Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We postulated whether interventions capable of restoring euglycemia would correct whole-body protein metabolism, shown previously to be elevated in hyperglycemic persons with non-insulin-dependent diabetes (NIDDM). The kinetics of protein metabolism were estimated in obese subjects with NIDDM in the hyper- and normoglycemic states during isoenergetic feeding and in the normoglycemic state induced by 4 wk of a very-low-energy diet (VLED) with constant protein intake. Seven NIDDM subjects [three males and four females with a body mass index (in kg/m2) of 39 +/- 2] were given a weight-maintaining, liquid formula providing 95 g protein/d for 15 d, followed in six subjects (two males and four females) for 27 d by a diet providing 1.7 MJ, 93 g protein derived from casein-soy, 13 g carbohydrate, 2 g fat, multivitamins and minerals, and a potassium bicarbonate supplement (32 mmol) per day. Exogenous insulin was given to achieve normoglycemia during the first 8 d of isoenergetic feeding. On days 6-8, 12-14, and 25-27, nitrogen flux rate was calculated from the urine [15N]urea enrichment by using the 60-h oral [15N]glycine method to obtain "integrated" feeding and fasting values. Rates of synthesis and breakdown were calculated from nitrogen flux. During isoenergetic feeding, normoglycemia was associated with more positive nitrogen balance (2.6 +/- 0.5 compared with -0.6 +/- 0.6 g N/d, P < 0.05); 18-23% lower nitrogen flux, and synthesis and breakdown rates (P < 0.05), and a 3% decrease in resting energy expenditure (P < 0.05). During the VLED, euglycemia was achieved but nitrogen balance, although it became less negative with time, never reached equilibrium. This was associated with significant (P < 0.05) decreases in the synthesis rate, resulting in net protein losses. Thus, the altered protein metabolism in moderately hyperglycemic NIDDM subjects was improved with exogenous insulin in doses sufficient to restore normoglycemia in the isoenergetic fed state, but it remained abnormal with a reduced non-protein energy intake. This suggests that protein metabolism is more sensitive to insulinization than was thought previously.
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PMID:Effect of glycemic control on the kinetics of whole-body protein metabolism in obese subjects with non-insulin-dependent diabetes mellitus during iso- and hypoenergetic feeding. 906 41

Type 1 diabetes is based on autoimmunity, and its development is in part determined by environmental factors. Among those, milk intake is discussed as playing a pathogenic role. Geographical and temporal relations between type 1 diabetes prevalence and cow's milk consumption have been found in ecological studies. Several case-control studies found a negative correlation between frequency and/or duration of breast-feeding and diabetes, but this was not confirmed by all authors. T-cell and humoral responses related to cow's milk proteins were suggested to trigger diabetes. The different findings of studies in animals and humans as well as the potential underlying mechanisms with regard to single milk proteins (bovine serum albumin, beta-lactoglobulin, casein) are discussed in this review. In contrast to type 1 diabetes, the etiology of type 2 diabetes, characterized by insulin resistance is still unclear. In a population with a high prevalence of type 2 diabetes, the Pima Indians, people who were exclusively breastfed had significantly lower rates of type 2 diabetes than those who were exclusively bottlefed. Studies in lactovegetarians imply that consumption of low fat dairy products is associated with lower incidence and mortality of diabetes and lower blood pressures. In contrast, preference for a diet high in animal fat could be a pathogenic factor, and milk and high fat dairy products contribute considerably to dietary fat intake. Concerning milk fat composition, the opposite effects of various fatty acids (saturated fatty acids, trans-fatty acids, conjugated linoleic acid) in vitro, in animals and in humans have to be considered.
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PMID:Milk and diabetes. 1075 42

Protein restriction is used conventionally in the prevention and treatment of diabetic nephropathy. Recently, the use of soy protein instead of animal protein has been postulated as a new preventive and treatment option. The aim of this study was to determine the qualitative and quantitative effects of dietary protein on biomarkers of diabetic nephropathy in a Type 2 diabetes mellitus mouse model (BKS.cg-m +Lepr(db)/+Lepr(db) mice). Diabetic (+Lepr(db)/+Lepr(db)) and control (m+/m+) mice (n = 24/group) consumed one of four different diets ad libitum [20% casein, 20% soy protein, 12% casein or 12% soy protein (energy-based percentages)] from 35 +/- 4 d of age until termination (184-217 d of age). Blood and urine were collected throughout the study to measure biomarkers of diabetes and diabetic nephropathy. Kidney tissue was collected at the end of the study for weight. In diabetic mice, a 20% casein diet increased urinary albumin excretion to macroalbuminuric levels, whereas a 20% soy protein diet led to no major changes in urinary albumin excretion. Low protein diets (12%), independently of protein type, decreased urinary albumin excretion to low microalbuminuric levels. There were no significant differences in plasma glucose concentrations. These findings show lower urinary albumin excretion when a soy protein diet or a low casein diet is fed, suggesting a delay in the progression of diabetic nephropathy.
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PMID:Altering dietary protein type and quantity reduces urinary albumin excretion without affecting plasma glucose concentrations in BKS.cg-m +Lepr db/+Lepr db (db/db) mice. 1261 36

Nutritional deprivation of the fetus and infant is associated with susceptibility to the development of impaired glucose tolerance or type 2 diabetes in adult life. Quantitative changes in mitochondrial DNA (mtDNA) seem to be associated with type 2 diabetes, but the effect of protein malnutrition on mtDNA content is not known. This study investigated the effects of protein malnutrition in fetus and early life on mtDNA content and glucose-insulin metabolism in adult life. Male offspring of dams fed a low-protein (LP) diet (8% casein) during pregnancy and lactation were weaned onto either a control (18% casein) diet (recuperated group, R) or a LP diet, and they were compared with the control group (C). The mtDNA content in the liver was lower in the R and LP groups than in the C group at 5 weeks of age, but higher in the R and LP groups than in the C group at 15 weeks of age. The mtDNA content in skeletal muscle and pancreas was significantly lower in the R and LP groups than in the C group at 25 weeks of age. Fetal-malnourished rats showed decreased pancreatic beta-cell mass and reduced insulin secretory responses to glucose load, but no differences in glucose tolerance or insulin sensitivity. Our findings imply that protein malnutrition in utero causes changes in mtDNA content, impaired beta-cell development, and insulin secretion, which may contribute to the development of type 2 diabetes in later life.
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PMID:Changes of mitochondrial DNA content in the male offspring of protein-malnourished rats. 1512 98

Soy protein was shown to exhibit several beneficial effects on renal function in nondiabetic patients with nephropathy, and to improve serum lipids. This study examined the effects of isolated soy protein consumption on urinary albumin excretion, serum lipids, plasma amino acids, and isoflavones in diabetic patients with nephropathy. Male patients (n = 14) with type 2 diabetes and nephropathy were followed in a crossover design for 7 mo. The study comprised two 8-wk intervention periods, placed between a 4-wk lead-in and two 4-wk washout periods. In the 2 intervention periods, 0.5 g/(kg. d) of the dietary protein was provided as either isolated soy protein (ISP) or casein, in random order. Blood and urine samples were collected at the beginning and end of each period. Data were analyzed by multiple linear regression for a repeated-measure design. ISP consumption led to changes of -9.5% in urinary albumin excretion (P < 0.0001), -0.45 in the total-to-HDL-cholesterol ratio (P < 0.05), -0.20 in the LDL-to-HDL cholesterol ratio (P < 0.05), and +4.3% in HDL cholesterol (P = 0.0040). Plasma arginine concentrations, the arginine-to-lysine ratio, and plasma isoflavone concentrations were higher after ISP consumption (P < 0.05). Urinary albumin excretion was negatively correlated with plasma total isoflavones (rho = -0.441), daidzein (rho = -0.326), and O-desmethylangolesin (rho = -0.389) (P < 0.05). The findings indicate that isolated soy protein consumption improves several markers that may be beneficial for type 2 diabetic patients with nephropathy.
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PMID:Isolated soy protein consumption reduces urinary albumin excretion and improves the serum lipid profile in men with type 2 diabetes mellitus and nephropathy. 1528 69

We examined the effects of intake of Korean foxtail millet protein (FMP) on plasma levels of lipid, glucose, insulin, and adiponectin in genetically type 2 diabetic KK-Ay mice. When mice were fed a normal FMP diet or a high-fat-high-sucrose diet containing FMP for 3 weeks, in both experiments plasma concentrations of high-density lipoprotein cholesterol (HDL-cholesterol) and adiponectin increased remarkably in comparison with a casein diet group, whereas concentrations of insulin decreased greatly and that of plasma glucose was comparable to that in the casein diet group. Considering the role of adiponectin, insulin, and HDL-cholesterol in diabetes, atherosclerosis, and obesity, it appears likely that FMP may improve insulin sensitivity and cholesterol metabolism through an increase in adiponectin concentration. Therefore, FMP would serve as another beneficial food component in obesity-related diseases such as type 2 diabetes and cardiovascular diseases.
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PMID:Effects of dietary protein of Korean foxtail millet on plasma adiponectin, HDL-cholesterol, and insulin levels in genetically type 2 diabetic mice. 1566 64

Dyslipidemia and hyperglycemia are integral components of the metabolic perturbations in type 2 diabetes. Apolipoprotein E-deficient (apoE(-/-)) mice develop severe hyperlipidemia and significant hyperglycemia when fed a western diet containing 21% fat (w/w), 0.15% cholesterol and 19.5% casein. Using an intercross between C57BL/6J (B6) and C3H/HeJ (C3H) apoE(-/-) mice, we performed quantitative trait locus (QTL) analysis to identify loci contributing to hyperglycemia and associated traits. Fasting plasma levels of glucose, insulin and serum amyloid-P (SAP) and body weight in 234 female F2 mice were measured after being fed the western diet for 12 weeks. QTL analysis revealed one significant QTL, named Bglu3 [95.8 cM, logarithm of odds ratio (OR)(LOD) 4.1], on chromosome 1 and a suggestive QTL on chromosome 9 (38 cM, LOD 2.3) that influenced plasma glucose levels. Bglu3 coincided with loci on distal chromosomal 1 that had a major influence on plasma SAP levels and body weight. Significant correlations between plasma glucose, SAP and body weight were observed in F2 mice. Thus, these results demonstrate genetic linkages of hyperglycemia and body weight with SAP, a marker of the acute-phase response, in hyperlipidemic apoE(-/-) mice and suggest a probability for the Sap gene to be a positional candidate of Bglu3.
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PMID:Genetic linkage of hyperglycemia, body weight and serum amyloid-P in an intercross between C57BL/6 and C3H apolipoprotein E-deficient mice. 1659 6

The balance between muscle protein synthesis (MPS) and muscle protein breakdown (MPB) is dependent on protein consumption and the accompanying hyperaminoacidemia, which stimulates a marked rise in MPS and mild suppression of MPB. In the fasting state, however, MPS declines sharply and MPB is increased slightly. Ultimately, the balance between MPS and MPB determines the net rate of muscle growth. Accretion of new muscle mass beyond that of normal growth can occur following periods of intense resistance exercise. Such muscle accretion is an often sought-after goal of athletes. There needs to be, however, an increased appreciation of the role that preservation of muscle can play in offsetting morbidities associated with the sarcopenia of aging, such as type 2 diabetes and declines in metabolic rate that can lead to fat mass accumulation followed by the onset or progression of obesity. Emerging evidence shows that consumption of different types of proteins can have different stimulatory effects on the amplitude and possibly duration that MPS is elevated after feeding; this may be particularly significant after resistance exercise. This effect may be due to differences in the fundamental amino acid composition of the protein (i.e., its amino acid score) and its rate of digestion. Milk proteins, specifically casein and whey, are the highest quality proteins and are quite different in terms of their rates of digestion and absorption. New data suggest that whey protein is better able to support MPS than is soy protein, a finding that may explain the greater ability of whey protein to support greater net muscle mass gains with resistance exercise. This review focuses on evidence showing the differences in responses of MPS, and ultimately muscle protein accretion, to consumption of milk- and soy-based supplemental protein sources in humans.
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PMID:The role of milk- and soy-based protein in support of muscle protein synthesis and muscle protein accretion in young and elderly persons. 2036 72

Arginine (Arg) is known to possess numerous useful physiological properties and have immunomodulatory effects. In vitro studies reported that Arg inhibits advanced glycation endproduct (AGE) formation; however, the effects of Arg on the receptor of AGE (RAGE) expression in inflammatory conditions are not clear. The present study investigated the effects of dietary Arg supplementation on inflammatory mediator production and RAGE expression in type 2 diabetic rats. There were one normal control (NC) group and two diabetic groups in the present study. Rats in the NC group were fed with a regular chow diet. One diabetic group (DM) was fed a common semi-purified diet while the other diabetic group received a diet in which part of the casein was replaced by Arg (DM-Arg) for 8 weeks. Diabetes was induced by an intraperitoneal injection of nicotinamide followed by streptozotocin. Rats with blood glucose levels exceeding 1800 mg/l were considered diabetic. Blood samples and the liver and lungs of the animals were collected at the end of the study for further analysis. Results showed that plasma glucose and fructosamine contents were significantly higher in the diabetic groups than those in the NC group. The DM group had higher fructosamine and C-reactive protein than the DM-Arg group. Immunohistochemical staining showed that the expressions of RAGE in liver and lung tissues were significantly lower in the DM-Arg group than in the DM group. These results suggest that supplemental dietary Arg can decrease AGE-RAGE interactions and consequently reduce tissue damage in rats with type 2 diabetes.
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PMID:Effects of dietary arginine on inflammatory mediator and receptor of advanced glycation endproducts (RAGE) expression in rats with streptozotocin-induced type 2 diabetes. 2038 49

Glucagon-like peptide-1 (GLP-1) is an intestinal hormone with well-established glucose-lowering activity. The in vitro and in vivo actions of natural putative secretagogues of GLP-1 were investigated. The acute GLP-1 releasing activity of olive leaf extract (OLE), glutamine (GLN), alpha casein (ACAS), beta casein (BCAS) and chlorogenic acid (CGA) were assessed in STC-1 cells and C57BL/6 mice. All compounds except ACAS significantly increased acute in vitro GLP-1 secretion (66-386%; P<0.05-0.001). Oral gavage of OLE and GLN modestly increased plasma GLP-1 concentrations (48% and 41%, respectively), but did not lower glycaemic excursions. OLE and GLN are potent stimulators of GLP-1 secretion both in vitro and in vivo and chronic studies should assess their suitability as nutritional therapies for type 2 diabetes.
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PMID:In Vitro and In Vivo Effects of Natural Putative Secretagogues of Glucagon-Like Peptide-1 (GLP-1). 2188 7


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