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Growth Hormone Diabetogenic

Biosynthetic 20-kilodalton Methionyl-human Growth Hormone Has Diabetogenic And Insulin-like Activities.

Biosynthetic 20-kilodalton Methionyl-human Growth Hormone Has Diabetogenic And Insulin-like Activities.

The anterior pituitary gland produces a 20-kilodalton (kDa) variant of human growth hormone (hGH) that differs from the predominant 22-kDa form of hGH in that amino acid residues 32-46 are deleted. Previous work has suggested that the 20-kDa variant possesses the full growth-promoting and lactogenic activities of 22-kDa hGH but lacks its intrinsic diabetogenic and insulin-like activities. In the present study, recombinant DNA techniques were used to prepare biosynthetic 20-kDa hGH, and some of the biological properties of the purified hGH variant were examined. The biosynthetic 20-kDa hGH variant was found to share the propensity for aggregation exhibited by its native counterpart. Moreover, like the native variant, biosynthetic 20-kDa hGH possessed full growth-promoting activity in the weight gain test in hypophysectomized rats. However, contrary to previous work suggesting that native 20-kDa hGH lacks diabetogenic and insulin-like activities, biosynthetic 20-kDa hGH was found to have substantial diabetogenic activity when administered chronically to ob/ob mice and to possess approximately 20% the in vitro insulin-like activity of biosynthetic 22-kDa hGH on isolated epididymal adipose tissue of hypophysectomized rats. The diabetogenic and insulin-like activities of biosynthetic 20-kDa hGH cannot be ascribed to contamination of the hormone preparation with the 22-kDa form of hGH or with other diabetogenic or insulin-like pituitary peptides. Therefore, the results strongly suggest that diabetogenic and insulin-like activities are also intrinsic properties of the 20-kDa variant of hGH. Continue reading >>

Growth Hormone (somatotropin)

Growth Hormone (somatotropin)

Growth hormone is a protein hormone of about 190 amino acids that is synthesized and secreted by cells called somatotrophs in the anterior pituitary. It is a major participant in control of several complex physiologic processes, including growth and metabolism. Growth hormone is also of considerable interest as a drug used in both humans and animals. Physiologic Effects of Growth Hormone A critical concept in understanding growth hormone activity is that it has two distinct types of effects: Direct effects are the result of growth hormone binding its receptor on target cells. Fat cells (adipocytes), for example, have growth hormone receptors, and growth hormone stimulates them to break down triglyceride and supresses their ability to take up and accumulate circulating lipids. Indirect effects are mediated primarily by a insulin-like growth factor-I (IGF-I), a hormone that is secreted from the liver and other tissues in response to growth hormone. A majority of the growth promoting effects of growth hormone is actually due to IGF-I acting on its target cells. Keeping this distinction in mind, we can discuss two major roles of growth hormone and its minion IGF-I in physiology. Effects on Growth Growth is a very complex process, and requires the coordinated action of several hormones. The major role of growth hormone in stimulating body growth is to stimulate the liver and other tissues to secrete IGF-I. IGF-I stimulates proliferation of chondrocytes (cartilage cells), resulting in bone growth. Growth hormone does seem to have a direct effect on bone growth in stimulating differentiation of chondrocytes. IGF-I also appears to be the key player in muscle growth. It stimulates both the differentiation and proliferation of myoblasts. It also stimulates amino acid uptake and p Continue reading >>

How Do Growth Hormones Work?

How Do Growth Hormones Work?

Originally Answered: In what ways do growth hormones work? Anterior pituitary secretes Growth Hormone (GH) which is released in blood. It stimulates the mitotic division in liver and produce certain factors called Insulin-like growth factors (IGFs). Out of these factors IGF-1 and IGF-2 play role in growth of the body. IGF-1 is the primary mediator of growth hormone which is released from the liver on the effect of growth hormone. It affects both soft and hard tissue. It binds to specific receptors on cells and tissues of the body and stimulates body growth by mitotic division on muscles, tissues, nerve, skin, liver, kidney, haemopoetic cells, cartilage (epiphysial cartilage) - leads to linear or longitudinal growth of bone etc. IGF-2 acts just like a sink for IGF-1 by binding to same receptors that IGF-1 binds but doesn't stimulates cell growth. So it basically lowers the excessive growth of body by IGF-1. The growth hormone is diabetogenic i.e. it increases blood sugar level by inhibiting uptake by cell, it promotes lipolysis and increases fatty acid for energy source and promote protein synthesis. GH-RF (Growth hormone releasing factor) and GH-IF (Growth hormone inhibiting factor) are hormones released from hypothalamus which regulate secretion of GH in turn regulating growth. Continue reading >>

Effects Of Growth Hormone On Glucose Metabolism.

Effects Of Growth Hormone On Glucose Metabolism.

Abstract Growth hormone (GH) counteracts in general the effects of insulin on glucose and lipid metabolism, but shares protein anabolic properties with insulin. Under physiological circumstances GH does not affect total glucose turnover directly. There is however evidence that GH acutely decreases glucose oxidation (secondary to an increase in lipid oxidation) and suppresses muscle uptake of glucose, suggesting that GH redistributes glucose fluxes into a non-oxidative pathway, which could be a build up of glycogen depots through gluconeogenesis. Since GH secretion is inhibited in the fed state these actions are mainly important in the postprandial or fasting state. Under pathological conditions of GH excess (e.g. acromegaly, poorly controlled tp. 1 diabetes or high dose GH treatment) the diabetogenic actions of GH become apparent. In these patients increased endogenous glucose production, decreased muscle glucose uptake and rising blood glucose levels are observed. In patients with intact beta-cell function these changes are counterbalanced by hyperinsulinemia--such hyperinsulinemia may in the long term induce increased cardiovascular morbidity and mortality ('Reavens syndrome X'). When stimulated with insulin these patients exhibit insulin resistance at the liver, in adipose tissue and in muscle. Few elaborate studies on the effects of GH on glucose metabolism in GH deficient patients have been conducted. These patients are hypersensitive to the actions of insulin on glucose metabolism and there is some evidence that when GH initially is given to such patients in the GH deprived state, paradox insulin-like effects of GH may be observed. Whether this may relate to increased activity of insulin-like growth factors is unsettled. Continue reading >>

On The Diabetogenic Effect Of Growth Hormone In Man: Effects Of Growth Hormone Of Glucagon And Insulin Secretion.

On The Diabetogenic Effect Of Growth Hormone In Man: Effects Of Growth Hormone Of Glucagon And Insulin Secretion.

Eur J Clin Invest. 1981 Apr;11(2 Suppl 1):115-9. On the diabetogenic effect of growth hormone in man: effects of growth hormone of glucagon and insulin secretion. The effects of human growth hormone (GH) on glucose homeostasis and the secretion of insulin and glucagon was investigated in eighteen healthy subjects. GH (40 microgram/kg) was given as a 30 min i.v. infusion and was followed immediately, or after 60 min, by either a glucose infusion, or an i.v. L-arginine infusion or i.v. insulin (0.05 IU/kg). An insulin-like effect of GH was seen about 15 min after the start of the GH infusion, and became a diabetogenic action 90 min later. Basal and glucose stimulated insulin secretion were suppressed 60 min after the start of the GH infusion, while insulin response to i.v. L-arginine, on the whole, was uninfluenced. Basal glucagon as well as glucagon response to arginine or hypoglycaemia were uninfluenced by GH. GH did not alter the degree of hypoglycaemia reached after i.v. insulin, whereas the rapidity of blood glucose fall was significantly decreased. The restitution of blood glucose after its nadir was not modified by the hormone. These results demonstrate that the diabetogenic action of GH is not mediated by GH effects on glucagon secretion, and that GH is of little importance in the acute counter-regulation of insulin-induced hypoglycaemia. Continue reading >>

Insulin-like And Diabetogenic Effects Of Growth Hormone In Healthy Subjects, Diabetics, And Low Insulin Responders

Insulin-like And Diabetogenic Effects Of Growth Hormone In Healthy Subjects, Diabetics, And Low Insulin Responders

The effect of two doses of GH (10 and 40 g/kg) on glucose homeostasis and insulin secretion was studied in 10 high insulin responders, 10 low insulin responders, and 6 subjects with chemical diabetes. GH was given as an iv infusion over 30min and, after a lag period of 60 min, a standard glucose infusion test (GIT) was performed. The insulin-like effect of GH was demonstrated in all groups under basal conditions but was more prominent in the diabetic than in the high and low insulin responders; it was evident even during the first 30 min of the GIT in the diabetics and low responders but not in the high responders. The insulin-like action of GH shifted to an antiinsulin one rather abruptly and was evident 30 min after discontinuation of the GIT. Hence, the GH-mediated decrease in the glucose disappearance rate, as seen after withdrawal of the GIT, wasof the same magnitude in all groups. The high GH dose seemed to have a more pronounced hypoglycemic effect than the low one, but the difference was not significant. As to the diabetogenic effect, there was no difference between the two GH doses. Both significantly suppressed basal insulin levels in all groups, and glucose stimulated insulin release in the diabetics and low insulin responders. In high insulin responders, the latter effect wasevident only in the presence of the high dose of the hormone, indicating that the diabetogenic effect is predominantly mediated by the peripheral effects of GH and not by the suppression of insulin release. In conclusion, it has been demonstrated that the insulin-like effect of GH as well as its inhibitory effect on insulin release were more pronounced in diabetic subjects and low insulin responders, whereas the diabetogenic effect seemed to be of the same magnitude in these two groups Continue reading >>

Diabetogenic | Definition Of Diabetogenic By Medical Dictionary

Diabetogenic | Definition Of Diabetogenic By Medical Dictionary

Diabetogenic | definition of diabetogenic by Medical dictionary /diabetogenic/ (-betah-jenik) producing diabetes. Want to thank TFD for its existence? Tell a friend about us , add a link to this page, or visit the webmaster's page for free fun content . Some of the risk factors predate transplant and could be used to risk-stratify patients and apply risk-reduction strategies such as lifestyle modification and use of less diabetogenic immunosuppressive protocols. Maternal and foetal outcomes in gestational diabetes mellitus inflammatory mediators, such as cytokines and chemokines, and reactive oxygen species, such as superoxide or hydroxyl radicals) (Sjostrand and Eriksson 2009; Tiganis 2011), should also be investigated (through immunoblots, immunohistochemical methods, and quantitative polymerase chain reaction) to pinpoint the exact mechanisms of the diabetogenic effects of noise exposure. Screening of free carnitine and acylcarnitine status in children with familial Mediterranean fever The onset of arterial hypertension due to disturbed circadian rhythm of blood pressure and diabetogenic profile potentiates atherosclerosis and can cause a cardiovascular disease (CVD) [31]. Giardiasis in streptozotocin--induced diabetic C57BL/6 mice 26-29] The different type of ADRs associated are hyperglycemic and diabetogenic, [30-32] adipogenic, [33-35] hyperlipidemia, [19,36,37] dyslipidemia, [38] spontaneous bleeding episodes, [39,40] dermatologic and sensitive reaction, [41-44] hepatic effect, [28,29,45-47] lactic acidosis and steatosis, [48-51] gastrointestinal symptoms, [6,15,19] teratogenic effect, [52] nervous system effect, [18,53-56] peripheral neuropathy, [56-58] hematologic effect, [59] immune reconstitution syndrome, [60,61] cardiovascular effect, [62] sulfonamide sens Continue reading >>

Human Growth Hormone As A Regulator Of Blood Glucose Concentration And As A Diabetogenic Substance

Human Growth Hormone As A Regulator Of Blood Glucose Concentration And As A Diabetogenic Substance

Human growth hormone as a regulator of blood glucose concentration and as a diabetogenic substance Human growth hormone (HGH) has recently been shown to play a prominent role in the control of blood glucose homeostasis. Furthermore, it has long been known that administration of growth hormone in animals can induce a diabetes-like state. In human subjects, exogenous administration of HGH or hypersecretion of the endogenous hormone in acromegaly is accompanied by glucose intolerance in only about 25 per cent of the cases. In this paper, data are presented which give a more diversified picture of the so-called diabetogenic action of HGH. It is suggested that HGH, although decreasing the peripheral utilization of glucose, is not a primary diabetogenic factor, since its insulinogenic action causes a compensatory hyperinsulinism, with normal glucose tolerance as the result. HGH is diabetogenic only in prediabetic subjects whose pancreas is unable to respond to the insulinogenic effect of the hormone. In such subjects, the diabetogenic action of HGH not being counterbalanced by a compensatory hyperinsulinism, glucose intolerance may result. Thus, HGH may be regarded as anadditional factor for the development of diabetes, the major prerequisite being a prexisting prediabetic state. Human growth hormoneGrowth hormoneInsulinDiabetes mellitusExperimental diabetesAcromegalyPathogenesis of diabetes mellitus Presented as an invited lecture at the VI Acta Endocrinologica Congress, Helsinki, Finland, August 8th12th, 1967. L'hormone de croissance humaine en tant que rgulateur de la concentration du glucose sanguin et en tant que substance diabtogne Il a t dmontr rcemment que l'hormone de croissance humaine (HGH) joue un rle prminent dans la rgulation normale de la glycmie. De plus, il Continue reading >>

Diabetogenic Action Of Pure Anterior Pituitary Growth Hormone

Diabetogenic Action Of Pure Anterior Pituitary Growth Hormone

Diabetogenic Action of Pure Anterior Pituitary Growth Hormone Nature volume 164, pages 209211 (06 August 1949) | Download Citation IN this laboratory, investigations designed to purify the diabetogenic principle of ox anterior pituitary tissue, the daily administration of which to the intact dog or cat induces a condition of diabetes mellitus, have been in progress for some time1-3. Methods involving precipitation in the presence or absence of neutral salts have yielded a potent preparation capable of inducing the appearance of glycosuria in a normal intact cat when administered in a dose of 4 mgm. protein/day (approximately 0.1 mgm. protein N/kgm. body weight/day) over a period of four days (graph a). We have found similar diabetogenic activity to be exhibited both by purified growth hormone prepared in our laboratory by the method of Li, Evans and Simpson4 and by the crystalline growth hormone obtained by the ethanol-precipitation method of Wilhelmi, Fishman and Russell5 (see graph b). We have also had the opportunity of testing, in the intact adult cat, the diabeto-genic activity of growth hormone prepared according to the method of Li et al4 by Dr. C. H. Li of the Institute of Experimental Biology, University of California (to whom we are grateful for his generous gift), and also of crystalline growth hormone prepared in the laboratories of Armour and Co., Chicago, by the method of Wilhelmi et al.5. For the gift of the latter preparation we are indebted to Dr. A. E. Wilhelmi, of the Department of Physiological Chemistry, Yale University, and to Dr. I. M. Bunding, of Armour and Co., Chicago. Both preparations were highly diabetogenic in the adult intact cat (graphs c and d), and, doubtless, similar activity can be demonstrated in the intact adult dog, since in our e Continue reading >>

Metabolic Basis For The Diabetogenic Action Of Growth Hormone In The Obese (ob/ob) Mouse.

Metabolic Basis For The Diabetogenic Action Of Growth Hormone In The Obese (ob/ob) Mouse.

Metabolic basis for the diabetogenic action of growth hormone in the obese (ob/ob) mouse. Cameron CM , Kostyo JL , Adamafio NA , Dunbar JC . The ob/ob mouse responds predictably to chronic treatment with large doses of pituitary GH with marked hyperglycemia and decreased glucose tolerance. The purpose of the present study was to characterize the metabolic alterations produced by GH that lead to this diabetogenic response in the ob/ob mouse in order to determine whether this animal might serve as a useful model for the study of the cellular mechanisms involved in the diabetogenic action of GH. Female ob/ob mice were treated sc for 3 days with either saline or 200 micrograms/day S-carboxymethylated human GH (RCM-hGH), a diabetogenic GH derivative lacking significant growth-promoting or insulin-like activities. Six hours before the start of the experiment, the animals were given a sc injection of 2 micrograms dexamethasone and deprived of food. RCM-hGH treatment produced marked increases in fasting blood glucose and plasma insulin concentrations, but had no effect on plasma glucagon or serum insulin-like growth factor I levels. It had no effect on liver glycogen level or in vitro hepatic glucose production in the absence or presence of pyruvate and lactate added to the incubation medium. By contrast, the in vitro stimulatory effects of insulin on [14C] glucose oxidation by isolated soleus muscle or segments of parametrial fat were greatly attenuated by RCM-hGH treatment, without changes in rates of basal glucose oxidation. This change in peripheral tissue responsiveness to insulin does not appear to involve glucose transport, since the in vitro stimulation by insulin of 3-O-[14C]methylglucose transport into isolated diaphragm muscle was not altered by RCM-hGH treatment. M Continue reading >>

Growth Hormone And Carbohydrate Metabolism

Growth Hormone And Carbohydrate Metabolism

GROWTH HORMONE AND CARBOHYDRATE METABOLISM JAMA. 1952;150(16):1602-1603. doi:10.1001/jama.1952.03680160052014 The various phases of carbohydrate metabolism, namely, the oxidation of sugar to carbon dioxide and water and its conversion to fat, glycogen synthesis, and the new formation of sugar from protein and possibly fat, are all under hormonal control. The importance of the islands of Langerhans, the adrenal medulla, the adrenal cortex, and the thyroid in carbohydrate metabolism are well recognized. Great progress has been made in establishing both the conditions that determine and the factors that regulate the secretory activity of these organs as well as the exact role of their various hormones in the chain of intermediary reactions involved in carbohydrate metabolism. Recent work has shown that still another endocrine factor must be added to the above list, namely, an anterior pituitary factor other than corticotropin, most probably growth hormone or some other hormone closely linked with it. The relation of the anterior pituitary to carbohydrate metabolism originally Continue reading >>

Studies Show Benefits Of Growth Hormone Therapy For Adults With Pws

Studies Show Benefits Of Growth Hormone Therapy For Adults With Pws

Studies Show Benefits Of Growth Hormone Therapy For Adults With PWS Studies Show Benefits Of Growth Hormone Therapy For Adults With PWS Children with PWS typically have growth hormone deficiency (GHD), and treating them with growth hormone has been shown to have beneficial effects on growth, body composition, motor function, and possibly cognitive development. What many people don't know is that studies show promising results for growth hormone therapy for adults with PWS. Testing for Growth Hormone Deficiency in Adulthood While growth hormone therapy for children with PWS has been approved by the FDA since 2000 without the need for prior laboratory confirmation of GHD, the picture is somewhat different once PWS children attain adult height. Guidelines recommend that adults with PWS should have an evaluation of thegrowth hormone/ IGF axis to confirm GHD prior togrowth hormone therapy. Unlike in children, where lack of linear growth is a good indicator of potential problems in the growth hormone/ IGF-1 axis, adult GHD is harder to diagnose because a low growth hormone level is also part of the normal aging process. GHD is usually diagnosed using provocative agents that stimulategrowth hormone secretion, but this method isnt perfect. Especially in the case of PWS, underlying obesity and the frequent presence of other hormonal imbalances can influence test results. Therefore, relying on provocative testing alone has the potential to exclude PWS patients who, based on these criteria may not be GHD, but may still benefit fromgrowth hormone therapy in adulthood. Not surprisingly, there is a wide variation in GHD diagnosis in adult PWS patients previous studies have shown that anywhere between 8-55% of PWS adults met criteria for severe GHD. Clinical Picture of Growth Hormone Continue reading >>

Diabetogenic Hormones (human Choriosomatomammotrophin And Ovine Growth Hormone): Anti-insulin Action In Hypophysectomized Rats

Diabetogenic Hormones (human Choriosomatomammotrophin And Ovine Growth Hormone): Anti-insulin Action In Hypophysectomized Rats

Three hormones were tested for effectiveness as diabetogenic, that is antiinsulin, agents: human choriosomatomammotrophin (HCS), ovine GH, and ovine prolactin. Female rats hypophysectomized at 28 days of age were used throughout the study. In a first series of experiments rats were injected once daily for a period of 10 days with HCS (100 g), GH (10 or 100 g) or prolactin (10 or 100 g), each thyroxine (T4, 0.5 g), and then challenged in a glucose tolerance test with glucose plus 0.03 units protamine zinc insulin (PZI) following a 6-h fast. Blood glucose levels (mg/100 ml) 50 min later were: saline control, 74; HCS, 98; prolactin, 85. No prior injections: fasting, 54; glucose only, 159. GH, 10 g, was as effective as HCS; a higher dose, 100 g, was no more effective than prolactin. T4 negated the anti-insulin effects of HCS and of GH. In a second series rats were pre-treated for a period of 22 days, beginning 14 days after hypophysectomy, and then injected with doses of PZI (0.4 units 1.6 units/day) that induced convulsions in unprotected (saline and prolactin-treated) rats run concurrently. HCS (200 g 400 g/day) staved off convulsions over the 10-day challenge period; HCS also stimulated growth of the thymus, markedly in combination with PZI and T4. Neither HCS nor PZI affected skeletal growth. In summary, HCS affords protection in the hypophysectomized rat against insulin-induced hypoglycaemia without introducing complications associated with growth. The parent HCS molecule or an active fragment of the diabetogenic hormones, we suggest, should be tested in humans for usefulness in protecting brittle diabetic against insulin hypoglycaemia. Continue reading >>

Effects Of Growth Hormone And Pioglitazone In Viscerally Obese Adults With Impaired Glucose Tolerance: A Factorial Clinical Trial

Effects Of Growth Hormone And Pioglitazone In Viscerally Obese Adults With Impaired Glucose Tolerance: A Factorial Clinical Trial

Effects of Growth Hormone and Pioglitazone in Viscerally Obese Adults with Impaired Glucose Tolerance: A Factorial Clinical Trial Affiliation Department of Medicine, Wayne State University, Detroit, Michigan, United States of America Affiliation Geriatric Research Education and Clinical Center, Veterans Affairs Palo Alto Health Care System, Palo Alto, California, United States of America Affiliation Department of Radiology, Veterans Affairs Palo Alto Health Care System, Palo Alto, California, United States of America *To whom correspondence should be addressed. E-mail: [email protected] Affiliation Department of Medicine, Stanford University, Stanford, California, United States of America Effects of Growth Hormone and Pioglitazone in Viscerally Obese Adults with Impaired Glucose Tolerance: A Factorial Clinical Trial Recombinant human growth hormone (GH) and pioglitazone (PIO) in abdominally obese adults with impaired glucose tolerance were evaluated under the hypothesis that the combination attenuates GH-induced increases in glucose concentrations, reduces visceral adipose tissue (VAT), and improves insulin sensitivity over time. Randomized, double-blind, placebo-controlled, 2 2 factorial design. Veterans Affairs Palo Alto Health Care System, Palo Alto, California, United States. 62 abdominally obese adults aged 4075 with impaired glucose tolerance. GH (8 g/kg/d, or placebo) and pioglitazone (30 mg/d, or placebo) for 40 wk. Baseline and after 40 wk of treatment, VAT content was quantified by CT scan, glucose tolerance was assessed using a 75-g oral glucose tolerance test, and insulin sensitivity was measured using steady-state plasma glucose levels obtained during insulin suppression test. Baseline: body mass index (BMI), plasma glucose, and visceral fat content w Continue reading >>

Growth Hormone Flashcards | Quizlet

Growth Hormone Flashcards | Quizlet

Insulin-like-growth-factor (IGF). stimulates GH. secreted by liver synthesized in anterior pituitary cells called somatotrophs (make up 40-50% of cells in anterior pituitary). Hormone is stored in large granules within somatotrphic cells. Growth hormone releasing hormone (GHRH) induces synthesis and stims secretion of GH. Somatostatin inhibits synthesis and secretion. Pulsatile release of GHRH causes similar pulsatile release of GH. Somatostatin inhibits effect of GHRH on somatotrophic cells. GHRH, Ghrelin (secreted in fasting situations by cells in stomach. tells hypothalamus to release GHRH), Protein Nutritional Deficiency, Decrease in FFA and glucose, fasting or caloric restriction, puberty, exercise, stage IV sleep, physiologic stress, estrogens and androgens somatostatin, increased blood glucose, increased blood FFA, administration of exogenous GH, obesity, senescence, somatomedins plasma levels GH greatest in children and peak in puberty, lowestest in senescence Variations in secretion: Circadian Rhythm GH secretion varies within the 24 hour sleep-wake cycle. Peak secretion ~ 1 hr after onset of deep sleep secretion greater in females, estradiol stims GH secretion with a peak just before ovulation, testosterone stims GH secretion in males is GH the magic pill, the fountain of youth? GH supplements to middle aged males did not enhance muscle mass and strength gains over placebo effect when both groups preformed weight training exercises. (so no.) Actions of GH & Somatomedins (IGF): Metabolic Effects 1. Increase protein synthesis (synergistic action with insulin): 2. mobilization of fatty acids and utilization of fatty acids: -stims release of fatty acids from adipose cells and therefore see increase in plasma FFA and ketoacids -increases oxidation of fatty acids b Continue reading >>

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