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Contribution of Plasma Galactose and Glucose to Milk Lactose Synthesis during Galactose Ingestion

Department of Pediatrics, Children’s Nutrition Research Center, U.S. Department of Agriculture/Agricultural Research Service, Baylor College of Medicine, Houston, Texas 77030

Address all correspondence and requests for reprints to: M. W. Haymond, M.D., Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030-2600. E-mail: mhaymond{at}bcm.tmc.edu.

	Abstract

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We have previously demonstrated that plasma glucose contributed 80% in the fed and 60% in the fasted state to lactose synthesis in humans, and de novo synthesis in the breast contributing to both the glucose and galactose moieties accounted for the remaining 20% and 40%, respectively, of lactose. The present study was conducted to determine, in lactating women, whether oral galactose is directly incorporated from plasma galactose into glucose and galactose in milk lactose or via conversion of galactose to glucose in the liver. Six healthy exclusively breast-feeding women (30 ± 2 yr) (mean ± SE) ingested galactose at 22 µmol·kg^-1·min^-1 for 9 h after an overnight fast during infusion of [6,6-²H₂]glucose and [1-¹³C]galactose. We observed that 69 ± 6% of glucose and 54 ± 4% of galactose in lactose were derived directly from plasma glucose, whereas 7 ± 2% and 12 ± 2% of glucose and galactose in lactose, respectively, were derived directly from plasma galactose. De novo synthesis of glucose and galactose via hexoneogenesis accounted for 25 ± 8% and 35 ± 6%, respectively. We conclude that during ingestion of galactose the contribution from plasma glucose to glucose and galactose in lactose was similar to that of a short-term fasting, but part of the de novo synthesis of glucose and galactose in the breast was replaced by direct uptake of galactose.

	Introduction

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WE HAVE RECENTLY DEMONSTRATED that plasma glucose contributed significantly but was not the exclusive substrate for milk lactose synthesis in humans (80% in the fed condition and 60% during short-term fasting) (1). In the course of these studies, we observed that the human mammary gland is capable of de novo synthesis of both the glucose and galactose moieties in lactose, a process we termed hexoneogenesis (1). In those studies, plasma glycerol contributed directly to the galactose moiety in lactose, but not the glucose moiety, formed by this process.

Recently, Obermeier et al. (2) and Kunz et al. (3), using [1-¹³C]galactose and nuclear magnetic resonance spectroscopy, reported that orally ingested ¹³C label was incorporated in milk, especially in lactose and neutral oligosaccharides. In some of the women, there was preferential labeling of the galactose, compared with glucose, immediately after galactose intake. However, the metabolic pathway(s) through which oral galactose contributes to milk lactose production remains unknown. The present studies were carried out to determine whether oral galactose is incorporated into glucose and galactose in milk lactose as a result of conversion of galactose to glucose in the liver and subsequent incorporation of this glucose into galactose and glucose in milk lactose as we have previously demonstrated (1) or as the result of the direct uptake of galactose into the breast and milk glucose and galactose.

	Materials and Methods

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Materials

Lactase (Aspergillus oryzae, 5500 ONPG, o-nitrophenyl ß-D-galactopyranoside, units per gram) was obtained from ICN Biochemicals, Inc. (Irvine, CA) and ß-galactosidase (Aspergillus oryzae, 9,600 U/g and Escherichia coli, grade VIII, 740,000 U/g) from Sigma-Aldrich (St. Louis, MO). BaOH, ZnSO₄, D-(+)glucose (dextrose, corn sugar), D-(+)galactose, and D-lactose (monohydrate) were purchased from Sigma-Aldrich. All organic solvents were HPLC grade. [1-¹³C]galactose and [6,6-²H₂]glucose were purchased from Cambridge Isotope Laboratory (Amherst, MA).

Glucose concentrations were determined using a biochemical analyzer model 2700 Select (Yellow Springs Instruments, Yellow Springs, OH). Galactose concentrations were determined using a glucose and L-lactate analyzer model 2300 Stat+, retrofitted to read galactose (Yellow Springs Instruments). BaOH solution (0.3N) and ZnSO₄ solution (0.3N) were purchased from Sigma-Aldrich.

Study design

Subjects. Six lactating women, between 24 and 35 yr of age (30 ± 2 yr), in good health, between 6 weeks and 3 months postpartum, took part in these studies. Their weight was 68 ± 3 kg, and body mass index was 24.7 ± 1.4 kg/m². The infants of these women were healthy and exclusively breast-fed at the time of the study. All of the volunteers underwent a general physical examination and had normal hemoglobin and screening studies for liver and renal function and a negative pregnancy test before they were accepted into the study.

Protocol design. Each woman and her infant were admitted to the Metabolic Research Unit (MRU) of the Children’s Nutrition Research Center or the General Clinical Research Center on the evening before the study. At 1800 h on the evening of admission, two iv catheters were introduced in the mother’s antecubital fossa or forearm vein under Emla (AstraZeneca Pharmaceuticals LP, Wayne, PA) cream analgesia, one for isotope infusion and the other for blood sampling. Subjects were fed a supper meal of 10 kcal/kg at 1800 h and were subsequently fasted, except for water overnight. At 0600 h, baseline breast milk and blood (5 ml) samples were obtained, and the subjects received primed constant infusions of [6,6-²H₂]glucose (20 µmol·kg^-1·min^-1, 0.33 µmol·kg^-1·min^-1) to measure glucose rates of appearance and the fraction of glucose and galactose in milk lactose derived from plasma glucose and [1-¹³C]galactose (20 µmol·kg^-1·min^-1 and 0.33 µmol·kg^-1·min^-1) to measure galactose rate of appearance and the fraction of galactose and glucose in lactose derived from plasma galactose. In addition, unlabeled oral galactose (22 µmol·kg^-1·min^-1) was administered every 15 min from 0600 h until completion of the study to increase the plasma galactose concentration; this was necessary to allow accurate measurement of galactose enrichments in plasma samples and clear separation of galactose from glucose during gas chromatography-mass spectrometry (GCMS) analysis. The total amount of galactose ingested over the 9-h study period would correspond to nine glasses of milk (240 ml each).

Blood samples (6–10 ml) were collected at 0600 h (just before start of the tracer infusions) and then at 0900, 1200, 1245, 1300, 1315, 1330, 1345, 1400, 1415, 1430, and 1500 h. The infants were breast-fed at approximately 3-h intervals (0600, 0900, 1200, and 1500 h). Maternal blood samples and milk samples were obtained immediately before each feeding. Indirect calorimetry was performed every 3 h. To determine the volume of milk consumed, the difference in weight of the infant (before and after feeding) was added to the volume of milk obtained for analyses (generally 5 cc each) (4).

Analyses

Plasma samples. Plasma glucose was measured using an enzyme-specific method (glucose analyzer, YSI, Inc.). Plasma insulin and C-peptide were measured using commercially available RIA kits (Linco Research, Inc., St. Charles, MO). Plasma free fatty acids and ß-hydroxybutyrate were determined by microfluorometric enzyme analyses as previously described using a Cobas Fara II analyzer (Roche Diagnostic Systems, Inc., Montclair, NY). The pentaacetate derivatives of glucose and galactose were prepared as described previously (5). The isotopic enrichments of [6,6-²H₂]glucose, [1-¹³C]galactose, and ¹³C-glucose, derived from [1-¹³C]galactose, were measured by GCMS using a quadrupole instrument (HP 6890/HP5973, Hewlett-Packard Co., Palo Alto, CA) and an SPB-17 column (30 m x 0.25 mm internal diameter, 0.25 µm phase thickness, Supelco, Inc., Bellefonte, PA). Positive chemical ionization (PCI) mode was used with methane as the reagent gas and selected ion monitoring of m/z 331–333 for both glucose and galactose. The conditions for the GCMS glucose and galactose analyses were: the temperature program used was an initial temperature, 70 C for 1 min, a temperature ramp at 30 C/min up to 280 C, followed by a 4-min hold. The ¹³C isotopic enrichments in breath CO₂ were measured by isotope ratio mass spectrometry (MS instrument, Tracermass Robeprep G, Europa Scientific, Crewe, UK). All measurements were made in the Stable Isotope Core Laboratory of the CNRC. To verify that the [1-¹³C]enrichment from galactose remained in position 1 when galactose was converted to glucose in the liver, GCMS was also employed in the electron impact mode monitoring the m/z 242–244 fragments, in which carbon 1 is cleaved off (6).

Milk samples. Milk samples were defatted, deproteinized, and hydrolyzed with lactase, using the method recently described (1). The hydrolyzed products were then derivatized (1) and analyzed by GCMS using a mass selective detector (GC model 6890 series, MS model 5973, Hewlett-Packard Co.) with an SPB-17 column (30 m x 0.25 mm internal diameter, 0.25 µm phase thickness, Supelco). The conditions for the gas chromatography were the same as for the analysis of the plasma samples. The PCI ions monitored were 331–333 for glucose and galactose.

Calculations

The rates of appearance (Ra) of glucose and galactose into the systemic circulation were calculated under near steady-state condition using standard equations:

where Ra is the rate of appearance, E_i and E_p are the enrichments of the isotope in the infusate and the plasma, respectively, and I is the rate of infusion of the isotope of interest.

Absolute splanchnic extraction of galactose was calculated by subtracting galactose Ra from ingested galactose, and the fractional splanchnic extraction was calculated by dividing absolute splanchnic extraction by ingested galactose.

The fraction of glucose Ra derived from galactose was calculated as E_{[¹³C]glucose}/E_{[¹³C]galactose}, where E_{[¹³C]glucose} is the plasma enrichment of ¹³C glucose derived from [1-¹³C]galactose, and E_{[¹³C]galactose} is the plasma enrichment of [1-¹³C]galactose. The flux of galactose converted to glucose was calculated as follows:

Potential sources for milk glucose and galactose in lactose are plasma glucose, plasma galactose, plasma glucose derived from the hepatic conversion of galactose to glucose, and finally the lactose could be produced within the breast, a process we have denoted hexoneogenesis (1). The M+2 glucose and M+2 galactose in lactose (derived from the [6,6-²H₂]glucose tracer) represent the direct contribution from plasma glucose. Thus, the proportion of glucose (M+2 Gluc_milk) and galactose (M+2 Gal_milk) in lactose derived from plasma glucose can be calculated using the following equation:

where M+2 Gluc_plasma is the M+2 in plasma glucose derived from [6,6-²H₂]glucose and M+2 Gluc_milk is the M+2 in glucose in lactose derived from [6,6-²H₂]glucose.

where M+2 Gal milk is the M+2 in galactose in lactose derived from [6,6-²H₂]glucose.

The M+1 of plasma glucose (M+1 Glu_plasma) and M+1 of glucose (M+1 Glu_milk) and M+1 of galactose in lactose (M+1 Gal_milk) are derived from the [1-¹³C]galactose tracer. Thus, the M+1 of plasma glucose represents glucose derived from galactose, i.e. galactose converted to glucose in the liver. The M+1 of glucose and galactose in lactose could be derived directly from plasma galactose or plasma glucose generated by hepatic conversion of galactose to glucose. The proportion of the glucose and galactose in lactose derived from plasma glucose should be equal whether calculated from the [6,6-²H₂]glucose or the [¹³C]glucose data, i.e.

Galmilkplasma M+1 glucose=(M+2 Galmilk/M+2 Glucplasma)*M+1 Glucplasma

Glucose and galactose in lactose derived directly from plasma galactose were calculated using the following equation:

where Gluc_{milkplasma galactose} is the glucose in lactose derived directly from plasma galactose.

where Gal_{milkplasma galactose} is the galactose in lactose derived directly from plasma galactose.

The fraction of glucose and galactose in lactose derived from the direct uptake of plasma galactose was then estimated on the basis of standard product/precursor relationship using the following equations:

where Gal_oxidation is the rate of galactose oxidation, ¹³CO₂ is the ¹³C enrichment inexpired CO₂, VCO₂ is the rate of CO₂ expired (µmol·kg^-1·min^-1), [1-¹³C]gal_plasma is the enrichment of [1-¹³C]galactose in the systemic circulation, and 0.8 corrects for recovery of labeled CO₂.

Statistical analysis

All data are expressed as mean ± SE. Substrate and hormone data from the overnight 12-h fast (baseline, 0600 h) were compared with the values measured from 1200 to 1500 h, i.e. after 6–9 h of ingesting galactose using paired t test. The glucose and galactose kinetic data (glucose and galactose Ra, fraction of glucose Ra derived from galactose, splanchnic extraction of dietary galactose, and oxidation rate of [1-¹³C]galactose) represent the average of the values measured between 1200 and 1500 h, i.e. after 6–9 h of galactose feeding. Isotope enrichments in milk glucose and galactose used for calculation of product-precursor relationships represent the mean of the values from the milk samples obtained at 6 and 9 h into the study.

	Results

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Plasma substrate and hormone concentrations

Following 6–9 h of continuous galactose ingestion, plasma galactose concentration increased from 0.07 ± 0.01 to 0.55 ± 0.15 mM, (P < 0.05). Plasma glucose concentrations did not change [5.74 ± 0.32 (baseline) vs. 5.96 ± 0.27 mM, P = NS]. Plasma lactate increased from 0.81 ± 0.12 (baseline) to 1.65 ± 0.15 mM, (P < 0.05). Plasma glucose, ß-hydroxybutyrate, free fatty acids, insulin, C-peptide, and glucagon remained unchanged throughout the study (Table 1).

The results on glucose and galactose kinetics are based on the data provided in Table 2 using the calculations described in Calculations. The concentration of plasma galactose was too low to assess accurately the plasma galactose enrichment in two subjects (low abundance). As a consequence, the analyses are based on an n = 6 for the maternal glucose kinetic data and an n = 4 for plasma galactose kinetics and the milk results. Plasma glucose and galactose Ra were 13.35 ± 1.05 (n = 6) and 9.15 ± 1.11 (n = 4) µmol·kg^-1·min^-1, respectively. The fraction of plasma glucose Ra derived from galactose was 41% ± 3%, and the rate of galactose converted to glucose was 5.51 ± 0.45 µmol·kg^-1·min^-1 (n = 6). The nongalactose-derived glucose production (i.e. after deducting the contribution of galactose to glucose Ra from the total glucose Ra) was 8.02 ± 1.28 µmol·kg^-1·min^-1. The rate of splanchnic extraction of galactose was 12.85 ± 1.11 µmol·kg^-1·min^-1, and the fractional extraction was 58% ± 5%.

Table 2 provides the enrichments of M+1 and M+2 in plasma glucose, galactose, and glucose in lactose between 6 and 9 h of study (6–9 h of isotope infusion). The M+2 enrichment of glucose in lactose was 69 ± 6% of that of plasma [6,6-²H₂]glucose enrichment (Fig. 1), and the M+2 enrichment of galactose in lactose was 54 ± 4% of that of the plasma [6,6-²H₂]glucose (i.e. 69% of the glucose and 54 of the galactose in lactose were derived directly from plasma glucose).

View larger version (22K): [in this window] [in a new window]   Figure 1. Fraction of glucose and galactose derived from hydrolyzed human lactose derived from plasma glucose (white bar), galactose (gray bar), and de novo synthesis (hatched bar) during ingestion of galactose at 22 µmol·kg-1·min-1. SE bars reflect the variance for each individual part of the contribution to lactose synthesis.

Indirect calorimetry data

The rate of galactose oxidation (regardless of the pathway of metabolism) was estimated to be 3.69 ± 0.64 µmol·kg^-1·min^-1, or 40 ± 3% of the galactose Ra and 17 ± 1% of the ingested amount of galactose.

Milk volume and lactose production

During the 9 h of galactose ingestion, milk production was 374 ± 58 ml. Assuming a lactose concentration of 7% or 220 mM in milk and that 61% [(69 + 54)/2] of lactose is derived from the plasma glucose in the fed state, the rate of glucose converted to lactose was approximately 1.40 µmol·kg^-1·min^-1 and the rate of galactose conversion to lactose 0.21 µmol·kg^-1·min^-1. This represents approximately 11% and 2% of the systemic rates of appearance of glucose and galactose, respectively. The rate of plasma clearance of glucose and galactose into lactose synthesis can be estimated from the rates of conversion of plasma glucose and galactose into lactose and the plasma concentrations. The clearance of plasma glucose and galactose into lactose synthesis was 0.24 and 0.38 ml/kg^-1·min^-1, respectively (i.e. the clearances are similar for glucose and galactose despite a 10-fold difference in their plasma concentrations).

	Discussion

Top Abstract Introduction Materials and Methods Results Discussion References

 
Using an iv infusion of [1-¹³C]galactose and oral administration of unlabeled galactose, the present study demonstrated that ingestion of galactose results in direct uptake of galactose by lactating mammary tissue with conversion to both glucose and galactose in lactose and uptake of plasma glucose (as a result of presumed hepatic conversion of galactose to glucose) and incorporation into glucose and galactose in milk lactose. In principle, these data are in agreement with those recently reported by Obermeier et al. (2) and Kunz et al. (3) in which they observed that following ingestion of [1-¹³C]galactose, the label was recovered in glucose and galactose in lactose. However, their study design precluded them from determining whether the labeled galactose was converted to labeled glucose in the liver and subsequently the labeled plasma glucose converted to labeled glucose and galactose in milk lactose or the direct uptake of labeled galactose by the breast.

We have previously demonstrated (1) that plasma glucose contributed approximately 90% of the glucose and approximately 60% of the galactose in lactose in the fed state, regardless of whether the feeding is glucose alone or a mixed liquid caloric meal. During fasting these values decreased to approximately 60% and approximately 50%, respectively (1). In the present study, we observed values of 69 ± 6% and 54 ± 4% for the contribution of plasma glucose to milk glucose and galactose, respectively. These values are slightly higher than our previous fasted values but lower than the fed data, which is not surprising because the women in the present study were really not fasting but receiving oral galactose at 22 µmol·kg^-1·min^-1. Despite the galactose ingested, it is interesting to note that the plasma glucose rates of appearance in this and our previous fasting studies (7) were essentially the same (i.e. the oral galactose did not increase maternal plasma glucose appearance rates).

Using the single- and double-labeled plasma glucose enrichments, we were able to partition the contributions of plasma glucose to milk glucose and galactose. In addition, we were able to determine the fractional contribution of plasma galactose to both carbohydrate moieties in milk lactose. Plasma galactose made a greater contribution to milk galactose than milk glucose, suggesting a ready pathway of transport and phosphorylation of the galactose in the mammary tissue. In our previous study (1), plasma glucose contributed approximately 60% and hexoneogenesis approximately 40% of milk lactose in the fasted state. During ingestion of galactose, the contribution from plasma glucose to lactose was virtually identical to that of the fasting state but the contribution from hexoneogenesis was approximately 10% lower (30%). This difference is accounted for by the direct conversion of plasma galactose to lactose.

In studies by Kunz et al. (3), an oral bolus dose of labeled galactose was administered (a total of 27 g). Assuming that the women weighed approximately 70 kg, this would correspond to 386 mg/kg or 2140 µmol/kg of which 7% was ¹³C-labeled galactose. We have previously demonstrated (8) that the uptake of galactose by the liver is saturable at about approximately 15 µmol·kg^-1·min^-1. Thus, it is impossible to determine how much of this bolus was extracted by the liver. In the present study, we administered the oral galactose over a period of 9 h. As a result, direct comparison of the results from these studies is of no value. The authors’ observation of the ¹³C appearing in the C-1 position in galactose and glucose in lactose (on the basis of their nuclear magnetic resonance data) does not prove that plasma [1-¹³C]galactose was the primary or only precursor for lactose synthesis. Using GCMS employing both electron impact (which cleaves C-1) (6) and PCI (which preserves the entire carbon skeleton) (6), we demonstrated that the plasma glucose (derived from galactose) was labeled exclusively in the C-1 position. This is consistent with direct hepatic conversion of [1-¹³C]galactose to [1-¹³C]glucose. Because Obermeier et al. (3) most likely achieved higher plasma galactose concentrations following their bolus ingestion than we did with our 9-h constant ingestion, they may have had somewhat higher direct conversion of plasma galactose to milk lactose than we observed. However, we demonstrated that under our study conditions, approximately 40% of the plasma glucose appearance rate was derived from galactose. With higher administration rates of galactose in the Kunz study (3), the vast majority of glucose would be derived from galactose (8).

In summary, during ingestion of galactose at 22 µmol·kg^-1·min^-1, 9.2 µmol·kg^-1·min^-1 appeared in the systemic circulation, 5.5 µmol·kg^-1·min^-1 appeared as plasma glucose, and 4 µmol·kg^-1·min^-1 was oxidized (i.e. we accounted for 85% of the oral galactose). Because plasma lactate concentrations doubled during ingestion of galactose, a portion of oral galactose was most likely converted to plasma lactate. Plasma galactose directly contributed approximately 10% of milk lactose with a larger proportion directed toward galactose in lactose, compared with glucose in lactose (12% vs. 7%). The direct contribution from plasma glucose to lactose was similar to that observed in the fasted state in our previous study (1). Thus, the carbon provided by plasma galactose replaced part of the carbons provided by hexoneogenesis during fasting. This study demonstrates that although plasma glucose is the primary source of milk lactose, plasma galactose is a potential substrate for milk lactose during ingestion of galactose. Milk is the primary dietary source of galactose. However, in milk the galactose is contained in the lactose molecule (i.e. galactose + glucose). We have previously demonstrated (8) that coingestion of galactose with glucose results in increased splanchnic uptake of galactose and thus very low plasma concentrations of galactose. Therefore, to achieve plasma concentrations of galactose that would enable us to determine whether galactose could contribute to milk lactose, in the present study, galactose was ingested alone at a rate that would correspond to nine glasses of milk (240 ml/each) over the 9-h study period.

	Acknowledgments

 
We acknowledge and thank the technicians in our laboratory (Patricia Breitenfelder, Shaji Chacko, Cindy Clarke, Dan Donaldson, and Kathryn Louie), our nurse coordinator (Andrea Jones, R.N.), and the staff in the Metabolic Research Unit and kitchen and the General Clinical Research Center who greatly facilitated the execution of these studies.

	Footnotes

 
This work was supported by grants from U.S. Department of Agriculture Cooperative Agreement #58-6250-6-001, NIH RO1DK 55478, and NIH HD37857. This work is a publication of the USDA/ARS Children’s Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine (Houston, TX). The contents of this publication do not necessarily reflect the views of policies of the U.S. Department of Agriculture, nor does mention of trade names, commercial products, or organizations imply endorsement from the U.S. Government.

Abbreviations: GCMS, Gas chromatography-mass spectrometry; PCI, positive chemical ionization; Ra, rates of appearance.

Received May 17, 2002.

Accepted September 12, 2002.

	References

Top Abstract Introduction Materials and Methods Results Discussion References

 

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