Type 2 diabetes caused by mineral deficiency,natural remedies for type 2 diabetes uk,diabetes type 2 pathophysiology flow chart - Review


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OA Texta€™s journals are led by prominent researchers, each embracing the concept that basic knowledge can foster sustainable solutions for society. Obesity and diabetes are currently a major health problem worldwide with growing in prevalence. One of these shared features is that osteoblasts and adipocytes differentiate from a common precursor cell in the bone marrow, the mesenchymal stem cells [5,6].
Osteoporosis, which bone mass is dramatically reduced with menopause and aging [20], has also been shown to induce in obesity, diabetes (type I and II) and inflammatory disease [21,22].
Various hormones and cytokines, which include leptin, adiponectin, insulin, epinephrine, cortisol, glucagon, TNF-α and other factors, are well known as key molecules that relate to obesity and diabetes. Bone is a dynamic tissue that undergoes continual adaptation during vertebrate life to attain and preserves skeletal size, shape and structural integrity and to regulate mineral homeostasis. Numerous pathological processes have the capacity to disrupt this equilibrium by leading to conditions where the rate of bone resorption outpaces and the rate of bone formation, leading to osteoporosis [20]. Osteoporosis is a major cause of increased morbidity and mortality affecting the aging population.
The TallyHo mouse is a polygenic model of early onset, naturally occurring type 2 diabetes mellitus and obesity [30,46].
As described above, there is growing evidence that abnormality and bone loss are induced in animal models for obesity and type 2 diabetes.
Anti-resorptive agents have been used the preferred standard of clinical care for the amelioration of bone loss in osteoporosis. Effect of nutritional zinc: Nutritional zinc has been demonstrated to stimulate osteoblastic bone for mation and suppress osteoclasti bone resorption in vitro and in vivo [51].
Effects of p-hydroxycinnamic acid: Cinnamic acid, a flavonoid, is present in many plant and fruits.
Interestingly, p-hydroxycinnamic acid was found to stimulate osteoblastogenesis and suppress adipogenesis using culture systems with mouse bone marrow cells and mouse 3T3-L1 preadipocytes in vitro [60].
Obesity and diabetes induce secondary diseases with various pathophysiologic states, which are important in clinical aspects including cardiovascular disease, neural disturbance, kidney disease, cancer and osteoporosis. We found that diabetic states and bone loss in type 1 diabetes were improved by the intake of zinc compound, β-cryptoxanthin and p-hydroxycinnamic acid, which is novel osteogenic factors. 7.Laudes M (2011) Role of WNT signalling in the determination of human mesenchymal stem cells into preadipocytes.
8.Gharibi B, Abraham AA, Ham J, Evans BA (2011) Adenosine receptor subtype expression and activation influence the differentiation of mesenchymal stem cells to osteoblasts and adipocytes. 11.Laudes M (2011) Role of WNT signalling in the determination of human mesenchymal stem cells into preadipocytes. 12.Gharibi B, Abraham AA, Ham J, Evans BA (2011) Adenosine receptor subtype expression and activation influence the differentiation of mesenchymal stem cells to osteoblasts and adipocytes.
21.Rossmeisl M, Rim JS, Koza RA, Kozak LP (2003) Variation in type 2 diabetes--related traits in mouse strains susceptible to diet-induced obesity.
24.Yamaguchi M, Weitzmann MN, Baile CA, Murata T (2012) Exogenous regucalcin suppresses osteoblastogenesis and stimulates adipogenesis in mouse bone marrow culture. 27.Chen G, Deng C, Li YP (2012) TGF-AZA? and BMP signaling in osteoblast differentiation and bone formation. 28.Johnell O, Kanis JA (2006) An estimate of the worldwide prevalence and disability associated with osteoporotic fractures. 30.Fajardo RJ, Karim L, Calley VI, Bouxsein ML (2014) A review of rodent models of type 2 diabetic skeletal fragility. 31.Rossmeisl M, Rim JS, Koza RA, Kozak LP (2003) Variation in type 2 diabetes--related traits in mouse strains susceptible to diet-induced obesity.
35.Cao JJ, Gregoire BR, Gao H (2009) High-fat diet decreases cancellous bone mass but has no effect on cortical bone mass in the tibia in mice. 36.Halade GV, Rahman MM, Williams PJ, Fernandes G (2010) High fat diet-induced animal model of age-associated obesity and osteoporosis.
43.Ealey KN, Fonseca D, Archer MC, Ward WE (2006) Bone abnormalities in adolescent leptin-deficient mice. 44.Hamrick MW, Pennington C, Newton D, Xie D, Isales C (2004) Leptin deficiency produces contrasting phenotypes in bones of the limb and spine. 52.Uchiyama S, Yamaguchi M (2003) Alteration in serum and bone component findings induced in streptozotocin-diabetic rats is restored by zinc acexamate. 55.Uchiyama S, Yamaguchi M (2005) Oral administration of beta-cryptoxanthin prevents bone loss in streptozotocin-diabetic rats in vivo. 56.Lai YL, Yamaguchi M (2006) Phytocomponent p-hydroxycinnamic acid stimulates bone formation and inhibits bone resorption in rat femoral tissues in vitro. 57.Yamaguchi M, Lai YL, Uchiyama S, Nakagawa T (2008) Phytocomponent p-hydroxycinnamic acid stimulates mineralization in osteoblastic MC3T3-E1 cells.
58.Lai YL, Yamaguchi M (2007) Phytocomponent p-hydroxycinnamic acid inhibits osteoclast-like cell formation in mouse bone marrow cultures.
59.Yamaguchi M, Uchiyama S, Lai YL (2007) Oral administration of phytocomponent p-hydroxycinnamic acid has a preventive effect on bone loss in streptozotocin-induced diabetic rats. 60.Yamaguchi M, Baile CA, Zhu S, Shoji M (2013) Bioactive flavonoid p-hydroxycinnamic acid stimulates osteoblastogenesis and suppresses adipogenesis in bone marrow culture.
The author was partly supported by Awards of the Mishima Kaiun Memorial Foundation (Japan), the Senji Miyata Foundation (Japan), and the Japan Society for Biomedical Research on Trace Elements.
Horizontal ridges on fingernails however can indicate a serious ailment, though it is not the case always.
Being one of the most important organs of the human body, kidneys are mainly responsible for the filtration of blood by the separation of solid wastes and excess water from it.
The major causes behind chronic kidney disease are high blood pressure and diabetes, which accounts for at least two-third of the total cases. Occurrence of glomerulonephritis, the state of inflammation and damage of the kidney filtration system, which is further caused by post infectious conditions. Diseases affecting human immune system, for example systemic lupus erythematosus and scleroderma.
Formation of large cysts in the kidney damaging the surrounding tissues, caused by inherited diseases like the polycystic kidney disease. Malformations in the mother’s womb during pregnancy, leading to narrowing and prevention of normal flow of urine resulting into backflow. Analgesic Nephropathy, another cause of chronic kidney disease, which is further caused by the use of analgesics like ibuprofen and acetaminophen.
Extensive research has determined that chronic kidney disease prevails in almost 16.8% of all adults above the age of 20 years.


The tests to be performed for the diagnosis of chronic kidney disease include blood tests and urinalysis, in which urine samples, collected for 24 consecutive hours, are analyzed to understand the functioning of the kidneys,.
Kidneys should always be monitored for proper functioning, and if any detection is made for chronic kidney disease, immediate treatment should be imparted reducing any life threat.
Obesity-Related Diseases - Welcome to Obesity in AmericaObesity and Type 2 Diabetes More than 80 percent of people with Type 2 diabetes, the most common form of the disease, are obese or overweight.
Obesity and diabetes induce secondary diseases with various pathophysiologic states including cardiovascular disease, neural disturbance, kidney disease, cancer and osteoporosis.
The incidence of metabolic disease, including type 2 diabetes with obesity, is increased to epidemic levels [1,2]. The pluripotency of mesenchymal stem cells is well known, and their ability to differentiate into osteoblasts, adipocytes, chondrocytes and myoblasts has been described extensively [7-14]. Bone marrow mesenchymal stem cells are multipotent cells, which among other cell lineages, give rise to adipocytes and osteoblasts. Disturbance of these factors may play an important role in pathophysiologic conditions of obesity and diabetes. Bone homeostasis, which maintains bone mass, is skillfully regulated through a delicate balance between osteoblastic bone formation and osteoclastic bone resorption [25-27].
Osteoporosis is a disease characterized by loss in bone density and bone strength and deterioration of bone microarchitecture, resulting in increased risk for bone fractures. It has been estimated that osteoporosis affects at least 200 million women worldwide, one third of women aged between 60 and 70 years and two thirds over 80 years [28,29]. We found that zinc acexamate reveals a potential anabolic effect on bone and that prevents bone loss in type 1 diabetic model rats induced by streptozotocin (STZ) [52,53]. Zinc acexamate, β-cryptoxanthin and p-hydroxycinnamic acid (HCA) stimulates osteoblastic bone formation and suppresses osteoclastin bone resorption, thereby increasing bone mass. The flavonoid p-hydroxycinnamic acid is an intermediate-metabolic substance in plant and fruits, and it is synthesized from tyrosine.
Bioactive flavonoid p-hydroxycinnamic acid, a novel osteogenic factor, may reveal preventive and therapeutic effects on osteoporosis associated with obese type 2 diabetes. These factors may be a useful tool in the prevention and improvement of diabetic osteoporosis, and development as new drugs will be expected in clinical aspects. This study was also supported by the Foundation for Biomedical Research on Bone Health and Nutrients, Japan.
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Ridges in finger nails indicate a medical problem like respiratory disorder, anaemia, iron deficiency or thyroid disease. A special type of horizontal ridges is called Beau’s lines and often indicates an underlying illness. Kidneys also help in regulation of various mineral levels like, sodium, calcium and potassium, in the human body. In order to test creatinin and urea in the blood, serum test and Blood Urea Nitrogen are the most commonly performed blood tests. Obesity increases the risk of developing a very large number of diseases, including: Type 2 (adult-onset) diabetes High blood pressure (hypertension) Stroke (cerebrovascular accident or CVA) Heart attack (myocardial infarction or MI) Heart failure (congestive heart failure) Cancer (certain forms such as cancer of the prostate and cancer of the colon and rectum) Gallstones and gall bladder disease (cholecystitis) Gout and gouty arthritis Osteoarthritis (degenerative arthritis) of the knees, hips, and the lower back Sleep apnea (failure to breath normally during sleep, lowering blood oxygen) Pickwickian syndrome (obesity, red face, underventilation, and drowsiness). Bone homeostasis is maintained through a delicate balance between osteoblastic bone formation and osteoclastic bone resorption. Obesity and diabetes induce secondary diseases with various pathophysiologic states, which are important in clinical aspects including cardiovascular disease, neural disturbance, kidney disease, cancer and osteoporosis [3,4]. There is an inverse relationship between differentiation of mesenchymal stem cells to osteoblasts and adipocytes.
We found that some functional food chemical factors, novel osteogenic factors, reveal improvement effects on diabetic conditions associated with osteoporosis using animal models.
Bone marrow mesenchymal stem cells are multipotent stromal cells, which among other cell lineages, that can differentiate into a variety of cell types including osteoblasts (bone cells), chondrocytes (cartilage cells), myoblasts (heart cells) and adipocytes (fat cells) [5,6]. Osteoporosis and obesity are now thought to be closely related and to share several features [5,6].
More recently, regucalcin, which is a suppressor protein of intracellular signaling systems, has been proposed to be a key molecule in obesity and diabetes associated with osteoporosis [23]. Osteoblasts are differentiated from bone marrow mesenchymal stem cells and stimulate bone formation and calcification.
The most dramatic expression of osteoporosis is represented by fractures of the proximal femur for which the number increases as the population ages [20].
There is also a lack of complete β-cell failure in the model, indicating that diabetes is not very severe [41]. Novel analogues, which are synthesized from bioactive chemicals derived from food factors, may be developed as new drugs that reveal potent-osteogenic effects for the treatment of osteolysis, which is induced in various diseases including inflammation, obesity and diabetes. Among cinnamic acid and its related compounds (cinnamic acid, p-hydroxycinnamic acid, ferulic acid, caffeic acid and 3, 4-dimethoxycinnamic acid), p-hydroxycinnamic acid has been shown to have specific-anabolic effects on bone in vitro [56]. While the vertical ridges in the finger nails do not indicate a medical problem and these become prominent with the age. But the normal functioning of this organ is hampered by the occurrence of a disease named chronic kidney disease, which results into gradual and permanent loss of functioning of the kidneys. Blood tests also help in testing of electrolyte levels and acid-base balance along with blood cell counts, thus monitoring the functioning of the kidneys. Aging and numerous pathological processes induce decrease in osteoblastic bone formation and increase in osteoclastic bone resorption, leading to osteoporosis with decrease in bone mass.
This review has been written to outline our recent advances that have been made concerning preventive effects of novel osteogenic factors on bone loss that is induced in type 1 diabetes. One of shared features for obesity with osteoporosis is that osteoblasts and adipocytes differentiate from a common precursor cell in the bone marrow mesenchymal stem cells. In addition, regucalcin has been demonstrated to stimulate adipogenesis in mouse bone marrow cell culture in vitro [24], suggesting an involvement as a stimulatory factor in adipogenesis.
Osteoporosis is a common metabolic disease and generally affects people at an advanced age and suffering from other chronic diseases. Body weight continues to increase with age, but obesity in these mice is less severe than some other diabetic models [49].
Development of osteogenic factors, which target the differentiation of bone marrow mesenchymal stem cells, may be importance in biomedical osteoporosis treatment. Bone loss in the femoral- metaphyseal tissues induced by STZ administration is shown in Figure 2. Administration of STZ caused a significant decrease in body weight and a significant increase in serum glucose, triglyceride, and calcium concentrations, indicating a diabetic state [55]. HCA was found to suppress adipogenesis from bone marrow mesenchymal stem cells, suggesting its preventive effects on obesity.


Bone mineral density was dramatically decreased in the femoral-metaphyseal tissues of rats treated with streptozotocin that causes type 1 diabetes.
Osteoblasts and adipocytes differentiate from a common precursor cell in the bone marrow mesenchymal stem cells. The incidence of metabolic disease including obesity and obese type 2 diabetes has increased to epidemic levels in recent years [2]. Insulin, which is secreted by feeding, stimulates adipogenesis from bone marrow mesenchymal stem cells.
Secondary causes of osteoporosis including obesity and diabetes are associated with bone marrow adiposity that greatly produces TNF-α [4,5]. Thus findings may support the view that osteoporosis are implicated with obesity and diabetes. Physiologic process of bone turnover through these bone cells underpins development and maintenance of the skeletal system.
According to a recent World Health Organization report, osteoporosis has become a global health problem with a disease incidence and mortality rate similar to that of cardiovascular diseases, diabetes and cancer [3,4]. Lower trabecular bone volumes are primary the result of increased osteoclast resorption as indicated by serum biomarkers and histomorphotometry [35-37], though bone formation is also decreased [38]. Hyperphagia, insulin resistance and hyperinsulinemia are all evident at 3 to 4 weeks of age, with obesity evident by 4 weeks [40].
Increased plasma triglycerides, cholesterol, and fatty acid levels are noticeable from 4 to 8 weeks of age [49]. Administration of STZ caused a significant increase in serum glucose, triglyceride and calcium concentrations and a significant decrease in body weight, serum zinc and inorganic phosphorus concentrations [52,53].
These alterations were prevented by the administration of β-cryptoxanthin for 14 days.
Oral administration of p-hydroxycinnamic acid was found to reveal preventive and restorative effects on hyperglycemia, hyperlipidemia and bone loss in type 1 diabetic rats induced by treatment with STZ in vivo [59], demonstrating that this factor reveals preventive and restorative effects on diabetic states. Obesity and osteoporosis are now thought to be closely related and to share several features. Bone remodeling and modeling underpin development and maintenance of the skeletal system [25]. Bone mass is dramatically reduced after menopause, which depresses secretion of ovarian hormone (estrogen) in women [20]. Interestingly, recent data indicate that whereas body weight and fasting glucose levels can return to normal after a return to a normal diet, trabecular bone loss prior to skeletal maturity may not be recoverable without some other types of intervention [34]. These factors were found to reveal preventive effects on diabetic condition and bone loss that are induced in animal models for type 1 diabetes. Moreover, calcium content, alkaline phosphatase activity and deoxyribonucleic acid (DNA) content in the femoral-diaphyseal and -metaphyseal tissues were significantly reduced in diabetic rats [52,53]. Administration of β-cryptoxanthin to normal rats for 14 days did not have a significant effect on body weight or on serum glucose, triglyceride, and calcium concentrations [55].
The fourth stage includes severe reduction in kidney function finally leading to kidney failure in the fifth and final stage. Bone modeling is responsible for growth and mechanically induced adaptation of bone, and it requires that the processes of bone formation and bone removal (resorption). The potential implications of those results are obvious considering the childhood obesity problem in the United States and other countries [30]. Other characteristics of the TallyHo mouse include enlarged pancreatic islets, hyperleptinemia, and poor wound healing [48,49]. The change in these serum and bone components of STZ-diabetic rats was found to improve after the oral administration of zinc acexamate. Calcium content, alkaline phosphatase activity, and DNA content in the femoral-diaphyseal and -metaphyseal tissues were significantly decreased in STZ-diabetic rats [55]. STZ administration caused a significant decrease in body weight and a significant increase in serum glucose, triglyceride, and calcium levels, indicating a diabetic state. Chronic kidney disease, having a prevalence of 39.4% among individuals above the age group of 60 years, can be detected by various types of symptoms, some of which are as follows.
Differentiation of bone marrow mesenchymal stem cells may be involved in the development of osteoporosis. Investigations of the skeletal phenotype in TallyHo mice have utilized two different control strains [47,50].
This preventive effect was also observed by the administration of zinc acexamate for 7 days [53]. In Western societies, mean body weight has increased dramatically in older people, and a similar trend exists in Asia. Postmenopausal osteoporosis is the archetypal osteoporotic condition in women after menopause and leads to bone destruction through complex and diverse metabolic and biochemical changes. This study demonstrates that the oral administration of zinc acexamate has preventive effects on diabetic condition and bone loss in type 1 diabetes in vivo.
Administration of β-cryptoxanthin to normal rats for 14 days caused a significant increase in calcium content, alkaline phosphatase activity, and DNA content in the femoral-diaphyseal and -metaphyseal tissues [55]. Calcium content in the femoral-diaphyseal and -metaphyseal tissues was significantly decreased in STZ-diabetic rats [59]. This mouse also have lower bone mass and markedly reduced bone formation in vertebrate and long bones compared to wild-type controls, and this deficiency can be corrected with leptin treatment [30, 42-45]. Thus, β-cryptoxanthin was found to reveal preventive effects on diabetic condition and bone loss in type 1 diabetic model rats. Such functional food factors may improve bone loss implicated with type 1diabetes and obese type 2 diabetes.
Alkaline phosphatase activity and DNA content in the diaphyseal and metaphyseal tissues was decreased in STZ-diabetic rats [59]. Devlin et al., using SWR mice as controls, showed that despite their greater body weight male TallyHo mice have reduced total body BMD as well as lowest trabecular bone volume at the distal femur. These decreases in STZ-diabetic rats were prevented after the administration of p-hydroxycinnamic acid [59]. Femoral three-point bending showed that male TallyHo mice have a higher maximum load but less postyield deformation than SWR control [50]. Thus, intake of p-hydroxycinnamic acid was found to reveal preventive effects on bone loss in type 1 diabetic model animals and that reveals partial restrative effects on serum biochemical findings in the diabetic state.



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