometry is generally considered as the single most easily obtainable, inexpensive, and noninvasive method that reflects body composition. At the University of La Réunion, a laboratory course involving students was designed to teach anthropometric measurements for the determination of body composition. Using skin fold thickness equations, students determined the fat and total muscular masses of their body composition. The influences of sex and their physical activity or inactivity on these different parameters were compared and interpreted at the end of the course. Positive and significant correlations were established between the students' body mass indexes values and their fat mass percentages and between their fat-free and muscular masses as well. A higher fat mass percentage was found in sedentary students compared with more active ones. Therefore, this laboratory makes the students practice and understand the use of classical techniques to evaluate the body composition of a person. It also alerts them to the correlation between a sedentary attitude and higher body fat content. This laboratory course constitutes an active introduction to a following lesson on more recent and actual techniques used to evaluate body composition.     

The Impact of Food Viscosity on Eating Rate,Subjective Appetite,Glycemic Response and Gastric Emptying Rate

Understanding the impact of rheological properties of food on postprandial appetite and glycemic response helps to design novel functional products. It has been shown that solid foods have a stronger satiating effect than their liquid equivalent. However, whether a subtle change in viscosity of a semi-solid food would have a similar effect on appetite is unknown. Fifteen healthy males participated in the randomized cross-over study. Each participant consumed a 1690 kJ portion of a standard viscosity (SV) and a high viscosity (HV) semi-solid meal with 1000 mg acetaminophen in two separate sessions. At regular intervals during the three hours following the meal, subjective appetite ratings were measured and blood samples collected. The plasma samples were assayed for insulin, glucose-dependent insulinotropic peptide (GIP), glucose and acetaminophen. After three hours, the participants were provided with an ad libitum pasta meal. Compared with the SV meal, HV was consumed at a slower eating rate (P = 0.020), with postprandial hunger and desire to eat being lower (P = 0.019 and P<0.001 respectively) while fullness was higher (P<0.001). In addition, consuming the HV resulted in lower plasma concentration of GIP (P<0.001), higher plasma concentration of glucose (P<0.001) and delayed gastric emptying as revealed by the acetaminophen absorption test (P<0.001). However, there was no effect of food viscosity on insulin or food intake at the subsequent meal. In conclusion, increasing the viscosity of a semi-solid food modulates glycemic response and suppresses postprandial satiety, although the effect may be short-lived. A slower eating rate and a delayed gastric emptying rate can partly explain for the stronger satiating properties of high viscous semi-solid foods.     

Effects of glucose supplementation on gastric emptying, blood glucose homeostasis, and appetite in the elderly

The aims of this study were to evaluate the effects of dietary glucose supplementation on gastric emptying (GE) of both glucose and fat, postprandial blood glucose homeostasis, and appetite in eight older subjects (4 males, 4 females, aged 65--84 yr). GE of a drink (15 ml olive oil and 33 g glucose dissolved in 185 ml water), blood glucose, insulin, gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), and appetite (diet diaries, visual analog scales, and food intake at a buffet meal consumed after the GE study) were evaluated twice, after 10 days on a standard or a glucose-supplemented diet (70 g glucose 3 times a day). Glucose supplementation accelerated GE of glucose (P < 0.05), but not oil; there was a trend for an increase in GIP (at 15 min, P = 0.06), no change in GLP-1, an earlier insulin peak (P < 0.01), and a subsequent reduction in blood glucose (at 75 min, P < 0.01). Glucose supplementation had no effect on food intake during each diet so that energy intake was greater (P < 0.001) during the glucose-supplemented diet. Appetite ratings and energy intake at the buffet meal were not different. We conclude that, in older subjects, glucose supplementation 1) accelerates GE of glucose, but not fat; 2) modifies postprandial blood glucose homeostasis; and 3) increases energy intake.     

Glycemic index, postprandial glycemia and cardiovascular disease

PURPOSE OF REVIEW: Several lines of evidence indicate that exaggerated postprandial glycemia puts individuals without diabetes at greater risk of developing cardiovascular disease. In large, prospective observational studies, including meta-analyses, higher 120 min post-load blood glucose and glycated hemoglobin (a measure of average blood glucose level over time) independently predict cardiovascular mortality and morbidity in individuals without diabetes. These findings imply that the glycemic nature of dietary carbohydrates may also be relevant. We aim to provide a clearer perspective on how the glycemic impact of carbohydrates may modulate development of cardiovascular disease. RECENT FINDINGS: In ecological studies, average dietary glycemic index (a measure of the postprandial glycemic potential of carbohydrates) and glycemic load (average glycemic index x amount of carbohydrate) predicts coronary infarct and cardiovascular disease risk factors, including HDL cholesterol, triglycerides and C-reactive protein. In short-term intervention studies of overweight and hyperlipidemic patients, low glycemic index diets lead to improvements in cardiovascular disease risk factors, including reduced LDL cholesterol and improved insulin sensitivity, as well as greater body fat loss on energy-restricted diets. Molecular studies indicate that physiological hyperglycemia induces overproduction of superoxide by the mitochondrial electron-transport chain, resulting in inflammatory responses and endothelial dysfunction. SUMMARY: Taken together, the findings suggest that conventional high-carbohydrate diets with their high glycemic index may be suboptimal, particularly in insulin-resistant individuals. Because around one in four adults has impairments in postprandial glucose regulation, the glycemic potential of carbohydrates warrants further investigation in cardiovascular disease prevention.     

Circadian Aspects of Postprandial Metabolism

Time‐dependent variations in the hormonal and metabolic responses to food are of importance to human health, as postprandial metabolic responses have been implicated as risk factors in a number of major diseases, including cardiovascular disease. Early work reported decreasing glucose tolerance in the evening and at night with evidence for insulin resistance at night. Subsequently an endogenous circadian component, assessed in constant routine (CR), as well as an influence of sleep time, was described for glucose and insulin. Plasma triacylglycerol (TAG), the major lipid component of dietary fat circulating after a meal, also appears to be influenced by both the circadian clock and sleep time with higher levels during biological night (defined as the time between the onset and offset of melatonin secretion) despite identical hourly nutrient intake. These time‐dependent differences in postprandial responses have implications for shiftworkers. In the case of an unadapted night shift worker, meals during work time will be taken during biological night. In simulated night shift conditions the TAG response to a standard meal, preceded by either a low‐fat or a high‐fat premeal, was higher after a nighttime meal than during a daytime meal, and the day/night difference was larger in men than in women. In real night shift workers in Antarctica, insulin, glucose, and TAG all showed an increased response after a nighttime meal (second day of night shift) compared to a daytime meal. Night shift workers are reported to have an approximately 1.5 times higher incidence of heart disease risk and also demonstrate higher TAG levels compared with matched dayworkers. As both insulin resistance and elevated circulating TAG are independent risk factors for heart disease, it is possible that meals at night may contribute to this risk.     

Effects of post-absorptive and postprandial exercise on glucoregulation in metabolic syndrome

Objective: The aim of this study was to investigate the effects of an acute exercise bout in the morning in the post‐absorptive or postprandial state on the glycemic and insulinemic response to three standardized meals throughout the day. It is hypothesized that post‐absorptive exercise enhances fat oxidation rate during exercise and thereafter attenuates the glucose and insulin response to subsequent meals. Research Methods and Procedures: Seven sedentary males with metabolic syndrome (age, 45 ± 11 years; BMI, 34 ± 3 kg/m²) were studied in a crossover design comparing three conditions: no exercise, postprandial and post‐absorptive exercise (at ～60% of the individual V?O_2max for 45 minutes). Substrate use was evaluated by indirect calorimetry during exercise. Venous blood samples were taken at regular (30‐ to 60‐minute) intervals throughout the day, and glucose, insulin, and triglyceride concentrations were determined. Results: During exercise, a higher fat oxidation rate was observed in the post‐absorptive than the postprandial state. The glycemic response to a standardized high‐carbohydrate breakfast was lower when exercising after breakfast than when exercising before breakfast. There was no effect of either exercise mode on glucose and insulin response to lunch and supper. Discussion: Post‐absorptive exercise has the advantage of promoting fat use, whereas postprandial exercise can attenuate the glycemic response to breakfast. Neither exercise mode acutely induces improved glucoregulation later during the day. The impact of meal timing on the effects of regular exercise training on glycemic control in this population remains to be studied.     

Mechanism of action of whole milk and its components on glycemic control in healthy young men

Milk reduces post-meal glycemia when consumed either before or within an ad libitum meal. The objective of this study was to compare the effect of each of the macronutrient components and their combination with whole milk on postprandial glycemia, glucoregulatory and gastrointestinal hormones and gastric emptying in healthy young men. In a randomized, crossover study, 12 males consumed beverages (500ml) of whole milk (3.25% M.F.) (control), a simulated milk beverage based on milk macronutrients, complete milk protein (16g), lactose (24g) or milk fat (16g). Whole and simulated milk was similar in lowering postprandial glycemia and slowing gastric emptying while increasing insulin, C-peptide, peptide tyrosine tyrosine (PYY) and cholecystokinin (CCK), but simulated milk resulted in higher (41%) glucagon-like peptide-1 (GLP-1) and lower (43%) ghrelin areas under the curve (AUC) than whole milk (P=.01 and P=.04, respectively). Whole and simulated milk lowered glucose (P=.0005) more than predicted by the sum of AUCs for their components. Adjusted for energy content, milks produced lower glucose and hormone responses than predicted from the sum of their components. The effect of protein/kcal on the AUCs was higher than fat/kcal for insulin, C-peptide, insulin secretion rate, GLP-1, CCK and paracetamol (P<.0001), but similar to lactose except for CCK and paracetamol, which were lower. The response in PYY and ghrelin was similar per unit of energy for each macronutrient. In conclusion, milk lowers postprandial glycemia by both insulin and insulin-independent mechanisms arising from interactions among its macronutrient components and energy content.     

Effect of a meal feeding schedule on hepatic glycogen synthesis and gluconeogenesis in rats

We investigated the effect of a meal feeding schedule (MFS) on food intake, hepatic glycogen synthesis, hepatic capacity to produce glucose and glycemia in rats. The MFS comprised free access to food for a 2-hour period daily at a fixed mealtime (8.00-10.00 a.m.) for 13 days. The control group was composed of rats with free access to food from day 1 to 12, which were then starved for 22 h, refed with a single meal at 8.00-10.00 a.m. and starved again for another 22 h. All experiments were performed at the meal time (i.e. 8.00 a.m.). The MFS group exhibited increased food intake and higher glycogen synthase activity. Since gluconeogenesis from L-glutamine or L-alanine was not affected by MFS, we conclude that the increased food intake and higher glycogen synthase activity contributed to the better glucose maintenance showed by MFS rats at the fixed meal time.     

Load-dependent effects of duodenal glucose on glycemia, gastrointestinal hormones, antropyloroduodenal motility, and energy intake in healthy men

Gastric emptying is a major determinant of glycemia, gastrointestinal hormone release, and appetite. We determined the effects of different intraduodenal glucose loads on glycemia, insulinemia, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and cholecystokinin (CCK), antropyloroduodenal motility, and energy intake in healthy subjects. Blood glucose, plasma hormone, and antropyloroduodenal motor responses to 120-min intraduodenal infusions of glucose at 1) 1 ("G1"), 2) 2 ("G2"), and 3) 4 ("G4") kcal/min or of 4) saline ("control") were measured in 10 healthy males in double-blind, randomized fashion. Immediately after each infusion, energy intake at a buffet meal was quantified. Blood glucose rose in response to all glucose infusions (P < 0.05 vs. control), with the effect of G4 and G2 being greater than that of G1 (P < 0.05) but with no difference between G2 and G4. The rises in insulin, GLP-1, GIP, and CCK were related to the glucose load (r > 0.82, P < 0.05). All glucose infusions suppressed antral (P < 0.05), but only G4 decreased duodenal, pressure waves (P < 0.01), resulted in a sustained stimulation of basal pyloric pressure (P < 0.01), and decreased energy intake (P < 0.05). In conclusion, variations in duodenal glucose loads have differential effects on blood glucose, plasma insulin, GLP-1, GIP and CCK, antropyloroduodenal motility, and energy intake in healthy subjects. These observations have implications for strategies to minimize postprandial glycemic excursions in type 2 diabetes.     

Effect of solid meal on gastric emptying of,and glycemic and cardiovascular responses to,liquid glucose in older subjects

Gastric emptying is a determinant of the postprandial glycemic and cardiovascular responses to oral carbohydrate. We evaluated the effects of a solid meal on gastric emptying and the glycemic and cardiovascular responses to oral glucose in healthy older subjects. Ten subjects aged 72.1 +/- 1.9 yr were studied. Each subject had measurements of gastric emptying, blood glucose, serum insulin, blood pressure, and heart rate after ingestion of a 50-g glucose drink (300 ml) with (mixed meal) or without (liquid only) a solid meal (300 g ground beef). Gastric emptying of liquid was initially slightly more rapid (P < 0.05) after the mixed meal compared with liquid only at 5 min (92.0 +/- 1.5 vs. 96.0 +/- 1.3%) and much slower (P < 0.05) after 120 min. The time to peak blood glucose was less (39.0 +/- 4.0 vs. 67.5 +/- 10.3 min; P < 0.01) and blood glucose subsequently lower (P < 0.01) after the mixed meal. The increase in serum insulin was greater (P < 0.001) after the mixed meal. Blood pressure fell (P < 0.05) in the first 30 min, with no difference between the two meals. Increase in heart rate after both meals (P < 0.005), was greater (P < 0.05) after the mixed meal. The presence of a noncarbohydrate solid meal had discrepant effects on early and subsequent emptying of a nutrient liquid, which affects postprandial glycemia and increased heart rate.     

Postprandial variations of plasma inflammatory markers in abdominally obese men

Objective: Abdominal obesity is associated with a fasting proinflammatory condition. However, not much is known of the potential variations in circulating inflammatory markers after food intake. The purpose of the present study was to examine postprandial changes in plasma tumor necrosis factor (TNF)‐α, interleukin (IL)‐6, and C‐reactive protein (CRP) concentrations in men and their potential associations with fat distribution and metabolic profile variables. Research Methods and Procedures: Thirty‐eight men were given a high‐fat meal in the morning after an overnight fast, and TNF‐α, IL‐6, and CRP levels were measured in plasma at 0, 4, and 8 hours after the meal. Physical and metabolic profiles were also assessed for each participant. Results: We observed a substantial increase in circulating IL‐6 levels (p < 0.0001) after the meal. Although postprandial variations in circulating TNF‐α levels across time failed to reach statistical significance (p = 0.02), we noted a significant decrease in plasma TNF‐α concentrations 4 hours (?10%, p < 0.001 vs. 0 hours) after food intake. Plasma CRP levels were not affected by the fat load. We also noted that insulin‐sensitive individuals displayed a less pronounced inflammatory response after food intake than insulin‐resistant subjects. Discussion: Results of the present study show that consumption of a high‐fat meal leads to an increase in plasma IL‐6 concentrations and transient decrease in circulating TNF‐α levels in overweight men. Our results suggest a possible role of insulin resistance in the modulation of the postprandial inflammatory response, which could, in turn, contribute to worsen the state of insulin resistance.     

Oral salmon calcitonin improves fasting and postprandial glycemic control in lean healthy rats

A novel oral form of salmon calcitonin (sCT) was recently demonstrated to improve both fasting and postprandial glycemic control and induce weight loss in diet-induced obese and insulin-resistant rats. To further explore the glucoregulatory efficacy of oral sCT, irrespective of obesity and metabolic dysfunction, the present study investigated the effect of chronic oral sCT treatment on fasting and postprandial glycemic control in male lean healthy rats. 20 male rats were divided equally into a control group receiving oral vehicle or an oral sCT (2?mg/kg) group. All rats were treated twice daily for 5 weeks. Body weight and food intake were monitored during the study period and fasting blood glucose, plasma insulin and insulin sensitivity were determined and an oral glucose tolerance test (OGTT) performed at study end. Compared with the vehicle group, rats receiving oral sCT had improved fasting glucose homeostasis and insulin resistance, as measured by homeostatic model assessment of insulin resistance index (HOMA-IR), with no change in body weight or fasting plasma insulin. In addition, the rats receiving oral sCT had markedly reduced glycemia and insulinemia during OGTT. This is the first report showing that chronic oral sCT treatment exerts a glucoregulatory action in lean healthy rats, irrespective of influencing body weight. Importantly, oral sCT seems to exert a dual treatment effect by improving fasting and postprandial glycemic control and insulin sensitivity. This and previous studies suggest oral sCT is a promising agent for the treatment of obesity-related insulin resistance and type 2 diabetes.     

Circadian aspects of postprandial metabolism

Time-dependent variations in the hormonal and metabolic responses to food are of importance to human health, as postprandial metabolic responses have been implicated as risk factors in a number of major diseases, including cardiovascular disease. Early work reported decreasing glucose tolerance in the evening and at night with evidence for insulin resistance at night. Subsequently an endogenous circadian component, assessed in constant routine (CR), as well as an influence of sleep time, was described for glucose and insulin. Plasma triacylglycerol (TAG), the major lipid component of dietary fat circulating after a meal, also appears to be influenced by both the circadian clock and sleep time with higher levels during biological night (defined as the time between the onset and offset of melatonin secretion) despite identical hourly nutrient intake. These time-dependent differences in postprandial responses have implications for shiftworkers. In the case of an unadapted night shift worker, meals during work time will be taken during biological night. In simulated night shift conditions the TAG response to a standard meal, preceded by either a low-fat or a high-fat premeal, was higher after a nighttime meal than during a daytime meal, and the day/night difference was larger in men than in women. In real night shift workers in Antarctica, insulin, glucose, and TAG all showed an increased response after a nighttime meal (second day of night shift) compared to a daytime meal. Night shift workers are reported to have an approximately 1.5 times higher incidence of heart disease risk and also demonstrate higher TAG levels compared with matched dayworkers. As both insulin resistance and elevated circulating TAG are independent risk factors for heart disease, it is possible that meals at night may contribute to this risk.     

The individual and combined effects of glycemic index and protein on glycemic response, hunger, and energy intake

Although high protein and low glycemic index (GI) foods are thought to promote satiety, little is known about the effects of GI, protein, and their interaction on hunger and energy intake several hours following a mixed meal. This study investigated the long term effects of GI, protein, and their combined effects on glucose, insulin, hunger, and energy intake in healthy, sedentary, overweight, and obese adults (BMI of 30.9 ± 3.7 kg/m²). Sixteen individuals participated separately in four testing sessions after an overnight fast. The majority (75%) were non‐Hispanic Blacks. Each consumed one of four breakfast meals (high GI/low protein, high GI/high protein, low GI/low protein, low GI/high protein) in random order. Visual analog scales (VAS) and blood samples were taken at baseline, 15 min, and at 30 min intervals over 4 h following the meal. After 4 h, participants were given the opportunity to consume food ad libitum from a buffet style lunch. Meals containing low GI foods produced a smaller glucose (P < 0.002) and insulin (P = 0.0001) response than meals containing high GI foods. No main effects for protein or interactions between GI and protein were observed in glucose or insulin responses, respectively. The four meals had no differential effect on observed energy intake or self‐reported hunger, satiety, and prospective energy intake. Low GI meals produced the smallest postprandial increases in glucose and insulin. There were no effects for GI, protein, or their interaction on appetite or energy intake 4 h after breakfast.     

Long-time alcohol intake modifies resistin secretion and expression of resistin gene in adipose tissue

Elevated serum resistin is implicated in insulin resistance associated with obesity and type 2 diabetes mellitus. Alcohol consumption interferes with the nutritional status, metabolic and hormonal activity of the drinker. Impact of ethanol intake on resistin level and resistin metabolic effects is unknown. Effect of long-time (28 days) ad libitum moderate alcohol (6% ethanol solution) intake on serum resistin and resistin mRNA level in adipose tissue of rats (A) was compared to control (C) and pair-fed (PF) animals. PF rats were fed the same caloric amount as A rats on previous day. Alcohol consumption resulted in reduction of food and energy intake, decreased body mass gain, epididymal fat pads mass and smaller adipocytes (vs. C rats). Alcohol intake significantly increased serum resistin and glucose, insulinemia remained unchanged. Systemic insulin resistance was not proved by HOMA, QUICKI and McAuley indexes, but impaired insulin effect on glucose transport in isolated adipocytes was present. Elevated serum resistin was positively correlated with glycemia (r = 0.88, p < 0.01) and negatively with fat cell size (r = -0.73, p < 0.05). High resistin level as the consequence of long-time alcohol intake could contribute to smaller adipocytes, higher glycemia, attenuation of insulin-stimulated glucose transport in adipocytes. Diminished resistin gene expression in adipose tissue of A and PF rats was present.     

Dilution of the 75-g oral glucose tolerance test increases postprandial glycemia: implications for diagnostic criteria

BACKGROUND: Dilution has been noticed to increase the glycemic response to various sugars, including glucose. This effect may contribute to the poor reproducibility of the oral glucose tolerance test (OGTT). To test this hypothesis we assessed the effect of diluting a 75-g OGTT on 2-hour postprandial blood glucose based diagnostic outcomes, incremental glycemia and area under the glucose curve. METHODS: On 3 different occasions, 10 subjects (mean age 40 [and standard error of the mean (SEM) 3.2] years; mean body mass index 27.2 [and SEM 1.2] kg/m2) without previously diagnosed dysglycemia were given a 300-mL, 600-mL or 900-mL 75-g OGTT in random order. The protocol followed the American Diabetes Association''s guidelines. Finger-prick capillary blood samples were obtained at fasting and then 15, 30, 45, 60, 90 and 120 minutes after the start of the test. RESULTS: At 30, 45 and 60 minutes, incremental glycemic concentrations were significantly higher with the 900-mL meal (means [and SEMs]: 4.9 [0.4] mmol/L, 5.1 [0.6] mmol/L and 4.6 [0.8] mmol/L, respectively) than with the 600-mL (means [and SEMs]: 4.0 [0.3] mmol/L, 4.2 [0.6] mmol/L and 3.6 [0.7] mmol/L, respectively) and the 300-mL meals (means and [SEMs]: 3.8 [0.5] mmol/L, 4.0 [0.5] mmol/L and 3.2 [0.6] mmol/L, respectively) (p < 0.05). The same was true for peak incremental blood glucose, regardless of time (p < 0.05). The area under the curve for the 900-mL meal (mean [and SEM] 404 [57] min.mmol/L) was significantly higher than for the 600-mL (mean [and SEM] 331 [51] min.mmol/L) and 300-mL meals (mean [and SEM] 280 [48] min.mmol/L) (p < 0.05). No other significant differences were observed. INTERPRETATION: Dilution of the 75-g OGTT will likely not affect current screening practices that use 2-h postprandial glucose levels as the basis for diagnosis. It may, however, bias the interpretation of older criteria that rely on intermediate time points because these midpoints appear to be sensitive to alterations in the total volume of the meal ingested.     

The common hepatic branch of the vagus is not required to mediate the glycemic and food intake suppressive effects of glucagon-like-peptide-1

The incretin and food intake suppressive effects of intraperitoneally administered glucagon-like peptide-1 (GLP-1) involve activation of GLP-1 receptors (GLP-1R) expressed on vagal afferent fiber terminals. Central nervous system processing of GLP-1R-driven vagal afferents results in satiation signaling and enhanced insulin secretion from pancreatic-projecting vagal efferents. As the vast majority of endogenous GLP-1 is released from intestinal l-cells following ingestion, it stands to reason that paracrine GLP-1 signaling, activating adjacent GLP-1R expressed on vagal afferent fibers of gastrointestinal origin, contributes to glycemic and food intake control. However, systemic GLP-1R-mediated control of glycemia is currently attributed to endocrine action involving GLP-1R expressed in the hepatoportal bed on terminals of the common hepatic branch of the vagus (CHB). Here, we examine the hypothesis that activation of GLP-1R expressed on the CHB is not required for GLP-1's glycemic and intake suppressive effects, but rather paracrine signaling on non-CHB vagal afferents is required to mediate GLP-1's effects. Selective CHB ablation (CHBX), complete subdiaphragmatic vagal deafferentation (SDA), and surgical control rats received an oral glucose tolerance test (2.0 g glucose/kg) 10 min after an intraperitoneal injection of the GLP-1R antagonist, exendin-(9-39) (Ex-9; 0.5 mg/kg) or vehicle. CHBX and control rats showed comparable increases in blood glucose following blockade of GLP-1R by Ex-9, whereas SDA rats failed to show a GLP-1R-mediated incretin response. Furthermore, GLP-1(7-36) (0.5 mg/kg ip) produced a comparable suppression of 1-h 25% glucose intake in both CHBX and control rats, whereas intake suppression in SDA rats was blunted. These findings support the hypothesis that systemic GLP-1R mediation of glycemic control and food intake suppression involves paracrine-like signaling on GLP-1R expressed on vagal afferent fibers of gastrointestinal origin but does not require the CHB.     

Persisting Neural and Endocrine Modifications Induced by a Single Fat Meal

1. High-fat diets, modify the neuroendocrine response and, when prolonged, result in positive energy balance and obesity. Little is known about the effects of fat on the mechanisms operating in the initial steps of the neural and endocrine disturbances. 2. The studies reported here were designed to access the impact of the consumption of a single exclusively animal fat meal (lard), 24 h following its ingestion a) on the response of the hypothalamic serotonergic system to a standard laboratory chow meal and b) on the circulating levels of glucose, insulin, and leptin. The release of serotonin in the extracellular medial hypothalamic space (including the paraventricular-PVN and ventromedian-VMH nuclei) was determined using electrochemical detection following HPLC in samples obtained in vivo by microdialysis, in nonanesthetized adult male Wistar rats. 3. A lard meal resulted in decreased hypothalamic serotonin release postprandially and attenuated (24 h later) the hypothalamic serotonin response that normally follows a balanced meal. 4. In permanently catheterized rats, postprandial glucose and insulin levels measured in samples obtained in vivo, were either not, or only slightly, modified after a lard meal, whereas plasma leptin levels were increased. Interestingly, 24 h after a meal, insulin and leptin levels were increased in those animals eating a fat meal compared with those eating chow. Next-day glucose levels remained identical after the absorption either of a chow, or a lard meal. 5. The changes induced by the fat meal on peripheral and central regulators of energy and glucose homeostasis represent either adaptive mechanisms or early alterations that could render the organism vulnerable to further insults.     

Effect of Glycemic Load on Peptide‐YY Levels in a Biracial Sample of Obese and Normal Weight Women

Black women suffer a disproportionately higher rate of obesity than their white counterparts. Reasons for this racial disparity may reflect underlying differences in the appetite suppressing peptide‐YY (PYY). The PYY response to food is differentially influenced by macronutrient content but the effect of glycemic load on PYY response is unknown. This study examined whether glycemic load influences fasting and postprandial PYY levels and whether fasting and postprandial PYY levels are lower in obese black women compared to normal weight black women and to white women. Data were collected from 40 women (20 black, 20 white; 10 each normal weight vs. obese) at the University of North Carolina Clinical and Translational Research Center (CTRC). Participants completed in counterbalanced order two 4½‐day weight‐maintenance, mixed macronutrient high vs. low glycemic load diets followed by a test meal of identical composition. Total PYY levels were assessed before and after each test meal. Results show no differences in fasting PYY levels but significantly less postprandial PYY area under the curve (PYY_AUC) in the group of obese black women compared to each other group (race × obesity interaction, P < 0.04). PYY_AUC was positively related to insulin sensitivity (P < 0.004) but was not affected by glycemic load (main and interactive effects, P > 0.27). These findings indicate that postprandial PYY secretion is not affected by glycemic load but is blunted in obese black women compared with normal weight black women and with white women; additionally, they begin to address whether blunted PYY secretion contributes uniquely to the pathogenesis of obesity in black women.     

Carbohydrates modulate opiate receptor mediated mechanisms during postprandial endocrine function

The present study was designed to determine the role of carbohydrates during naloxone-induced opiate receptor blockade upon the postprandial rise of plasma somatostatin (SLI), insulin and pancreatic polypeptide (PP) levels in response to protein and fat test meals in conscious dogs. Test meals consisting of 50 g liver extract + 50 g sucrose or 50 g corn oil + 50 g sucrose dissolved in 300 ml water were instilled intragastrically, respectively. Additionally, liver extract and fat meals were given with a concomitant intravenous infusion of glucose. To all test meals either naloxone (4 mg) or saline was added. The addition of sucrose to liver extract or the infusion of i.v. glucose during the liver meal abolished the inhibitory effect of naloxone on the rise of postprandial somatostatin levels which has been described recently. The addition of carbohydrate either orally or intravenously to the fat meal resulted in an even stimulatory effect of naloxone upon the rise of postprandial somatostatin levels. Insulin levels were not changed during liver extract + sucrose or i.v. glucose, respectively. When sucrose or i.v. glucose was administered together with the fat meal the addition of naloxone augmented postprandial insulin secretion. Pancreatic polypeptide (PP) release was augmented during the combination of sucrose or i.v. glucose with the fat and liver meal when naloxone was present in the meals. The present data demonstrate that the addition of carbohydrates either orally or intravenously to fat and protein meals modulates the effect of endogenous opiates in the regulation of postprandial somatostatin, insulin and pancreatic polypeptide release in dogs in a way that carbohydrates induce inhibitory mechanisms that are mediated via endogenous opiate receptors.