Galactose and its metabolites, primarily derived from lactose, may have toxic effects on the ovary. We aimed to prospectively examine the associations of galactose and lactose intakes with the onset of natural menopause. The data of a population-based cohort study in a Japanese community (the Takayama study) initiated in 1992 were analysed, with follow-up data collected in 2002. Among the participants of the Takayama study, premenopausal women (n 3115) aged 35–56 years at baseline were included in this study. Dietary intake, including lactose and galactose was assessed only at baseline using a FFQ. The menopausal status and age at menopause were determined based on the participants’ self-reports, and natural menopause was defined as the absence of menstruation for 12 months or more. Cox proportional hazards models were used to estimate the hazard ratios (HR) and 95 % CI. A total of 1790 women experienced natural menopause within the 10-year follow-up. Lactose and galactose intakes were associated with a later onset of natural menopause after adjusting for potential confounding factors and the HR (95 % CI) for the highest v. lowest quartile were 0·80 (0·69, 0·92) (P-trend = 0·001) in lactose and 0·86 (0·74, 1·00) in galactose (P-trend = 0·036), respectively. High intakes of lactose and galactose were associated with a later onset of natural menopause. Despite the presumed ovotoxicity effects, lactose and galactose intakes at usual levels may not be deleterious to the ovarian aging process among Japanese community-dwelling women.

The present paper reviews the physiological responses of human liver carbohydrate metabolism to physical activity and ingestion of dietary sugars. The liver represents a central link in human carbohydrate metabolism and a mechanistic crux point for the effects of dietary sugars on athletic performance and metabolic health. As a corollary, knowledge regarding physiological responses to sugar ingestion has potential application to either improve endurance performance in athletes, or target metabolic diseases in people who are overweight, obese and/or sedentary. For example, exercise increases whole-body glycogen utilisation, and the breakdown of liver glycogen to maintain blood glucose concentrations becomes increasingly important as exercise intensity increases. Accordingly, prolonged exercise at moderate-to-high exercise intensity results in depletion of liver glycogen stores unless carbohydrate is ingested during exercise. The exercise-induced glycogen deficit can increase insulin sensitivity and blood glucose control, and may result in less hepatic lipid synthesis. Therefore, the induction and maintenance of a glycogen deficit with exercise could be a specific target to improve metabolic health and could be achieved by carbohydrate (sugar) restriction before, during and/or after exercise. Conversely, for athletes, maintaining and restoring these glycogen stores is a priority when competing in events requiring repeated exertion with limited recovery. With this in mind, evidence consistently demonstrates that fructose-containing sugars accelerate post-exercise liver glycogen repletion and could reduce recovery time by as much as half that seen with ingestion of glucose (polymers)-only. Therefore, athletes aiming for rapid recovery in multi-stage events should consider ingesting fructose-containing sugars to accelerate recovery.

Circumstantial evidence suggests that substitution of glucose or sucrose by the low-glycaemic index sugar galactose in the diet may lead to greater thermogenesis and/or fat oxidation. Using ventilated hood indirect calorimetry, we investigated, in twelve overnight-fasted adults, the resting energy expenditure (REE) and respiratory quotient (RQ) for 30 min before and 150 min after ingestion of 500 ml of water containing 60 g of glucose, fructose or galactose in a randomised cross-over design. REE increased similarly with all three sugars, reaching peak values after 50–60 min, but its subsequent fall towards baseline values was faster with galactose and glucose than with fructose (P < 0·001). RQ increased with all three sugars, but to a much greater extent with galactose and fructose than with glucose, particularly after 1 h post-ingestion. When ingested as a sugary drink, postprandial thermogenesis and utilisation of fat after galactose are not higher than after glucose or fructose.

The present study was conducted to assess whether glucagon-like peptide-1 (GLP-1) release and appetite after a breakfast with or without an additional galactose/guar gum stimulation is different in normal-weight compared with overweight/obese subjects. Twenty-eight overweight/obese (BMI 30·3 (sd 2·7) kg/m2; age 44·3 (sd 9·7) years) and thirty normal-weight subjects (BMI 22·8 (sd 1·4), age 31·5 (sd12·8) years) participated in a crossover study. Fasting and postprandial plasma GLP-1, insulin, glucose and free fatty acid concentrations were measured in response to either a galactose (50 g)/guar gum (2·5 g) load (836 kJ) and a standard breakfast (1·9 MJ; GG), or water (250 ml) and the standard breakfast (W) every 30 min relative to the ingestion for 120 min. Appetite was assessed using 100 mm visual analogue scales. GLP-1 concentrations were significantly increased after GG at 30 and 60 min compared with W in both groups. Plasma GLP-1 concentrations in the W condition were higher in normal-weight than overweight/obese subjects (P=0·03). No difference was observed in the GG condition between groups. Satiety was increased in normal-weight compared with overweight/obese subjects in the GG condition at 30 (P=0·02) and 60 (P=0·04) min. We conclude that after a standard breakfast with water, GLP-1 release was lower in the overweight/obese than the normal-weight subjects. However, postprandial GLP-1 release in overweight/obese subjects was no different from that of normal-weight subjects when galactose/guar gum was added to the breakfast. The latter was not mirrored by subjective feelings of satiety. Disturbed perception of the physiological feedback of a satiety hormone rather than disturbed feedback itself might contribute to obesity.

During a routine inspection of Cheddar cheese manufactured at a commercial factory in New Zealand, some lots of 6-month-old cheese were found to have developed a pinkish colouration on the surface of the 20 kg blocks of cheese. Colouration did not always occur uniformly on all six faces of the rectangular cheese block, or even on a single face of the block. Furthermore, not all blocks from within the same day's manufacture were equally affected. When an affected block was removed from its bag and cut across, colouration was sometimes found to penetrate approximately 1–2 cm down into the cheese. In those blocks where a plug of cheese had been removed previously, a pinkish zone surrounded the plug-hole cavity.

The pinkish colouration was observed to fade slowly (over about 12–24 h) when the cheese surface was exposed to air.

Annatto, known to cause pink discolouration in “coloured” Cheddar cheese (Govindarajan & Morris, 1973) and in processed cheese made using coloured Cheddar, was not used in the manufacture of the present cheeses and could therefore be excluded as a cause of the colouration.

The flavour profiles of all affected cheeses were considered by experienced industry cheese graders to be easily within the normal range of flavour profile expected for a cheese of this type i.e. there was no evidence of any off-flavour development.

The present short communication describes the microbiological and chemical investigations carried out to determine the origin and nature of the pinkish colouration in Cheddar cheese.

The behaviour of Streptococcus thermophilus in combination with Lactococcus lactis subsp. cremoris or subsp. lactis mesophilic starters in experimental Cheddar cheese is reported. In a standard manufacturing procedure employing a 38 °C cook temperature, even very low levels (0·007%) of Str. thermophilus combined with normal levels of the mesophilic starter (1·7%) resulted in increased rates of acid production, the formation of significant amounts of galactose (∼ 13 mmol/kg cheese), and populations nearly equivalent to those of the mesophilic lactic starter in the curd before salting. At a 41 °C cook temperature, the Str. thermophilus attained a higher maximum population (∼ log 8·2 colony forming units (cfu)/g) than the Lc. lactis subsp. cremoris (∼ log 6·8 cfu/g) and formed more galactose (∼ 28 mmol/kg). Lactobacillus rhamnosus, deliberately added to a cheese made using Str. thermophilus starter and which contained 24 mmol galactose/kg at day one, utilized all the galactose during the first 3 months of cheese ripening. Adventitious non-starter lactic acid bacteria had the potential to utilize this substrate too, and a close relationship was demonstrated between the increase in this flora and the disappearance of the galactose. Some possible consequences for cheese quality of using Str. thermophilus as a starter component are discussed.

The capacity of intestinal lactase (EC 3.2.1.23) of piglets to hydrolyse lactose in vivo was investigated by measuring the response of blood galactose to doses of lactose, galactose plus glucose and both whole and skimmed milk. Following the administration of oral doses of lactose dissolved in water to piglets from 2 to 18 d of age the adjusted galactose area under the curve (AUC) was between 1·12 and 1·36 arbitrary units, while following a dose of galactose plus glucose dissolved in water it was between 1·56 and 1·98 arbitrary units. Whereas these results suggest that the rate of digestion of lactose appeared to limit the amount of galactose reaching the peripheral blood after a dose of lactose dissolved in water, there was no significant correlation between the capacity of piglets to hydrolyse physiological amounts of lactose and the age of the piglets (2- to 18-d-old piglets; r 0·11). Following oral doses of sow's milk containing either lactose, or galactose plus glucose, the adjusted galactose AUC values were 0·94 and 1·00 arbitrary units respectively, in 10-d-old piglets. Thus, the limitation to the digestion of lactose observed when it was present in water was not evident for lactose in sow's milk. Since there was no significant difference between the adjusted galactose AUC following a dose of whole milk (0·95 arbitrary units) and that following a dose of skimmed milk (1·03 arbitrary units), the presence of fat in sow's milk did not appear to affect the utilization of lactose by the sucking piglets.

The kinetics of the response in the blond of piglets to physiological oral intakes of galactose and glucose, and intravenous administration of galactose are described. Following the intravenous administration of galactose to 2- and 10-d-old piglets (n 7), the half-life was 7.98 (SD 0.75) and 7.99 (SD 1.89) min respectively, and efficient elimination rate was 9.09 (SD 2.15) and 8.75 (SD 0.79) % per min respectively. The turnover of galactose in the piglets was 100-3 μg/min per kg body weight. These observations demonstrate that galactose was rapidly removed from the blood of the piglets. While the dosing and sampling procedures stimulated hyperglycaemia, they had no effect on the concentration of galactose in the peripheral plasma. The galactose area under the curve (adjusted to the plasma volume of the animal) following a dose of either galactose or galactose plus glucose was 1.75 (SD 0.15) and 1.95 (SD 0.14) arbitrary units respectively in 2-d-old piglets and 1.96 (SD 0.26) and 1.98 (SD 0.10) arbitrary units respectively in 10-d-old piglets. Since the presence of glucose did not lower the adjusted area under the curve for galactose in the peripheral blood, the effect of glucose on the metabolism of galactose in piglets was more like that reported for rats than that for man, guinea-pigs or mice. It is suggested that the galactose moiety of lactose may make an important contribution to the replenishment of liver glycogen in the neonatal piglet.