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Biomedical subjects

G A Wittert

Publications and source records attributed to G A Wittert.

At least 19 recordsLinked to original sources
PubMed2006

Relative androgen deficiency in relation to obesity and metabolic status in older men.

BACKGROUND: Although androgen deficiency in men has been linked with obesity and the metabolic syndrome, whether it predisposes to, or is a consequence of, type 2 diabetes mellitus (T2DM) is still unclear. OBJECTIVE: To determine the relationship between plasma androgen levels, obesity, metabolic status and T2DM in men of 70 years or older. DESIGN AND METHODS: A sample of 195 men from the Australian Longitudinal Study of Ageing with a mean age of 76.2 +/- 0.3 years were followed up for 8 years. Total testosterone (TT), fasting plasma glucose (FPG), urate, serum creatinine, total cholesterol (TC), HDL cholesterol (HDL-C), LDL cholesterol (LDL-C), triglycerides (TG), blood pressure (BP), body mass index (BMI), waist circumference (WC) and diabetic status were assessed at baseline. Self-reported diabetic status was obtained after 8 years. Metabolic syndrome was diagnosed based on the Third National Cholesterol Education Program Adult Treatment Panel clinical criteria. RESULTS: TT levels were lower in diabetic men compared with non-diabetic men (12.1 +/- 0.7 vs. 14.2 +/- 0.4 nmol/l, p = 0.026). TT levels in healthy, non-diabetic men over 80 years of age were lower (11.9 +/- 0.8 vs. 15.0 +/- 0.5 nmol/l, p = 0.002) than TT levels in those aged 70-79 years, inversely related to BMI (r = -0.26, p = 0.001), WC (r = -0.30, p < 0.001) and TG (r = -0.22, p = 0.005) and positively related to LDL-C (r = 0.25, p = 0.002). Men with the metabolic syndrome had significantly lower levels of TT and HDL-C, and higher values of BP, FPG, TG, BMI and WC, compared with those without. However, no significant difference in plasma TT levels was noted between men with incident T2Dm and healthy men. Stepwise linear regression analysis revealed that only LDL-C and WC related significantly to the variance of TT. Multiple logistic regression revealed FPG to be the only independent predictor of incident diabetes (odds ratio = 60.2, p = 0.003). CONCLUSIONS: Testosterone levels continue to decline even in healthy men over the age of 80 years. Although TT levels were inversely related to visceral obesity and several components of the metabolic syndrome, our data do not support a predictive or causative role for decreasing TT levels in the development of incident T2Dm. Androgen deficiency is consequent upon, rather than a cause of, poor metabolic status.

Aged↗
PubMed2005

A 6-month study of the efficacy and safety of tadalafil in the treatment of erectile dysfunction: a randomised, double-blind, parallel-group, placebo-controlled study in Australian men.

The efficacy and safety of tadalafil for the treatment of erectile dysfunction (ED) were assessed in a 6-month, randomised, double-blind, placebo-controlled study. Australian men with mild, moderate or severe ED of organic, psychogenic or mixed aetiology were randomised to tadalafil 20 mg as needed (n = 93) or placebo (n = 47). Efficacy assessments included the international index of erectile function (IIEF) and the sexual encounter profile (SEP) diary. Tadalafil significantly improved erectile function compared with placebo (p < 0.001, all measures). At the end of the study, the mean per-patient proportion of successful sexual intercourse attempts (SEP question three) was 73.5% for patients treated with tadalafil and 26.8% for placebo-treated patients. Improved erections were reported by 78% of tadalafil-treated patients compared to 12.8% of placebo-treated patients. The most common treatment-emergent adverse events--headache and dyspepsia--were generally mild or moderate. Tadalafil was effective and well tolerated in Australian men with mild to severe ED.

Adult↗
PubMed2004

Long-term effects of a high-protein, low-carbohydrate diet on weight control and cardiovascular risk markers in obese hyperinsulinemic subjects.

OBJECTIVE: To compare the long-term compliance and effects of two low-fat diets differing in carbohydrate to protein ratio on body composition and biomarkers of cardiovascular disease risk in obese subjects with hyperinsulinemia. DESIGN: Outpatient, parallel, clinical intervention study of two groups of subjects randomly assigned to either a standard protein (SP; 15% protein, 55% carbohydrate) or high-protein (HP; 30% protein, 40% carbohydrate) diet, during 12 weeks of energy restriction (approximately 6.5 MJ/day) and 4 weeks of energy balance (approximately 8.3 MJ/day). Subsequently, subjects were asked to maintain the same dietary pattern for the succeeding 52 weeks with minimal professional support. SUBJECTS: A total of 58 obese, nondietetic subjects with hyperinsulinemia (13 males/45 females, mean age 50.2 y, mean body mass index (BMI) 34.0 kg/m2, mean fasting insulin 17.8 mU/l) participated in the study. MEASUREMENTS: : Body composition, blood pressure, blood lipids, fasting glucose, insulin, CRP and sICAM-1 were measured at baseline and at weeks 16 and 68. Urinary urea/creatinine ratio was measured at baseline, week 16 and at 3 monthly intervals thereafter. RESULTS: In total, 43 subjects completed the study with similar dropouts in each group (P=0.76). At week 68, there was net weight loss (SP -2.9+/-3.6%, HP -4.1+/-5.8%; P<0.44) due entirely to fat loss (P<0.001) with no diet effect [corrected]. Both diets significantly increased HDL cholesterol concentrations (P<0.001) and decreased fasting insulin, insulin resistance, sICAM-1 and CRP levels (P<0.05). Protein intake was significantly greater in HP during the initial 16 weeks (P<0.001), but decreased in HP and increased in SP during 52-week follow-up, with no difference between groups at week 68, indicating poor long-term dietary adherence behaviour to both dietary patterns. CONCLUSION: Without active ongoing dietary advice, adherence to dietary intervention is poor. Nonetheless, both dietary patterns achieved net weight loss and improvements in cardiovascular risk factors.

Adult↗
PubMed2004

Ghrelin and measures of satiety are altered in polycystic ovary syndrome but not differentially affected by diet composition.

Polycystic ovary syndrome (PCOS) is a common endocrine condition in women of reproductive age associated with obesity. It may involve dysregulation of ghrelin, a hormone implicated in appetite regulation. The effect of diet composition on ghrelin is unclear. Overweight women with and without PCOS were randomized to a high-protein (40% carbohydrate, 30% protein; 10 PCOS, six non-PCOS) or standard protein diet (55% carbohydrate, 15% protein; 10 PCOS, six non-PCOS) for 12 wk of energy restriction and 4 wk of weight maintenance. Diet composition had no effect on fasting or postprandial ghrelin or measures of satiety. Non-PCOS subjects had a 70% higher fasting baseline ghrelin (P = 0.011), greater increase in fasting ghrelin (57.5 vs. 34.0%, P = 0.033), and greater maximal decrease in postprandial ghrelin after weight loss (-144.1 +/- 58.4 vs. -28.9 +/- 14.2 pg/ml, P = 0.02) than subjects with PCOS. Subjects with PCOS were less satiated (P = 0.001) and more hungry (P = 0.007) after a test meal at wk 0 and 16 than subjects without PCOS. Appetite regulation, as measured by subjective short-term hunger and satiety and ghrelin homeostasis, may be impaired in PCOS.

Adult↗
PubMed2002

The low dose dexamethasone suppression test: effect of time of administration and dose.

The dexamethasone suppression test (DST) is used to determine the sensitivity of the hypothalamic-pituitary-adrenal axis (HPA-axis) to negative feedback. Dexamethasone is usually administered at 23:00 h or at midnight but this is often not convenient. The aim of this study was to determine whether the administration of dexamethasone at 21:00 h as compared to 23:00 h would alter the degree to which 08:00 h plasma cortisol was suppressed the following morning. Three healthy males (mean+/-SE: 32+/-7 yr) and 3 healthy females (mean+/-SE: 35+/-7 yr) took part in the study. Each subject was orally administered 1 of 3 doses of dexamethasone (0.25 mg, 0.5 mg, or 1.0 mg) on 3 separate occasions in random order at least a week apart. Each dose of dexamethasone was taken at either 21:00 h or 23:00 h so that each subject underwent 6 tests. The differences in cortisol suppression between times and doses of dexamethasone were assessed using Analysis of Variance. Plasma cortisol was suppressed less in response to 0.25 mg dexamethasone at both 21:00 h and 23:00 h as compared with doses of dexamethasone of 0.5 mg or 1.0 mg (p=0.004). Suppression of plasma cortisol in response to each dose of dexamethasone was similar regardless of the timing of dexamethasone administration (p=0.5). We conclude that in healthy subjects 0.25 mg dexamethasone suppresses plasma cortisol less than either 0.5 mg or 1.0 mg and that 0.5 mg dexamethasone suppresses plasma cortisol to a similar extent as 1.0 mg dexamethasone. Moreover, changing the administration time of dexamethasone from 23:00 h to 21:00 h does not effect the degree to which cortisol is suppressed in healthy subjects.

Adult↗
PubMed2002

Antropyloroduodenal, cholecystokinin and feeding responses to pulsatile and non-pulsatile intraduodenal lipid infusion.

The contribution of the pulsatile nature of gastric emptying to small intestinal feedback mechanisms modulating antropyloroduodenal motility and appetite is unknown. On separate days, eight healthy male volunteers (18-34 years) received randomized, single-blind, intraduodenal (ID) infusions of 10% Intralipid (2 kcal min(-1)), either continuously [CID], or in a pulsatile manner [PID] (5 s on/15 s off) and 0.9% saline (control) administered continuously, each at a rate of 1.8 mL min(-1) for 3 h. During each infusion, subjective ratings of appetite were assessed and antropyloroduodenal pressures recorded with a 16-lumen manometric assembly incorporating a pyloric sleeve sensor. Plasma cholecystokinin was measured from blood collected at regular intervals throughout the infusion. At the end of each infusion the manometric assembly was removed, subjects were offered a buffet meal and the energy and macronutrient content of the meal was measured. Both ID lipid infusions stimulated isolated pyloric pressure waves (IPPWs) (P < 0.001) and basal pyloric pressure (P < 0.01) and suppressed antral (P < 0.05) and duodenal (P < 0.05) pressure waves when compared to controls; there was no difference in the effects of CID and PID lipid on antropyloroduodenal pressures. Infusions of lipid significantly increased plasma CCK concentrations (P < 0.05) compared with saline, but concentrations were not different between the two modes of lipid delivery (P > 0.05, CID vs. PID). Both intraduodenal lipid infusions decreased hunger (P < 0.05), increased fullness (P < 0.05) and reduced energy intake (P < 0.05) when compared with controls; again there was no difference between CID and PID lipid. We conclude that at the infusion rate of similar 2 kcal min(-1), the acute effects of intraduodenal lipid on antropyloroduodenal pressures, plasma CCK concentration and appetite are not modified by a pulsatile mode of lipid delivery into the duodenum.

Adolescent↗
PubMed2002

Defining 'relative' androgen deficiency in aging men: how should testosterone be measured and what are the relationships between androgen levels and physical, sexual and emotional health?

In men, bioavailable and free testosterone levels decline by about 1.0 and 1.2% per year, respectively, after the age of 40. The definition of clinically relevant androgen deficiency in the aging male remains uncertain. Clinical features common to both aging and androgen deficiency include decreased muscle mass and strength, and increased fatigue, increased fat mass, loss of libido, erectile dysfunction, impaired cognitive function and depression. It is, however, difficult to separate the effect on plasma testosterone of concomitant disease, compared with the effects of a decrease in testosterone levels alone. Testosterone supplementation has been shown to be effective in improving many of the clinical features of androgen deficiency in the older male, and is safe, at least in the short term. The maximum benefit occurs in those men with the lowest testosterone levels.

Adipose Tissue↗
PubMed2001

Bone densitometry in clinical practice: longitudinal measurements at three sites in postmenopausal women on five treatments.

We report sequential changes in bone mineral density (BMD) at the forearm, hip and spine in 340 consecutive postmenopausal women referred by 103 general practitioners and six specialists, and who were either untreated or being treated with calcium, estrogen, norethisterone or calcitriol for a median period of 25 months (range 11-52). The mean annual rate of change in BMD at the three sites was: 1.39% in 44 women on norethisterone; 0.94% in 107 women on estrogen (both p < 0.001); 0.24% (not significant) in 52 women on calcitriol; -0.53% in 92 women on calcium; and -1.06% in 45 women on no treatment (both p < 0.01). The mean annual rate of change at the three sites in the 295 treated women was 0.43%, which was significantly positive (p < 0.001) and was 1.49 percentage points more positive than in the untreated women (p < 0.001). The greatest mean difference between treated and untreated patients was seen at the forearm, where it was 2.16 percentage points (p < 0.001). This was significantly greater than the difference at the femoral neck (1.21 percentage points (p = 0.037)) and lumbar spine (1.10 percentage points (p = 0.044)). The data did not change significantly after correction for age, years since menopause or baseline BMD. Those who started the treatments at baseline gained bone faster than those who were continuing on existing therapies, but this difference was not significant at any site. In the hormone- and calcitriol-treated groups, there was no significant difference between those who had a calcium supplement and those who did not. We conclude that the effects of treatment on BMD in clinical practice are comparable to those predicted from clinical trials, that there are significant differences between the responses to treatment at different sites and that the forearm appears to be the most sensitive site, in this series at least.

Absorptiometry, Photon↗
PubMed2000

Peripheral administration of CRF and urocortin: effects on food intake and the HPA axis in the marsupial Sminthopsis crassicaudata.

The hypothalamic peptides corticotrophin releasing factor (CRF) and urocortin (UCN) decrease food intake and increase energy expenditure when administered either centrally or peripherally to rodents. The effects of CRF and UCN on food intake in other mammals (for example marsupials), however, are not known. Peripherally administered CRF induced cortisol release in the marsupial Sminthopsis crassicaudata via the CRF1 receptor, and central CRF administration potently decreased food intake, as in rodents. When peripherally administered, both CRF and UCN decreased food intake in S. crassicaudata, but UCN was considerably more potent ( approximately 50 fold) in this regard. The anorectic effects of CRF and UCN were not blocked by the CRF1 receptor antagonist antalarmin, suggesting that the peripheral effects of CRF and UCN on food intake are mediated primarily by the CRF2 receptor.

Adrenal Glands↗
PubMed2000

Cloning of leptin cDNA and assignment to the long arm of chromosome 5 in the marsupial Sminthopsis crassicaudata.

We have isolated and sequenced full-length cDNA clones for leptin in the dasyurid marsupial Sminthopsis crassicaudata (fat-tailed dunnart). Southern and in situ hybridisation data indicated a single leptin gene in the S. crassicauda- ta genome, localised to arbitrary chromosome bands 5q24--> q31 on the long arm of chromosome 5, the short-arm terminus of which bears the only nucleolar organising region. The nucleotide sequence of the cDNAs revealed that the primary translation product of S. crassicaudata leptin is composed of 167 amino acid residues, with a potential signal peptide of 21 residues. The mature protein of 146 amino acids is 82% similar to both the mouse and human proteins and is predicted to have a molecular weight of 16.26 kDa. Northern blot analysis revealed that the corresponding mRNA is approximately 3.9 kb in size and is expressed only in white adipose tissue of this marsupial species. Evolutionary analyses indicate that S. crassicaudata leptin cDNA has evolved at a significantly faster rate than cDNAs from eutherian mammals.

Amino Acid Sequence↗
PubMed1999

Effect of dietary macronutrients on food intake, body weight, and tail width in the marsupial S. crassicaudata.

The role of dietary fat, as opposed to total energy intake, in the etiology of obesity is controversial. The aim of this study was to determine the effect of macronutrient content, specifically changes in dietary fat on body weight, fat stores, and food intake in S. crassicaudata, a marsupial that stores about 25% of total body fat in its tail. Female animals were divided into three groups (n = 7-9) matched for food intake per gram of body weight. Each group of animals was fed, ad lib an isocaloric diet (1.01 kcal/g), which contained either 10, 20, or 40% of calories from fat. Body weight, food intake, and tail width (an index of body fat stores) were measured daily. Over 21 days, cumulative energy intake was less (p = 0.026) in the 40% fat group compared to the 10% fat group. Despite the differences in food intake, body weight in each group remained stable throughout the study, so that at day 21 there were no differences in the body weights between the three groups. In contrast, tail width increased in the animals who received the 40% fat diet compared to either the 10% (p = 0.016) or 20% (p = 0.001) fat intake groups, whereas there was no significant change in tail width in either of these two groups. These observations indicate that macronutrient composition has a role, independent of total calories in the regulation of food intake and body fat stores, specifically that dietary fat promotes adiposity, independent of total caloric intake.

Animals↗
PubMed1999

Evidence that nitric oxide stimulates feeding in the marsupial Sminthopsis crassicaudata.

Nitric oxide (NO) synthase inhibitors reduce food intake in rodents and chickens, suggesting that NO may stimulate feeding. We used two competitive, non-selective inhibitors of NO synthase (NOS), (NG-monomethyl-L-arginine ester [L-NMMA] and NG-nitro-L-arginine methyl ester [L-NAME]), to evaluate the role of NO mechanisms in the control of food intake in a marsupial model previously used in studies of appetite regulation. Adult male Sminthopsis crassicaudata (n = 11-16, 15 +/- 0.3 g, mean +/- S.E.M.) received L-NMMA (50, 100, 200 and 1000 mg/kg), L-NAME (50, 100 and 200 mg/kg), L-arginine (L-arg) the precursor of NO (1000 and 2000 mg/kg), L-NAME (200 mg/kg) in combination with L-arg (2000 mg/kg), or saline (0.9%). All drugs were administered intraperitoneally after 24 h of food deprivation, after which food was immediately made available ad libitum. Food intake was measured 0, 0.5, 1, 2, 4 and 24 h after treatments. In addition, we studied the effect of acute L-NAME administration on hypothalamic, cortical, hepatic and cardiac NOS activity by quantifying citrulline production. L-NMMA (1000 mg/kg) and L-NAME (100 and 200 mg/kg) suppressed food intake by 25%, 21%, and 30%, respectively, over 24 h after treatments (P < 0.05). L-arg (1000 and 2000 mg/kg) by itself had no significant effect on food intake when compared with saline (P > 0.05). When administered in combination with L-NAME (200 mg/kg), L-arg (2000 mg/kg) reversed L-NAME induced suppression of appetite (P> 0.05). Furthermore, L-NAME (200 mg/kg) significantly decreased hypothalamic (P < 0.01), cortical (P < 0.01) and hepatic (P < 0.03) NOS activity. L-NAME had no effect on cardiac NOS activity (P> 0.05). These data show that peripheral administration of L-NAME has a significant central effect, particularly in brain areas involved in appetite regulation, and suggest in marsupials, as in other mammals and birds, that NO plays a role in the regulation of food intake.

Animals↗
PubMed1999

Effects of small-intestinal fat and carbohydrate infusions on appetite and food intake in obese and nonobese men.

To determine whether the satiating effects of nutrients in the small intestine are lower in obese than in nonobese people, 9 healthy, obese men [age: 18-33 y; body mass index (BMI; in kg/m2) 30.4-40.8] and 11 healthy, nonobese men (age: 18-33 y; BMI: 19.1-26.4) received an intraduodenal infusion of saline (control), lipid ( 11.97 kJ/min, or 2.86 kcal/min), or glucose (11.97 kJ/min) for 120 min on separate days. Fullness, hunger, and nausea were assessed by visual analogue scales. After the infusions, a meal was offered and food intake was quantified. There was no difference in appetite ratings between the obese and nonobese subjects during the infusions, in the amount or macronutrient composition of food eaten after the infusions, or in the time taken to eat the meals. Both the lipid and glucose infusions were associated with greater fullness than the control infusion. The energy content of the food eaten was less after the lipid infusion than after either the control or glucose infusion (P < 0.01): lipid infusion suppressed energy intake by 22% compared with the control infusion and by 15% compared with the glucose infusion. Suppression of energy intake after intraduodenal nutrient infusions was due to slower eating (P < 0.01). Intraduodenal infusions of fat suppressed appetite and food intake more than did equienergetic infusions of carbohydrate in both obese and nonobese young men, and the responses to intraduodenal fat and glucose were not affected by obesity. The latter observation suggests that established obesity is not associated with reduced small-intestinal responses to dietary fat or carbohydrate.

Adolescent↗
PubMed1999

Effect of diet on the response to leptin in the marsupial Sminthopsis crassicaudata.

The aim of this study was to determine in the marsupial Sminthopsis crassicaudata 1) the effect of leptin on food intake, body fat stores, and metabolism and 2) whether leptin can prevent a diet-induced increase in adiposity. In response to 21 days of feeding with mealworms (2.99 kcal/g, 30% fat), body weight (P < 0. 0001) and tail width (P < 0.0001) increased, compared with control animals fed with laboratory diet (1.01 kcal/g, 20% fat). Subsequently, S. crassicaudata were randomly allocated to receive either laboratory diet or a choice between laboratory diet and mealworms. For 13 days, one-half of the animals in each dietary group received intraperitoneal human leptin (2.5 mg/kg twice daily), while the other one-half received phosphate-buffered saline. In animals receiving laboratory diet alone, leptin induced a decrease in body weight (P < 0.0001), tail width (P < 0.0001), and energy intake (P < 0.01). In animals receiving both laboratory diet and mealworms, leptin had no effect on body weight or tail width, although the proportion of laboratory diet eaten was reduced (P = 0. 0001), and there was a nonsignificant fall in overall energy intake (P = 0.07). We conclude that in S. crassicaudata, 1) a high-calorie, higher-fat diet induces an increase in adiposity and 2) leptin induces weight loss, but 3) an increase in dietary calories and fat content is associated with resistance to the actions of leptin.

Animals↗
PubMed1999

Effect of nitric oxide synthase inhibitors on short-term appetite and food intake in humans.

Animal studies suggest that nitric oxide (NO) may be a physiological regulator of appetite; NO synthase (NOS) inhibition suppresses food intake in rats, mice, and chickens. It is not known whether NO has any effect on appetite in humans. We have used NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine methyl ester (L-NAME), both competitive, nonselective inhibitors of NOS, in two separate studies to evaluate the role of NO in the short-term regulation of appetite in humans. In study I, 13 men (18-25 yr) underwent paired studies, in randomized, double-blind fashion, after an overnight fast. L-NMMA (4 mg. kg-1. h-1) or saline (0.9%) was infused intravenously at a rate of 40 ml/h for 1.5 h. In study II, eight men (18-26 yr) underwent three randomized, double-blind studies after an overnight fast. L-NAME (75 or 180 micrograms . kg-1. h-1) or saline (0.9%) was infused intravenously at a rate of 20 ml/h for 120 min. Hunger and fullness were measured using visual analog scales; blood pressure and heart rate were monitored, and 30 min before the end of the infusion, subjects were offered a cold buffet meal. Total caloric intake and the macronutrient composition of the meal were determined. Both L-NMMA (P = 0.052) and L-NAME (P < 0.05; both doses) decreased heart rate, L-NMMA increased diastolic blood pressure (P < 0.01), and L-NAME increased systolic blood pressure (P = 0.052). Neither drug had any effect on caloric intake or sensations of hunger or fullness. Despite having significant effects on cardiovascular function in the doses used, neither L-NMMA nor L-NAME had any effect on feeding, suggesting that NO does not affect short-term appetite or food intake in humans.

Adolescent↗
PubMed1998

Interaction of insulin, glucagon-like peptide 1, gastric inhibitory polypeptide, and appetite in response to intraduodenal carbohydrate.

The relation between gastrointestinal incretin hormones in the control of insulin release and short-term satiety by intestinal carbohydrate was investigated in 8 fasted, healthy male volunteers. Insulin, gastric inhibitory polypeptide (GIP), glucagon-like peptide 1 (GLP-1), and appetite ratings were measured during, and food intake was measured after, intraduodenal infusions of glucose or saline. Studies were conducted under hyperinsulinemic and euglycemic conditions. Raising plasma insulin with intravenous insulin infusion to concentrations slightly above usual postprandial concentrations (356.4 +/- 4.8 pmol/L) had no effect on GIP, GLP-1, or appetite ratings before the intraduodenal infusions began. Intraduodenal glucose infusion resulted in a further increase in plasma insulin to a peak of 779.4 +/- 114.0 pmol/L, caused an early increase in plasma GIP and a later increase in GLP-1 concentrations (P < 0.01), suppressed appetite (P < 0.05), and reduced energy intake (P < 0.01) compared with intraduodenal infusion of saline. There was a close association between the increase in GLP-1 and decrease in appetite. Infusion of octreotide to suppress the release of gastrointestinal hormones prevented the rise in insulin, GIP, and GLP-1 induced by intraduodenal glucose infusion and reversed the suppression of appetite and reduction in energy intake. These results suggest that 1) when infused to result in plasma concentrations slightly above usual postprandial concentrations, insulin does not inhibit its own release and 2) the effects of intraduodenal glucose on appetite may be mediated through the release of GLP-1 and not insulin.

Adult↗
PubMed1998

Effect of intravenous glucose and euglycemic insulin infusions on short-term appetite and food intake.

To investigate the short-term effects of insulin on feeding, 14 fasting, young adults received 150-min euglycemic intravenous infusions of control (C), low-dose (LD, 0.8 mU.kg-1.min-1), and high-dose (HD, 1.6 mU.kg-1.min-1) insulin and ate freely from a buffet meal during the last 30 min. Steady-state preprandial plasma insulin concentrations were 5.9 +/- 0.7 (C), 47 +/- 2 (LD), and 95 +/- 6 (HD) microU/ml and increased 56-59 microU/ml during the meal. No effect of treatment type of hunger or fullness ratings, duration of eating, or the weight, energy content (1,053 +/- 95 kcal, C; 1,045 +/- 101 kcal, LD; 1,066 +/- 107 kcal, HD; P = 0.9), and composition of food eaten was observed. On a fourth study day, 12 of the subjects received an intravenous infusion of glucose only (Glc) that was identical to the glucose infusion on their HD insulin day. Mean venous glucose concentration was 9.3 +/- 0.5 mmol [P < 0.001 vs. C (5.3 +/- 0.1), LD (5.2 +/- 0.2), and HD (5.2 +/- 0.2)], and plasma insulin increased to 45 +/- 2.3 microU/ml at the start and 242 +/- 36 microU/ml at the end of the meal. Energy intake during the meal was (approximately 15%) reduced (1,072 +/- 97 kcal, C; 1,086 +/- 102 kcal, LD; 1,088 +/- 105 kcal, HD; 919 +/- 115 kcal, Glc; P < 0.05 Glc vs. C, LD, and HD). Plasma insulin normally increases to approximately 100 microU/ml after a mixed meal in lean subjects. Therefore, in the absence of altered blood glucose concentrations, physiological concentrations of insulin are unlikely to play a role in meal termination and the short-term control of appetite.

Adult↗