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Query: KEGG:D00046 (lactose)
 16,692 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Induction of alloxan diabetes in 5 lactating goats resulted in reduced milk yields in 3 of the animals, while the yield was unchanged in two. After treatment of the diabetic goats with insulin for 4--5 days--the last 24 h intravenously--lactose secretion returned to the control values before alloxan administration provided that normoglycemia developed. In 2 experiments infusion of a large dose of insulin caused hypoglycemia and a 20--30 per cent reduction in lactose secretion rates. In the course of 1 h after withdrawal of the insulin infusion, patent signs of insulin deficiency developed as evidenced by steadily increasing plasma glucose concentrations. Nevertheless, lactose secretion continued at the same rate as during insulin infusion for the 4 h studied after discontinuation of the insulin infusion. In the goats where lactose secretion was reduced due to insulin-induced hypoglycemia, lactose secretion returned to control values when following discontinuation of insulin infusion the plasma glucose concentrations increased into normal and diabetic ranges. It is concluded that during insulin deficiency of short term duration, mammary lactose secretion was maintained at a normal rate. Since lactose is the major product of mammary glucose utilization, it is suggested that glucose uptake in the mammary gland was not reduced by short term insulin deficiency.
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PMID:Maintenance of lactose secretion during acute insulin deficiency in lactating goats. 67 68

A new disaccharidase inhibitor, AO-128, showed 190-3900-fold more potent inhibition of purified rat small intestine sucrase-isomaltase (S-1) complex and 23-33-fold more potent inhibition of semipurified porcine small intestine disaccharidases than acarbose. AO-128 suppressed elevation of the blood glucose concentration after oral sucrose, maltose, and starch, but not after oral glucose, fructose, and lactose. The chronic addition of AO-128 to the diet produced antiobesity and antidiabetic actions in obese and/or diabetic animals. Undesirable side effects, such as diarrhea and soft feces, were observed only for the first 5-7 d and suppression of intestinal disaccharidase activities was observed even at the end of the experiment, suggesting that the suppressive or delaying effect of AO-128 on elevation of the postprandial blood glucose concentrations is involved in reduction in body weight gain and prevention and/or amelioration of the diabetic state. Thus, AO-128 is useful as an adjunct to the dietary management of obesity and diabetes.
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PMID:Effect of an intestinal disaccharidase inhibitor (AO-128) on obesity and diabetes. 172 46

Gestational diabetes is the most common complication of pregnancy. If maternal hyperglycemia is not well controlled, excess glucose is transmitted to the fetus, which can lead to fetal macrosomia and maternal and fetal complications. Dietary treatment for gestational diabetes varies among practitioners. A case review is presented of a 32-year-old white woman with gestational diabetes whose condition was complicated by her blood glucose intolerance to lactose in milk. By following a carefully monitored regimen using specific dietary manipulation to maintain normoglycemia, the woman was able to deliver a normal, healthy baby by spontaneous vaginal delivery.
Diabetes Educ
PMID:Euglycemic control of gestational diabetes mellitus by specific dietary manipulation: a case study presentation. 193 53

Milk volume and composition were examined in a diabetic mother on days 3-7 postpartum. By day 5 milk volume produced and concentrations of sodium, potassium, chloride, lactose, protein, calcium, magnesium, and citrate were within limits of a reference population. Fat content of the milk was slightly lower. Free fatty acids were 2% of total lipid on day 3 but increased to 23% on days 4-7, suggesting impaired esterification in the mammary gland. Total milk lipoprotein lipase increased approximately fourfold during days 4-5. Other changes were 1) low cholesterol content, only one-fifth of normal milk; 2) decreased medium-chain fatty acids, suggesting impairment of fatty acid synthesis in the mammary gland; 3) increased oleic acid; and 4) high concentrations of polyunsaturated fatty acids, suggesting increased chain elongation. These results suggest that diabetes produces changes in lipid metabolism in the mammary gland that alter the composition of milk produced by the diabetic mother.
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PMID:Milk composition and volume during the onset of lactation in a diabetic mother. 259 26

A study was undertaken to define an appropriate marker of lactogenesis II (the onset of copious milk secretion) in mothers, and to determine the effect of diabetes on this marker. Changes in the concentrations of three milk components--lactose, citrate, and glucose--were measured in 38 normal mothers and 6 type I diabetic mothers up to 10 days after birth. Milk yield was measured in 12 of the normal mothers, and all mothers were asked to note the time of milk "coming in" (the feeling of overfullness of the breasts). The average concentrations of lactose, citrate, and glucose in milk were low for the first 24 h after birth, then between 24 and 48 h after birth there was a rapid increase in the concentrations of lactose and citrate, and this transitional period was followed by a plateau period that began between 60 and 84 h after birth. For individual mothers the transitional period for citrate began 32 +/- 9 h (n = 13) and finished 77 +/- 10 h (n = 17) after birth, and for lactose the transitional period finished at 53 +/- 12 h (n = 29) after birth. For diabetic mothers these times were significantly later. The average 24-h milk intake by infants increased from 82 to 556 ml/24 h between 24 and 144 h after birth. Milk intakes were correlated with the concentration of lactose (r = 0.52, n = 51, p less than 0.001), citrate (r = 0.47, n = 47, p less than 0.001), and glucose (r = 0.69, n = 50, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Milk lactose, citrate, and glucose as markers of lactogenesis in normal and diabetic women. 262 26

Diet therapy is an important factor in overall care of most GI patients. Historically, diets have been used unscientifically in many of these patients without positive results. Nutritional care and diet therapy are critical for two reasons. First, malnutrition is an expected sequelae to most, if not all, GI diseases or disorders. Failure to eat, digest, or assimilate nutrients can provoke malnutrition in just a few weeks, although careful assessment of anthropometric, clinical, biochemical, and nutritional history by a trained professional can protect against this. Diet therapy through the elimination of offending foods such as wheat gluten or lactose, or inclusion of specialized products such as medium chain triglycerides or elemental formulas, can sustain nutritional status. Dietary components such as insoluble fiber appear to have physiologic effects, while soluble fibers may have metabolic effects important to diabetes and cardiovascular disease. There is a high potential for malnutrition in Crohn's disease during active and remittent phases. Elemental enteral formulas or TPN are used during the active phase to ensure optimal nutritional status and bowel rest. Hyperalimentation using the GI tract during remittent stage maintains this. Avoiding offending foods by Crohn's patients is an acceptable practice as long as entire categories of foods are not deleted. Avoiding all foods containing gluten from wheat, rye, barley, and oats, however, is a crucial prerequisite to recovery from celiac disease. Gluten is commonly used as a stabilizer, emulsifier, and extender in the food industry and is not always shown on food labels. Careful consultation with a registered dietitian can identify hidden sources of gluten in the diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary therapy in gastrointestinal disease. 264 90

The Inuit (Eskimo) gene pool is in many respects similar to that of East Asian populations. Some polymorphisms imply frequent occurrence of disorders comparatively rare in Western Europe (e.g. lactose and sucrose malabsorptions). Low frequencies of alleles for slow isoniazid acetylation and sparteine/debrisoquine oxidation indicate slow elimination of a multitude of drugs. Autoimmune disorders (e.g. rheumatoid arthritis, insulin-dependent diabetes mellitus, Graves' disease and psoriasis) are rare, possibly explained by the associations of these disorders with HLA-alleles rare in the Inuit (e.g. HLA-B8). A correspondingly high incidence of reactive arthritis may be explained by a frequent HLA-B27 allele. The prevalence of disorders due to instability of mesenchymal tissues (e.g. spondylolisthesis, osteoarthrosis, hernia, heart block) still requires a biochemical explanation. Attention is drawn to the urgency of genetic studies in the Arctic because of the accelerating hybridization of the Inuit in all circumpolar areas.
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PMID:Genetic epidemiology of Greenland. 268 6

This study examined the hypothesis that the glucose component of food and not the total carbohydrate is the major determinant of the glycemic response in patients with insulin-dependent diabetes mellitus. Patients were given glucose alone, fructose alone, glucose + fructose, lactose, and glucose + fat + protein. Fructose given alone increased the blood glucose almost as much as a similar amount of glucose (78% of the glucose-alone area, p less than 0.05). However, the same amount of fructose given with glucose produced no greater glycemic response than did glucose alone (108%). Similarly, galactose contributed only slightly to the glycemic response when given as lactose (122%, p less than 0.01) whereas protein and fat had no additional glycemic effect (101%). To test the above hypothesis in natural foods, patients were fed an amount of bread (high glycemic index) or apple (low glycemic index) that contained 25 g glucose. Both challenges produced glycemic responses very similar to 25 g purified glucose.
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PMID:Glycemic responses in insulin-dependent diabetic patients: effect of food composition. 259 39

A 42-year-old male patient, who suffered from insulin-dependent diabetes mellitus (IDDM) and intolerance of lactose, presented with extreme metabolic acidosis (lactic acidosis). On arrival, an arterial blood sample showed: pH 6.79, PO2 18.8 kPa, PCO2 0.9 kPa, base excess-33 mmol l-1, blood glucose 38 mmol l-1 and oesophageal temperature 30 degrees C. Apart from the uncontrolled hyperglycaemia, a fluid balance disorder elicited by diarrhoea and disturbed tissue perfusion were possible aetiological factors. The patient was treated with a low-dose insulin regimen and infusion of isotonic sodium bicarbonate with a satisfactory result.
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PMID:Extreme metabolic acidosis. Case report. 330 70

Cellular accumulation of galactitol has been suggested to cause the apparent dietary-independent, long-term complications in classic galactosemia. Experimental animals rendered hypergalactosemic by galactose feeding accumulate tissue galactitol, as well as millimolar quantities of galactose, and manifest biochemical, physiological and pathological abnormalities which are generally eliminated or curtailed by the concomitant administration of an aldose reductase inhibitor. This includes reduced cellular content of the cyclic polyol, myo-inositol, which like galactitol may function as an alternate intracellular osmolyte. However, the abnormalities detected in experimental galactosemic animals are more compatible with findings in experimental diabetes mellitus than in human galactosemia. Because patients with galactokinase deficiency fail to manifest the CNS and ovarian complications which characterize classic galactosemia, yet during long-term lactose restriction excrete comparable urinary quantities of galactitol, this polyol alone is not likely to play an important role during postnatal life in the pathogenesis of long-term complications. Notwithstanding, a role for either galactitol or myo-inositol in an intrauterine toxicity cannot be dismissed.
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PMID:The role of polyols in the pathophysiology of hypergalactosemia. 767 66


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