Home Remedies for Hyperglycemia

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Protracted Hyperglycemia Had A Detrimental Effect On pCell Neogenesis

The observation that IN injected at day 1 post-SZ promoted p-cell neogenesis raised the question as to whether the hormone would have a similar effect after a protracted hyperglycemic period. This possibility is of obvious importance because it could determine the outcome in patients with a long history of diabetes. We found that an extended period of hyperglycemia did not inhibit the appearance of NBCs (54). However, the presence of these cells was transient and they quickly disappeared from the islets (Fig. 7). These observations suggest that

General Characteristics

The foregoing data indicate that we may anticipate an increase in the worldwide prevalence of DM. The focus has been and remains on treatment of hyperglycemia and the vascular complications of long-term diabetes. Using epidemiological data and historical perspectives, we are beginning to develop better programs aimed at early intervention and prevention.

Therapy for Diabetes Mellitus

Diabetes mellitus is a metabolic syndrome with a diversity of etiologies, clinical presentations, and outcomes. It is characterized by insulinopenia, fasting or postprandial hyperglycemia, and insulin resistance. Type 1 diabetes mellitus, referred to as juvenile or insulin-dependent diabetes mellitus is typically characterized by insulinopenia, hyperglycemia, and secondary insulin resistance (14). Type 2 diabetes mellitus, referred to as adult onset or non-insulin-dependent diabetes mellitus, is characterized by hyperglycemia and varying degrees of primary insulin resistance with elevated plasma insulin concentrations, but a decreased insulin response to challenge by a secretagogue (15). Diabetes mellitus need not be overt and grossly hyperglycemic to induce detrimental metabolic changes. A growing body of evidence suggests that there are detrimental consequences to normal physical challenges such as aging, which may be inherently linked to alterations in body composition. Such...

Metabolic and endocrine effects

Both acute and chronic sleep deprivation impair glucose tolerance during wakefulness. Sleep deprivation alters glucose uptake in the cell membrane and cytoplasm. It also reduces the initial insulin response to glucose, probably because of increased sympathetic activity which regulates pancreatic beta cell function and insulin release. There may also be effects on the later increase in plasma insulin because of impaired synthesis of insulin in response to a raised blood glucose level.

Hormonal Influences on Homeostatic Mechanisms

Insulin is secreted in response to increased levels of blood glucose. This may occur after a meal or if glucagon is released and circulating glucose increases. Increased insulin levels cause glucose to enter cells more quickly where it is either used for fuel or, in the case of fat cells, is converted to triglycerides and stored. Blood glucose levels then drop. Data support the contention that hunger and eating are initiated when nutrient levels, especially glucose levels, decrease in the blood. Thus a high insulin level could lead to hunger because it decreases blood glucose. Furthermore, insulin levels can be influenced by the hypothalamus, and disruption of this control by hypothalamic lesions may explain some of the effects of such lesions on eating behavior and body weight.

Islet Cell Neogenesis In Adult Mice

A series of experiments were performed to demonstrate that the new p cells visualized after SZ treatment were newly differentiated IN+ cells rather than old p cells that evaded the effect of the toxin. Because chronic hyperglycemia results in p-cell degranulation and decreased levels of insulin, it could be argued that acute hyperglycemia, such as that found in mice 1 day after the injection of the drug (at 1 day post-SZ), had similar effect. If old p cells survived the effect of the toxin, these cells would become degranulated at 1 day post-SZ, thus evading detection by immunohistochemical staining. After the reestablishment of normoglycemia by exogenous insulin injection, these cells would have restored the intracellular insulin concentration to normal levels and would stain again for insulin. To address this issue, we stained islets from 1 day post-SZ mice with aromatic L-amino acid decarboxylase (AADC), a neuronal enzyme localized in the cytoplasm of all the endocrine cells of the...

PCell Neogenesis Is Curtailed In Islets Of Nod Mice

Occurring in type I diabetes in humans (reviewed in ref. 55). In NOD mice, the inflammatory insulinitis leads to diabetes between 13 and 30 weeks of age (55). We examined islets of mutant 1- to 4-month-old NOD mice for the presence of two putative P-precursor cells, the PDX-1 SOM+ and the Glut2 GLU+ cells. All 1-month-old NOD mice examined were normoglycemic and contained islets that had an apparent normal morphology, whereas 2-month-old NOD mice, which were still normoglycemic, had islets with mild to severe insulinitis. At 4 months, one of the NOD mice analyzed had mild hyperglycemia (blood glucose 156 mg dL), whereas the other three mice were severely hyperglycemic (blood glucose 400 mg dL). Pancreata of both normoglycemic and hyperglycemic 4-month-old NOD mice contained islets with different degrees of lymphocyte infiltration and p-cell number. As expected, the number of affected islets was greater in hyperglycemic animals. The percentage of SOM+PDX-1+ cells was always higher in...

Extrapancreatic stem cells

Although important improvements have been performed in this area, several issues need to be still resolved with respect to the use of pancreatic precursors or ASCs from extra-pancreatic tissues. It is clear that adult -cells have a limited capacity to expand and differentiate and pancreatic ductal tissue has inadequate insulin content to restore hyperglycemia in transplantation protocols. Therefore, the search for strategies to increase -cell proliferation in vitro or insulin production from ductal tissue will be instrumental in taking more advantage of pancreases from cadaveric donors. On the other hand, transdifferentiation from extra-pancreatic tissues requires further study to clarify certain caveats, including genetic reprogramming mediated by either cell fusion events or extracellular signals generated after implantation in specific niches.

Selection of Insulin Producing Cells From Spontaneously Differentiating ES Cell Cultures

It has been shown previously that genetic selection against heterologous cell types generated during the course of spontaneous ES cell differentiation can result in enrichment for the cell types of interest. For example, this approach has been used to obtain purified cardiomyocyte- and neural-like cells from mouse ES cell cultures (21,22). Soria and coworkers used a similar strategy to select insulin-producing cells from spontaneously differentiating mouse ES cells (43). They introduced into the ES cells a plasmid conferring resistance to two antibiotics. The first antibiotic-resistance gene was under control of a constitutive promoter, and the second gene was under control of an insulin promoter. During the first stage of the culture the undifferentiated ES cells were selected for resistance to the first antibiotic. This allowed generation of a stable cell line in which every cell carried the plasmid. After this step, the ES cells were transferred into differentiation medium...

The Hypothyroid Obese Individual

Hypothyroidism can cause or aggravate hypertension and high cholesterol, which are risk factors for cardiovascular disease and can also lead to atherosclerosis (clogged arteries) and congestive heart failure, discussed in Chapter 25. When type 2 diabetes is in the picture, some individuals may need to be on more intensive diabetes control and may even require insulin, since hypothyroidism can affect blood sugar control, which in turn increases the risk of heart attack and stroke.

Liver Directed Cell Therapy for Type 1 Diabetes Mellitus

Of transcription factors observed in liver cells. Moreover, in response to Pdx-1 transgene expression, cells began to express insulin in a regulated fashion, although all elements of p-cell phenotype were not reproduced (103). Nonetheless, transplantation of Pdx-1-expressing immortalized fetal human liver cells in diabetic immunotolerant mice resulted in correction of hyperglycemia.

Lowering Fat and Healthy Eating

Dietary guidelines from nutrition experts, government nutrition advisories and panels, and registered dieticians have not changed in fifty years. A good diet is a balanced diet representing all food groups, based largely on plant foods, such as fruits, vegetables, legumes, and grains (also known as carbohydrates), with a balance of calories from animal-based foods, such as meats (red meat, poultry), fish, and dairy (also known as protein and fat). Nutrition research spanning the last fifty years has only confirmed these facts. What has changed in fifty years is the terminology used to define good diet, and the bombardment of information we receive about which foods affect which physiological processes in the body, such as cholesterol levels, triglycerides, blood sugar levels, and insulin. There are also different kinds of fats and carbohydrates, which

Stem Cellderived Islets And Intervention Therapy

Despite the high profile of type 1 diabetes and the implementation of new genetic screening programs for families and newborns to identify high-risk individuals, the incidence of type 1 diabetes is increasing worldwide. Type 1 diabetes is an especially insidious disease with clinical symptoms usually not being detected until after the patient's own immune system has destroyed 90 of the total insulin-producing P-cells of the endocrine pancreas (Eisenbarth, 1986 Harris, 1999). Although routine insulin injections can provide diabetic patients with their daily insulin requirements, blood glucose excursions are common, resulting in hyperglycemic episodes. Hyperglycemia represents the major health problem for the diabetic patient, especially long term. When inadequately controlled, chronic hyperglycemia can lead to microvascular complications (e.g., retinopathy and blindness, nephropathy and renal failure, neuropathy, foot ulcers, and amputation), and macrovascular complications (e.g.,...

Niacin and Nicotinic Acid

Superphysiological doses of niacin (1.5 to 3 g daily) have been used successfully in the treatment of hypercholesterolemia, and this practice diminishes mortality by reducing a coronary artery disease risk factor. Side effects of high-dose niacin include flushing, hyperuricemia, hyperglycemia, and elevations in liver enzymes.

Autologous Hsct In Recentonset Autoimmune Type 1 Diabetes Mellitus

The possibility of autoimmune disease relapse or recurrence and benefit of relief from hyperglycemia must be balanced against the risks of autologous HSCT. The acute risk of mortality resulting from induction toxicity and infections after autologous HSCT is approximately 1-2 (43). Although the potential for durable disease remission in patients with debilitating autoimmune disease favors autologous HSCT in spite of the risk of acute mortality, recent-onset type 1 diabetes can be controlled with exogenous insulin therapy in the majority of patients. The potential benefit of autologous HSCT thus does not balance the risk of HSCT in patients with recent-onset type 1 diabetes because (1) high probabil

General Properties and Possible Metabolic Functions

Nickel supplemented in high amounts may affect glucose and lipid metabolism through affecting the action of insulin. In 1926, it was reported that nickel intensified and prolonged the hypogly-cemic action of insulin administered to dogs and rabbits.122123 About 40 years later, it was found that nickel enhanced glucose uptake, its oxidation to carbon dioxide and incorporation into fat-pad lipids in vitro, thus simulating the action of insulin.124 Nickel chloride (10 mg kg body weight) injected before streptozotocin prevented streptozotocin-induced hyperglycemia in rats.125 Long-term high nickel ingestion (200 mg L as NiCl2 in drinking water) by rats was found to increase insulin binding by their epididymal adipocytes.126 Additionally, a decreased sensitivity to the anti-lipolytic response to insulin was found in adipocytes from the rats fed high nickel. This latter effect may explain why nickel-supplemented controls fed a high 20-mg Ni kg diet had higher, while those fed a moderate 1...

Randall S Sung Jeffrey D Punch

Transplant Rectum

Insulin-dependent diabetes mellitus (IDDM, also known as type I diabetes mellitus) is an autoimmune disease resulting from destruction of the islets of Langerhans. It usually occurs in lean, young persons and is characterized by an absence of insulin secretion in response to hyperglycemia and a tendency toward ketosis. Hyperglycemia leads to deleterious secondary complications including retinopathy, neuropathy, and fll renal insufficiency.1 ' The goal of pancreatic transplantation is to restore true euglycemia. Despite advances including multiple dosing regimens, ultralong-acting insulin, and continuous infusion pumps, no regimen of exogenous insulin administration reproduces physiologic glucose control. The rationale behind maintaining euglycemia is that this is the only known means of preventing the progression of diabetic complications. In addition, the recipient of a functional vascularized pancreatic graft or functional islet cells has the benefit of freedom from dangerous...

Effect Of Spirulina On Fatty Liver

No known treatment exists for fatty liver. The widely accepted treatment goal is to eliminate the potential causes and risk factors, since fatty liver due to obesity or alcoholism is reversible. Such actions as the discontinuation of drugs or toxins, body weight control and the prescription of hyperlipidemia and hyperglycemia help to reach this goal. Many other treatments have also been tested, including ursodeoxycholic acid (UDCA), metformin, rosiglitazone,betaine,and vitamins E and C. Although more investigations are required before recommendations can be made for NAFLD patients, UDCA and metformin seem promising. UDCA is a non-toxic natural bile acid that is initially used to dissolve gallstone and is now used to reduce liver fat deposition. Metformin, an antidiabetic drug and an insulin-sensitizing agent, is potentially useful for the fatty liver caused by insulin resistance and hyperisulinemia.

Basis for Sports Nutrition Interest

There is some limited evidence that molybdenum may have insulin mimetic effects. Feeding high amounts of molybdenum (0.5-1.0 g L in water plus 1.5-2.0 g kg diet) prevented fructose-induced hyperglycemia, hyperinsulinemia and hypertension and partially prevented increased plasma triglyceride concentrations in rats.97 Treating rats with sodium molybdate (100 mg kg body weight per day) significantly reversed changes in carbohydrate metabolizing (both oxidation and storage) enzymes, and regulated blood sugar concentrations in rats with alloxan-induced diabetes.98 The doses of molybdenum used in these two studies were extremely high. The estimated dietary requirement of the rat is 150 g Mo kg, and 100-mg Mo kg diet not high in sulfur apparently is toxic because it reduced growth.99 Thus, it would be irresponsible to suggest that ingesting supra nutritional intakes of molybdenum would result in insulin-like actions that could help athletic performance.

Heat Shock Proteins in the NOD Mouse

In a later paper, Elias et al. repeated a number of elements of the experiments using human hsp 60 in place of the mycobacterial hsp 60 (48). The major difference was that immunization with hsp 60 did not reduce the incidence of IDDM but instead rapidly induced hyperglycaemia. An epitope of human hsp 60 was also identified which stimulated a T-cell response in NOD mouse. This peptide, p277, comprised amino acids 437-460 and differs by only one amino acid from mouse hsp 60, but it contains more limited sequence homology with mycobacterial hsp 65. Using the T-cell clones generated against mycobacterial hsp 65, it was found that in several cases the responses to human hsp 60 were stronger, implying that this antigen was more closely related to the P-cell target protein than mycobacterial hsp 65. Three T-cell clones responded to the peptide p277, and only these clones produced insulitis and hyperglycemia in transfer experiments. The other T-cell clones, which responded more strongly to...

Case Reports Editorials Letters to the Editor Book Reviews and Other Publication Models

I think that highest accolades go to those case reports that change what we do in practice. For example, in 2001 Muench and Carey reported a case of a 38-year-old patient with schizophrenia who suddenly developed diabetes mellitus and ketoacidosis 12 months after starting the atypical antipsy-chotic medication olanzapine. The authors note that, including their case, there have been 30 such reports in the literature. What is noteworthy, in my opinion, is that on November 10, 2003, my clinician colleagues and I received a Dear Healthcare Provider letter from a pharmaceutical manufacturer stating that, The Food and Drug Administration (FDA) has requested all manufacturers of atypical antipsychotics to include a warning regarding hyperglycemia and diabetes mellitus in their product labeling. (Muench J, Carey M. Diabetes mellitus associated with atypical antipsychotic medications new case report and review of the literature. J Am Board Fam Pract 2001 14 278-282 and Letter from Janssen...

Low Blood Sugar or Thyrotoxicosis

Low blood sugar, also known as hypoglycemia, triggers the very same adrenaline rush reaction that can occur in a panic attack. Low blood sugar can be measured, and a reading below 50 mg dl (or in Canada, 3.5 mmol L) is considered too low. But many people assume they suffer from low blood sugar even when their blood sugar levels are normal because they feel shaky and irritable when hungry, which is relieved by food. In fact, the common feature to panic attacks and true hypoglycemic attacks is a rapid activation of the adrenergic system (adrenaline release), the same system enhanced by thyrotoxicosis. In this way, thyrotoxicosis can be confused for both panic attacks and hypoglycemia. Treatment of these adrenergic symptoms by beta-blockers can relieve most of these symptoms, and correction of the underlying thyrotoxicosis relieves the rest of them.

In Vivo Differentiation Of Pancreatic Stem Cells To Islets Of Langerhans

Pax6 And Nkx2

Islets of Langerhans are compact clusters of endocrine hormone-producing cells that, for most vertebrate species, are embedded within the acinar tissue of the pancreas (Fig. 1A). These clusters have evolved a cellular organization that optimizes rapid and highly regulated responses to elevated blood glucose levels. During embryogenesis, the pancreas forms from a fusion of the dorsal and ventral primordia. These two primitive glands, which In individuals genetically predisposed to type 1 (or autoimmune) diabetes, the organization and function of the islet clusters is disrupted due to the specific destruction of the Pcell population by a progressive and relentless attack from the body's own immune system (Fig. 1B). Since pancreatic P-cells per se have a limited capacity to proliferate after post-fetal development of the islets of Langerhans, the P-cell mass is rapidly lost despite comprising more than 60 of the total islet mass. Once the autoimmune attack is completed, the inflammatory...

Streaming Pancreas Islet Cell Kinetics Zajicek G Et Al

Zalzman M, Gupta S, Giri RK, Berkovich I, Sappal BS, Karnieli O, Zern MA, Fleischer N, Efrat S. Reversal of hyperglycemia in mice by using human expandable insulin-producing cells differentiated from fetal liver progenitor cells. Proc Natl Acad Sci USA 2003 100 7253-7258. 79. Ferber S, Halkin A, Cohen H, Ber I, Einav Y, Goldberg I, Barshack I, Seijffers R, Kopolovic J, Kaiser N, Karasik A. Pancreatic and duodenal homeobox gene 1 induces expression of insulin genes in liver and ameliorates streptozotocin-induced hyper-glycemia. Nat Med 2000 6 568-572.

Allogeneic Hsct In Recentonset Autoimmune Type 1 Diabetes Mellitus

In contrast to autologous HSCT, allogeneic HSCT may cure autoimmunity, and consequently preserve remaining pancreatic islets in patients with recent-onset type 1 diabetes. The rationale for allogeneic HSCT for patients with recent-onset type 1 diabetes is based on the following observations (1) allogeneic HSCT will halt autoimmune-mediated destruction of islet p cells (2) preservation of intact islet p cells is beneficial to the patient even in the absence of full metabolic control (3) because hyperglycemia is more easily managed in patients with functional islet p cells, chronic complications are less likely to develop and (4) there is a low probability of disease relapse or recurrence after allogeneic HSCT. Allogeneic HSCT is difficult to justify in recently diagnosed patients, however, because chronic effects of hyperglycemia are unlikely to manifest before complete loss of islet p cells. In patients likely to receive maximum therapeutic benefit from allogeneic HSCT, therefore,...

The Contradictions Of Hsp 60 Autoimmunity

Autoimmunity to hsp 60 is also present regularly in diseases restricted to certain organs. We found, for example, that T-cell autoimmunity to a particular peptide epitope of hsp 60 is commonly present in mice of the NOD strain spontaneously developing insulin-dependent diabetes mellitus (IDDM) (11,12), in humans newly diagnosed as suffering from the same disease (13), and in mice of the C57BL ksj strain induced to develop IDDM by exposure to a low dose of the p-cell toxin streptozotocine (14). This peptide, designated p277 by its order number in the peptide synthesizer, is composed of the string of amino acids in positions 437-460 of the human or mouse hsp 60 sequences. A functional role of p277 immunity in IDDM also was supported by the observation that hyperglycemia and insulitis could be induced in several nondiabetic strains of

Autoimmune Type 1 Diabetes Mellitus

Type 1 diabetes is characterized by insulin deficiency secondary to progressive T-cell-mediated destruction of insulin-producing pancreatic p cells within the islets of Langerhans. Clinical therapy is supportive blood glucose is controlled by insulin injections, diet, and exercise. Nevertheless, homeostatic maintenance of blood glucose through shifting physiologic conditions is clearly unrealistic, and long-term complications of chronic hyperglycemia, including retinopathy, peripheral neuropathy, stroke, cardiovascular disease, and nephropathy, frequently develop. Although tight glycemic control delays the development of chronic complications (16), the incidence of acute, life-threatening episodes of hypoglycemia is more than three times higher with this treatment (17).

Mechanisms Mediating the Beneficial Effects of Exercise

Exercise reduces blood glucose through an increase of insulin-dependent and insulin-independent glucose transport to working muscles 13 . Exercise increases the translocation of glucose transporter 4 (GLUT 4) to the surface of muscle cells 14 . There is evidence for the presence of two distinct pools of GLUT4 in skeletal muscle, one responding to exercise and one responding to insulin 15, 16 . Muscle contraction increases the AMP ATP and creatinine phosphocrea-tinine ratios, which rapidly activate adenosine monophosphate protein kinase (AMPK), a key mediator of fatty acid oxidation 17 and glucose transport 18 in mammalian cells. During muscle contraction, AMPK appears to produce the translocation of GLUT 4 of either the insulin-dependent 16 or the insulin-independent 15 pools. In type 2 diabetic subjects, physical training increases insulin-stimulated nonoxidative glucose disposal 19,20 , presumably activating glycogen synthesis. The beneficial effects of regular physical activity on...

Nestin As A Marker Of Islet Progenitor Cells

Using the same protocol, another group (66) subsequently demonstrated that although a number of nestin-positive ES cells did form clusters that stained positively for insulin, these clusters neither accumulated insulin transcript nor showed staining with an antibody specific for C-peptide, a protein that results from the cleavage of proinsulin to insulin. In addition, many of the insulinpositive cells were positive in the TUNEL assay, suggesting that they were undergoing apoptosis. Finally, it was demonstrated that cells were capable of taking up exogenous insulin from the medium, perhaps explaining their staining patterns and their failure to reverse hyperglycemia in streptozotocin-induced diabetic animals.

Management Of Perforations And Fistulas

Poorly controlled hyperglycemia or hypercarbia limits the caloric delivery. Those with low-output fistulas require 30 to 35 kcal kg day, with 1.0 to 2.0 g protein kg body weight day. Those with high-output fistulas require more calories up to 1.5 to 2.0 times normal energy expenditure, with a protein supply of 1.5 to 2.5 g kg day.1 ' This is especially true for duodenal fistulas, with losses of gastric, duodenal, biliary, and pancreatic exocrine protein-rich secretions. Prealbumin levels should be


If you do happen to have both conditions, an overactive thyroid will often make the diabetes worse and more difficult to control with insulin. Once your thyroid condition is treated, though, you will find it easier to regain control over the diabetes. On the other hand, there are not usually any problems of glucose control directly related to hypothyroidism. If true hypoglycemia is documented by low blood sugar levels (often this is inappropriately diagnosed see Chapter 4) in people with hypothyroidism, it is important to see if the pituitary gland is abnormal, causing both hypothyroidism and loss of adrenal function (causing the low blood sugar). Autoimmune destruction of the pituitary gland, as well as pituitary tumors, might be responsible.

Mechanisms of Action

It is tempting to assume that the implanted cells, being multipotent, simply replace the missing components of the damaged tissue. However, there is increasing evidence that this may not be the only or even the primary mechanism. In some experimental conditions, paracrine effects and immune regulation of the implanted cell populations play a role in functional restoration that appears to be much greater than their structural contribution to the repair tissue.70-73 For instance, the transplantation of c-kit positive bone marrow cells in a mouse model of diabetes mellitus reduced hyperglycemia mainly by triggering regeneration of the recipient's own pancreatic cells rather than by a direct contribution of the donor's cells to the regenerated tissue.70 In another study, the administration of human cord blood-derived CD34 positive cells to immunocompromised mice subjected to experimental stroke 48 hours earlier induced neovascularisation in the ischaemic zone, thereby providing an...

Diabetes mellitus

Type 1 diabetes (T1D) accounts for up to 10 of all diabetes, and is usually diagnosed in children and adolescents, although demographics are changing, predominantly due to the emergence of Type 2 diabetes (T2D) in adolescents, most likely as a consequence of the recent epidemic of obesity in this generation.2 T1D is characterised by abnormally high blood glucose levels following autoimmune f cell destruction, and can lead to serious long-term complications including blindness, kidney failure, stroke, heart and vascular diseases.3 T1D is currently incurable, and is most commonly


The effects of these drugs are practically identical. This group of drugs is characterized by three main side effects (1) hyperuricemia, (2) hyperglycemia, and (3) irregular electrolytic balance that can be characterized by hypercalcemia, hypochloremic and metabolic alkalosis.

Property 1 Coherence

Each component endpoint must measure not just the same disease process, but the same underlying pathophysiology. When each component endpoint is measuring the progression of the same pathology, the investigator can be assured that the component endpoint is measuring the process that is best understood to excite the production of the disease's manifestations. However, the component endpoints should not be so closely related that a single patient is too likely to experience all of them. These types of component endpoints are termed coincident endpoints. If a patient experiences one of two coincident endpoints, they are likely to experience the other. In this situation, there is no real advantage in using the combined endpoint instead of one of its component endpoints. Constructing component endpoints that are too interrelated will make the combined endpoint redundant. An example of coincident endpoints would be the (1) blood sugar reductions (in mg dl) and (2) reduction in glycosylated...

Type D

Type D (Table 10.1) causes enterotoxemia in sheep,4 and is probably most prevalent in young lambs suckling heavily-lactating ewes. It is also the predominant cause of death in weaned animals up to nearly 1 year old, often in those fed rich rations in feedlots. The frequent association of enterotoxemia with upsets in the gut flora caused by an unmanaged change to a rich diet gives rise to the common name of the disease - overeating disease.91 Multiplication of the organism, production of e-toxin,92 and absorption from the gut83 lead to a toxemia with little enteritis. Peritoneal and pericardial effusions are typical.93 e-Toxin's effects on the central nervous system and other tissues result in sudden death, although some animals display dullness, opisthotonos, and convulsions before death.83'91 Hyperglycemia and glycosuria are pathognomonic,83'94 and pulpy kidney, another common name for the disease, derives from the commonly-found post mortem autolysis which rapidly occurs in...

Risk factor diabetes

Thomas Willis Diabetes

There are two main types of diabetes. Type 1 diabetes, in which the pancreas stops making insulin, accounts for 10 to 15 of cases. The majority of people with diabetes have type 2 disease, in which insulin is produced in smaller amounts than needed, or is not properly effective. This form is preventable, because it is related to physical inactivity, excess calorie intake and obesity. People with type 1 diabetes need insulin injections to lower blood sugar, but many people with type 2 do not.

The Role of Insulin

The molecular structure of the complicated protein insulin was determined in Cambridge in the 1950s at the Laboratory of Molecular Biology by Frederick Sanger in the course of his first Nobel Prize work. The physiology of insulin and the control of glucose metabolism is complex. Before active insulin is available, a non-active molecule called C-peptide must be cleaved from the parent molecular proinsulin. There is an important basal secretion of insulin, but on the intake of food, insulin granules, stored in the P cells, are released in a pulsatile manner simultaneously from a number of P cells, in amounts relating to the ambient blood glucose concentration in the islets. The timing is critical. If released too early or too late, high insulin blood levels will cause inappropriate, possibly dangerous, hypoglycemia. If not enough insulin is available at the appropriate time, normal glucose metabolism cannot take place and the blood sugar level will rise. There is a considerable reserve...

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