Ian Chapman

Relation between food intake and visual analogue scale ratings of appetite and other sensations in healthy older and young subjects

Objective: Visual analogue scales are widely used in appetite research, yet the validity of these scales to evaluate appetite and mood has not been assessed in older subjects. The aim of this study was to determine the relations between food intake and visual analogue scale (VAS) ratings of appetite and nonappetite sensations in healthy older and young subjects.Design: Retrospective combined analysis of four single-blind, randomised, controlled appetite studies.Setting: All studies were conducted in the University of Adelaide, Department of Medicine, Adelaide, Australia.Subjects: A total of 45 healthy young men (n=24) and women (n=21) aged 18–35 y and 45 healthy older men (n=24) and women (n=21) aged 65–85 y were recruited by advertisement.Interventions: Oral, intraduodenal or intravenous administration of treatments which suppressed food intake were compared to control. Up to 90 min after treatment, a test meal was offered and subjects ate freely for between 30 and 60 min. Perceptions were assessed by 100-mm visual analogue scales administered at regular intervals.Results: Food intake at the test meal was positively related to perceptions of hunger, drowsiness, and calmness at both baseline and premeal (r>0.16, P<0.05), and inversely related to premeal ratings of fullness (r> 0.2, P<0.05) in both older and young subjects. Food intake was related to VAS ratings at least as strongly, if not more so, in older as in young subjects.Conclusions: These observations (i) confirm that food intake is related to perceptions of hunger and fullness as assessed by VAS in healthy older and young subjects, and (ii) suggest that sensations, not obviously associated with appetite, including ‘drowsiness’ and ‘calmness’, are also associated with food intake.

The nutritional status of 250 older Australian recipients of domiciliary care services and its association with outcomes at 12 months.

OBJECTIVES: To identify predictors and consequences of nutritional risk, as determined by the Mini Nutritional Assessment (MNA), in older recipients of domiciliary care services living at home.

Vitamin D, glucose, insulin, and insulin sensitivity

This review examines available evidence of links between abnormalities of glucose and insulin metabolism and vitamin D deficiency. Possible mechanisms of action of vitamin D include stimulation of insulin secretion and effects on insulin sensitivity. Sun exposure usually implies greater outdoor physical activity, which in itself may have beneficial effects on insulin sensitivity, unrelated to serum 25-hydroxyvitamin D concentrations. The observed associations in humans among vitamin D, insulin, and glucose metabolism have not yet been confirmed by intervention studies and, hence, a causal association has not been established. Clinical trials are needed to determine whether vitamin D treatment of vitamin D-deficient individuals is able to prevent or treat diabetes mellitus.

Circulating leptin concentrations in polycystic ovary syndrome : relation to anthropometric and metabolic parameters

OBJECTIVE To determine the relation between metabolic and anthropometric parameters and circulating leptin concentrations in women with polycystic ovary syndrome (PCOS).

Glucose tolerance and vitamin D: Effects of treating vitamin D deficiency

OBJECTIVE We investigated the effects of vitamin D treatment on plasma glucose, serum insulin, and insulin sensitivity in vitamin D-deficient individuals without diabetes mellitus. METHODS Thirty-three adults with vitamin D insufficiency (serum 25-hydroxyvitamin D concentration < or = 50 nmol/L) and without diabetes (12 with impaired glucose tolerance) were given two oral doses of 100 000 IU of cholecalciferol, 2 wk apart. Before the first dose and 2 wk after the second dose, a 75-g oral glucose tolerance test was performed. Plasma glucose, serum insulin, 25-hydroxyvitamin D, and parathyroid hormone concentrations were measured and insulin sensitivity was calculated from the oral glucose tolerance test. RESULTS Mean serum 25-hydroxyvitamin D increased from 39.9 +/- 1.5 (SEM) to 90.3 +/- 4.3 nmol/L (P < 0.0001) and mean serum parathyroid hormone decreased from 6.7 +/- 1.2 to 4.5 +/- 0.6 pmol/L (P = 0.055). There was no change in blood glucose mean of 0-120 min (6.1 +/- 0.3 before versus 6.2 +/- 0.3 mmol/L, P = 0.63) or insulin mean of 0-120 min (47.8 +/- 5.35 versus 48.9 +/- 5.22 mU/L, P = 0.67) concentrations, and no change in insulin sensitivity (Avignons insulin sensitivity index [SiM], P = 0.97; insulin sensitivity index at 0 and 120 min [ISI(0,120)], P = 0.74; Quantitative Insulin Sensitivity Check Index [QUICKI], P = 0.88; homeostasis model assessment [HOMA], P = 0.99) after vitamin D treatment. Results did not differ between subjects, with and without, impaired glucose tolerance. CONCLUSION In adults without diabetes, correction of vitamin D deficiency is not associated with any effect on blood glucose or insulin concentrations or insulin sensitivity as assessed during an oral glucose tolerance test. These observations do not support an association between glucose/insulin homeostasis and vitamin D, at least in the short term.

Body weight, anorexia, and undernutrition in older people.

Ideal body weight for maximum life expectancy increases with advancing age. Older people, however, tend to weigh less than younger adults, and old age is also associated with a tendency to lose weight. Weight loss in older people is associated with adverse outcomes, particularly if unintentional, and initial body weight is low. When older people lose weight, more of the tissue lost is lean tissue (mainly skeletal muscle) than in younger people. When excessive, the loss of lean muscle tissue results in sarcopenia, which is associated with poor health outcomes. Unintentional weight loss in older people may be a result of protein-energy malnutrition, cachexia, the physiological anorexia of aging, or a combination of these. The physiological anorexia of aging is a decrease in appetite and energy intake that occurs even in healthy people and is possibly caused by changes in the digestive tract, gastrointestinal hormone concentrations and activity, neurotransmitters, and cytokines. A greater understanding of this decrease in appetite and energy intake during aging, and the responsible mechanisms, may aid the search for ways to treat undernutrition and weight loss in older people.

Effect of small intestinal nutrient infusion on appetite, gastrointestinal hormone release, and gastric myoelectrical activity in young and older men

OBJECTIVE:The mechanisms responsible for the reduction in appetite and slowing of gastric emptying in older persons are poorly understood. The aim of this study was to evaluate the effects of aging on small intestinal regulation of appetite, GI hormone release, and gastric myoelectrical activity.METHODS:Thirteen older (65–84 yr) and 13 young (18–32 yr) healthy men received isovolumetric, intraduodenal (ID) infusions of saline (control), lipid, and glucose for 120 min, on separate days. The energy content of the lipid and glucose infusions was identical at 2.86 kcal/min. Immediately after the ID infusions, each subject was offered a buffet meal, and ad libitum food intake was quantified. Blood glucose and plasma insulin, glucagon-like peptide 1, and glucose-dependent insulinotropic peptide were measured. Gastric myoelectrical activity was measured by surface electrogastrography (EGG).RESULTS:ID lipid suppressed food intake in both the young and older men (p < 0.05), whereas ID glucose suppressed food intake only in the older men (p < 0.05). The blood glucose (p < 0.01) and insulin (p < 0.05) responses to ID glucose were greater in older than young men. However, there were no differences in glucagon-like peptide 1 or glucose-dependent insulinotropic peptide responses to any of the infusions. There was a greater increase in the EGG power ratio both during and after ID glucose infusion in the young (p < 0.05) than the older men, and an attenuation of EGG frequency by nutrient infusions in older, but not young, men.CONCLUSIONS:Our findings indicate that aging is associated with nutrient-specific changes in appetite, hormonal, and gastric myoelectrical (EGG) responses to ID nutrients. An enhanced satiating effect of small intestinal carbohydrates may potentially contribute to the anorexia of aging.

Effect of the once-daily human GLP-1 analogue liraglutide on appetite, energy intake, energy expenditure and gastric emptying in type 2 diabetes

AIMS Liraglutide reduces bodyweight in patients with type 2 diabetes mellitus (T2DM). This study aimed to investigate the mechanisms underlying this effect. METHODS The comparative effects of liraglutide, glimepiride and placebo on energy intake, appetite, nausea, gastric emptying, antral distension, bodyweight, gastrointestinal hormones, fasting plasma glucose and resting energy expenditure (REE), were assessed in subjects with T2DM randomised to treatment A (liraglutide-placebo), B (placebo-glimepiride) or C (glimepiride-liraglutide). Assessments were performed at the end of each 4-week treatment period. RESULTS Energy intake was less (NS) with liraglutide vs placebo and glimepiride, and 24-h REE was higher (NS) with liraglutide vs placebo and glimepiride. Fasting hunger was less (p=0.01) with liraglutide vs placebo and glimepiride, and meal duration was shorter with liraglutide (p=0.002) vs placebo. Paracetamol AUC(0-60 min) and C(max) were less (p<0.01) and fasting peptide YY was lower (p ≤ 0.001) after liraglutide vs placebo and glimepiride. Bodyweight reductions of 1.3 and 2.0 kg were observed with liraglutide vs placebo and glimepiride (p<0.001). There were no differences on antral distension, nausea, or other gastro-intestinal hormones. CONCLUSION Liraglutide caused decreased gastric emptying and increased reduction in bodyweight. The mechanisms of the liraglutide-induced weight-loss may involve a combined effect on energy intake and energy expenditure.

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) μU/ml and increased 56-59 μU/ml during the meal. No effect of treatment type on 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 μU/ml at the start and 242 ± 36 μU/ml at the end of the meal. Energy intake during the meal was (∼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 ∼100 μU/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.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.

Effects of oral fructose and glucose on plasma GLP-1 and appetite in normal subjects.

Oral glucose is a potent stimulant of glucagon-like peptide-1 (GLP-1) secretion. The effect of oral fructose on GLP-1 secretion in humans is unknown. The aims of this study were to determine (i) whether oral fructose stimulates GLP-1 secretion and (ii) the comparative effects of oral glucose and fructose on appetite. On 3 separate days, 8 fasting healthy males received, in single-blind randomized order (i) 75 g glucose, (ii) 75 fructose, or (iii) 75 g glucose followed by 75 g fructose I h later. Venous glucose, insulin and GLP-1 were measured. Appetite was assessed by visual analog questionnaires and intake of a buffet meal. Whereas glucose and fructose both increased plasma glucose, insulin and GLP-1 (P < 0.000)] for all), the response to glucose was much greater (P < 0.005 for all). There was no increase in plasma GLP-1 when fructose was given after glucose. There was no difference in food intake after oral glucose or fructose. We conclude that oral fructose (75 g) stimulates GLP-1 (and insulin) secretion, but the response is less than that to 75 g glucose. These observations suggest that neither GLP-1 nor insulin play a major role in the regulation of satiation.