Metformin

General Information about Metformin

Aside from its approved use within the administration of diabetes, metformin has additionally been shown to be effective within the treatment of polycystic ovary syndrome (PCOS). PCOS is a hormonal dysfunction that impacts many ladies of reproductive age. It is characterized by excessive ranges of male hormones, insulin resistance, and irregular intervals. Metformin can help regulate the menstrual cycle, improve insulin sensitivity, and cut back the levels of male hormones in girls with PCOS.

Metformin, additionally known by its brand name Glucophage, is an oral medicine commonly used to treat kind 2 diabetes. It belongs to the category of medication often identified as biguanides, which work by lowering the amount of sugar produced by the liver and lowering the absorption of sugar within the intestines. Metformin is also used within the treatment of polycystic ovary syndrome (PCOS) and has been shown to have potential benefits in other circumstances such as weight problems and cardiovascular ailments.

Metformin works by concentrating on the primary drawback in type 2 diabetes - high blood sugar levels. It does this in a quantity of methods. Firstly, it reduces the quantity of glucose produced by the liver. Normally, the liver produces glucose, particularly in periods of fasting or in response to emphasize. However, in people with diabetes, the liver produces extra glucose even when it is not needed. Metformin reduces this production, serving to to lower blood sugar ranges.

In conclusion, metformin is an effective and widely used medicine for the treatment of sort 2 diabetes and PCOS. It works by lowering the amount of glucose produced by the liver, enhancing insulin sensitivity, and decreasing the absorption of sugar in the intestines. Additionally, it could produce other well being benefits such as weight loss and cardiovascular safety. As with any medication, it is necessary to observe your physician's instructions and report any side effects to ensure safe and efficient remedy.

Type 2 diabetes is a chronic condition characterised by high ranges of sugar (glucose) in the blood. This happens when the physique either doesn't produce sufficient insulin or doesn't use it effectively. Insulin is a hormone that helps regulate the amount of glucose in the blood. In individuals with kind 2 diabetes, the pancreas may produce enough insulin, however the physique's cells don't reply to it properly, resulting in high blood sugar ranges.

Metformin is normally taken orally within the form of tablets and should be taken with meals to reduce the chance of stomach upset. The dosage and frequency of metformin intake will depend upon the affected person's needs, other medical situations, and response to the medication. It is typically started at a low dose and gradually increased to attain the desired results.

Like any medicine, metformin can cause unwanted effects. The most common unwanted side effects embrace nausea, vomiting, abdomen upset, and diarrhea. These side effects are usually gentle and go away as the body adjusts to the medicine. Other much less frequent unwanted side effects embrace complications, dizziness, and sweating. In rare cases, metformin may cause a severe condition called lactic acidosis, so you will want to search medical consideration if you experience symptoms such as muscle ache, weakness, or issue breathing whereas taking this medicine.

Metformin additionally has a couple of other advantages. It has been proven to reduce the absorption of sugar in the intestines, resulting in decrease blood sugar levels. It can also assist to reduce urge for food, leading to weight loss, which is beneficial for people with obesity and diabetes. Additionally, this treatment could have some cardiovascular advantages, such as lowering the risk of heart attack and stroke in people with diabetes.

Secondly, metformin improves the physique's sensitivity to insulin. Insulin resistance is a serious problem in folks with sort 2 diabetes, the place the body's cells are not able to reply correctly to insulin. This ends in excessive blood sugar ranges. Metformin works by improving the cells' response to insulin, making it simpler for insulin to do its job and regulate blood sugar ranges.

Chapter 82 Female Physiology Before Pregnancy and Female Hormones Effect of Estrogens on the Fallopian Tubes diabetes type 1 zelfzorg purchase metformin without prescription. They cause the glandular tissues of this lining to proliferate, and especially important, they cause the number of ciliated epithelial cells that line the fallopian tubes to increase. These cilia always beat toward the uterus, which helps propel the fertilized ovum in that direction. The primordial bone fracture, especially fracture of the vertebrae, many postmenopausal women are treated prophylactically with estrogen replacement to prevent the osteoporotic effects. In fact, under the influence of appropriate hormones, the masculine breast during the first 2 decades of life can develop sufficiently to produce milk in the same manner as the female breast. Estrogens cause (1) development of the stromal tissues of the breasts, (2) growth of an extensive ductile system, and (3) deposition of fat in the breasts. The lobules and alveoli of the breast develop to a slight extent under the influence of estrogens alone, but it is progesterone and prolactin that ultimately complete the growth and function of these structures. In summary, the estrogens initiate growth of the breasts and of the milk-producing apparatus. They are also responsible for the characteristic growth and external appearance of the mature female breast. However, they do not complete the job of converting the breasts into milkproducing organs. Estrogens inhibit gens cause a slight increase in total body protein, which is evidenced by a slight positive nitrogen balance when estrogens are administered. This effect mainly results from the growthpromoting effect of estrogen on the sexual organs, the bones, and a few other tissues of the body. The enhanced protein deposition caused by testosterone is much more general and much more powerful than that caused by estrogens. Estrogens increase the whole-body metabolic rate slightly, but only about one-third as much as the increase caused by testosterone. Estrogens also cause deposition of increased quantities of fat in the subcutaneous tissues. As a result, the percentage of body fat in females is considerably greater than that in the males whose bodies contain more protein. In addition to deposition of fat in the breasts and subcutaneous tissues, estrogens cause deposition of fat in the buttocks and thighs, which is characteristic of the feminine figure. As discussed in Chapter 80, at least part of this effect is due to stimulation of osteoprotegerin, which is also called osteoclastogenesis inhibitory factor, a cytokine that inhibits bone resorption. At puberty, when the female enters her reproductive years, her growth in height becomes rapid for several years. However, estrogens also cause uniting of the epiphyses with the shafts of the long bones. This effect of estrogen in the female is much stronger than the similar effect of testosterone in the male. As a result, growth of the female usually ceases several years earlier than growth of the male. A female eunuch who is devoid of estrogen production usually grows several inches taller than a normal mature female because her epiphyses do not unite at the normal time. After menopause, almost no estro- trogens do not greatly affect hair distribution. Androgens formed in increased quantities by the female adrenal glands after puberty are mainly responsible for this development of hair. Estrogens cause the skin to develop a texture that is soft and usually smooth, but even so, the skin of a woman is thicker than that of a child or a castrated female. Estrogens also cause the skin to become more vascular, which is often associated with increased warmth of the skin and greater bleeding of cut surfaces than is observed in men. The chemi- cal similarity of estrogenic hormones to adrenocortical hormones has been discussed previously. Estrogens, like aldosterone and some other adrenocortical hormones, cause sodium and water retention by the kidney tubules. This effect of estrogens is normally slight and rarely of significance, but during pregnancy the tremendous formation of estrogens by the placenta may contribute to body fluid retention, as discussed in Chapter 83. This estrogen deficiency leads to (1) increased osteoclastic activity in the bones, (2) decreased bone matrix, and (3) decreased deposition of bone calcium and phosphate. In some women this effect is extremely severe, and the resulting condition is called osteoporosis, described in Chapter 80. A major function of progesterone is to promote secretory changes in the uterine endometrium during the latter half of the monthly female sexual cycle, thus preparing the uterus for implantation of the fertilized ovum. In addition to this effect on the endometrium, progesterone decreases the frequency and intensity of uterine contractions, thereby helping to prevent expulsion of the implanted ovum. Proliferative Phase (Estrogen Phase) of the Endometrial Cycle Occurs Before Ovulation. These secretions are necessary for nutrition of the fertilized, dividing ovum as it traverses the fallopian tube before implantation. Progesterone promotes development of the lobules and alveoli of the breasts, causing the alveolar cells to proliferate, enlarge, and become secretory. However, progesterone does not cause the alveoli to secrete milk; as discussed in Chapter 83, milk is secreted only after the prepared breast is further stimulated by prolactin from the anterior pituitary gland.

As explained in Chapter 68 us diabetes prevention buy metformin 850 mg on line, this conversion occurs during the normal degradation of glucose by the glycolytic system. Because fatty acids are actually large polymers of acetic acid, it is easy to understand how acetyl-CoA can be converted into fatty acids. However, the synthesis of fatty acids from acetyl-CoA is not achieved by simply reversing the oxidative degradation described earlier. Combination of Fatty Acids With -Glycerophosphate to Form Triglycerides Once the synthesized fatty acid chains have grown to contain 14 to 18 carbon atoms, they bind with glycerol to form triglycerides. The enzymes that cause this conversion are highly specific for fatty acids, with chain lengths of 14 carbon atoms or greater, a factor that controls the physical quality of the triglycerides stored in the body. During triglyceride synthesis, only about 15% of the original energy in the glucose is lost in the form of heat; the remaining 85% is transferred to the stored triglycerides. The ability of the different cells of the body to store carbohydrates in the form of glycogen is generally slight; a maximum of only a few hundred grams of glycogen can be stored in the liver, the skeletal muscles, and all other tissues of the body put together. Therefore, fat synthesis provides a means by which the energy of excess ingested carbohydrates (and proteins) can be stored for later use. Indeed, the average person has almost 150 times as much energy stored in the form of fat as stored in the form of carbohydrate. Each gram of fat contains almost two and a half times the calories of energy contained by each gram of glycogen. Therefore, for a given weight gain, a person can store several times as much energy in the form of fat as in the form of carbohydrate, which is exceedingly important when an animal must be highly motile to survive. When insufficient insulin is available, Synthesis of Triglycerides From Proteins Many amino acids can be converted into acetyl-CoA, as discussed in Chapter 70. Therefore, when people have more proteins in their diets than their tissues can use as proteins, a large share of the excess is stored as fat. Regulation of Energy Release From Triglycerides Carbohydrates Are Preferred Over Fats for Energy When Excess Carbohydrates Are Available. Second, lack of glucose in the fat cells greatly reduces the availability of -glycerophosphate, which also makes it difficult for the tissues to form triglycerides. First, fats in adipose tissue cells are present in two forms: stored triglycerides and small quantities of free fatty acids. When excess -glycerophosphate is present (which occurs when excess carbohydrates are available), the excess -glycerophosphate binds the free fatty acids in the form of stored triglycerides. As a result, the equilibrium between free fatty acids and triglycerides shifts toward the stored triglycerides; consequently, only minute quantities of fatty acids are available to be used for energy. Because -glycerophosphate is an important product of glucose metabolism, the availability of large amounts of glucose automatically inhibits the use of fatty acids for energy. Second, when carbohydrates are available in excess, fatty acids are synthesized more rapidly than they are degraded. This effect is caused partially by the large quantities of acetyl-CoA formed from the carbohydrates and by the low concentration of free fatty acids in the adipose tissue, thus creating conditions appropriate for the conversion of acetyl-CoA into fatty acids. An even more important effect that promotes conversion of carbohydrates to fats is the following: the first step, which is the rate-limiting step, in the synthesis of fatty acids is carboxylation of acetyl-CoA to form malonyl-CoA. The rate of this reaction is controlled primarily by the enzyme acetyl-CoA carboxylase, the activity of which is accelerated in the presence of intermediates of the citric acid cycle. When excess carbohydrates are being used, these intermediates increase, automatically causing increased synthesis of fatty acids. Thus, an excess of carbohydrates in the diet not only acts as a fat-sparer but also increases fat stores. In fact, all the excess carbohydrates not used for energy or stored in the small glycogen deposits of the body are converted to fat for storage. All the fat-sparing effects of carbohydrates are lost and actually reversed when carbohydrates are not available. The equilibrium shifts in the opposite direction, and fat is mobilized from adipose cells and used for energy in place of carbohydrates. Also important are several hormonal changes that take place to promote rapid fatty acid mobilization from adipose tissue. Among the most important of these hormonal changes is a marked decrease in pancreatic secretion of insulin caused by the absence of carbohydrates. This decrease in insulin not only reduces the rate of glucose utilization by the tissues but also decreases fat storage, which further shifts the equilibrium in favor of fat metabolism in place of carbohydrates. At least seven of the hormones secreted by the endocrine glands have significant effects on fat utilization. Some important hormonal effects on fat metabolism, in addition to lack of insulin, are noted here. Probably the most dramatic increase that occurs in fat utilization is that observed during heavy exercise. This increase results almost entirely from release of epinephrine and norepinephrine by the adrenal medullae during exercise, as a result of sympathetic stimulation. These two hormones directly activate hormone-sensitive triglyceride lipase, which is present in abundance in the fat cells, and this activation causes rapid breakdown of triglycerides and mobilization of fatty acids. Sometimes the free fatty acid concentration in the blood of an exercising person rises as much as eightfold, and the use of these fatty acids by the muscles for energy is correspondingly increased. Other types of stress that activate the sympathetic nervous system can also increase fatty acid mobilization and utilization in a similar manner. Thyroid hormone indirectly causes rapid mobilization of fat by increasing overall rate of energy metabolism in all cells of the body under the influence of this hormone. The resulting reduction in acetyl-CoA and other intermediates of both fat and carbohydrate metabolism in the cells is a stimulus to fat mobilization.

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However blood sugar problems symptoms order metformin 850 mg on line, it has been difficult to determine the precise role of genetics in contributing to obesity because family members generally share many of the same eating habits and physical activity patterns. Current evidence suggests that 20% to 25% of cases of obesity may be caused by genetic factors. Genes can contribute to obesity by causing abnormalities of (1) one or more of the pathways that regulate the feeding centers and (2) energy expenditure and fat storage. All these monogenic forms of obesity account for only a very small percentage of obesity. Possible interactions of adverse intrauterine environment, epigenetic, and development factors in programming increased risk for obesity in multiple generations. The intrauterine environment of an obese mother may influence development of the embryo, including epigenetic effects on germ cells that become sperm or oocytes. The sperm and oocytes of male and female parents may also be altered by epigenetic changes that occur secondary to obesity, thus predisposing subsequent generations to increased risk for developing obesity. It is likely that many gene variations interact with environmental factors to influence the amount and distribution of body fat. Parents May Contribute to Obesity in Their Offspring Through Epigenetic Mechanisms. However, additional research is needed to further assess the impact of germ cell epigenetics in predisposing human beings to become obese. We previously pointed out that lesions in the ventromedial nuclei of the hypothalamus cause an animal to eat excessively and become obese. Progressive obesity often develops in people with hypophysial tumors that encroach on the hypothalamus, demonstrating that obesity in human beings, too, can result from damage to the hypothalamus. Although hypothalamic damage is almost never found in obese people, it is possible that the functional organization of the hypothalamic or other neurogenic feeding centers in obese individuals is different from that in persons who are not obese. Also, abnormalities of neurotransmitters or receptor mechanisms may be present in the neural pathways of the hypothalamus that control feeding. In support of this theory, an obese person who has reduced to normal weight by strict dietary measures usually develops intense hunger that is demonstrably far greater than that of a normal person. Also, diet-induced weight loss in obese people is associated with substantial "metabolic adaptation," which refers to slowing of metabolic rate and energy expenditure by greater amounts than predicted for the change in body composition caused by loss of fat and muscle mass. Studies in experimental animals also indicate that when food intake is restricted in obese animals, marked neurotransmitter changes occur in the hypothalamus that greatly increase hunger and oppose weight loss. Studies in humans have confirmed that diet-induced weight loss is accompanied by increased levels of hunger-stimulating hormones. These hormonal changes persist for at least 1 year after the weight loss, perhaps explaining, in part, why it is so difficult for most people to achieve sustained weight loss by dieting alone. Treatment of Obesity Treatment of obesity depends on decreasing energy input below energy expenditure and creating a sustained negative energy balance until the desired weight loss is achieved. Typically, such an energy deficit, if it can be achieved and sustained, will cause a weight loss of about 1 to 2 pounds per week, or about a 10% weight loss after 6 months. However, it is important to prevent vitamin deficiencies during the dieting period. For most people, increasing physical activity is also an important component of successful long-term reductions in adiposity. Almost all current guidelines for treatment of obesity therefore recommend lifestyle modifications that include increased physical activity combined with a reduction in caloric intake. Various drugs for decreasing the degree of hunger have been used in obesity treatment. The most widely used drugs are amphetamines (or amphetamine derivatives), which directly inhibit the feeding centers in the brain. One drug for treating obesity combines phentermine, a sympathomimetic that reduces food intake and increases energy expenditure, with topiramate, which has been used as an anticonvulsant drug. The danger in using sympathomimetic drugs is that they simultaneously overexcite the sympathetic nervous system and raise blood pressure. A commonly used sympathomimetic drug, sibutramine, was removed from the United States market in 2010 for obesity treatment because clinical studies demonstrated that it increased the risk for myocardial infarction and stroke. For example, orlistat, a lipase inhibitor, reduces the intestinal digestion of fat, causing a portion of the ingested fat to be lost in the feces and therefore reducing energy absorption. However, fecal fat loss may cause unpleasant gastrointestinal side effects, as well as loss of fat-soluble vitamins in the feces. All of the drugs that are currently approved for long-term treatment of obesity produce modest weight loss, usually only 5% to 10%, or less in some cases, and are most effective when used in combination with lifestyle modifications aimed at increased physical activity and a healthier diet. Gastric bypass surgery involves construction of a small pouch in the proximal part of the stomach that is then connected to the jejunum with a section of small bowel of varying lengths; the pouch is separated from the remaining part of the stomach with staples. Gastric banding surgery involves placing an adjustable band around the stomach near its upper end; this procedure also creates a small stomach pouch that restricts the amount of food that can be eaten at each meal. A third procedure that is now becoming more 886 Chapter 72 Dietary Balances; Regulation of Feeding; Obesity and Starvation; Vitamins and Minerals widely used is vertical sleeve gastrectomy, which removes a large part of the stomach with the remaining part stapled back together. These surgical procedures generally produce substantial weight loss in obese patients. The gastric bypass and vertical sleeve procedures often lead to rapid remission of type 2 diabetes mellitus and hypertension, important complications of obesity, even before substantial weight loss has occurred. These procedures are major operations, however, and their long-term effects on overall health and mortality are still uncertain. Inanition, Anorexia, and Cachexia Inanition is the opposite of obesity and is characterized by extreme weight loss.