Free Fatty Acids, Niacin and Growth Hormone

These studies below show that reducing the concentration of free fatty acids (FFA) in the blood will increase the responsiveness of the pituitary to Growth Hormone Releasing Hormone (GHRH), in everyone and especially in the obese and elderly.

In these experiments the researchers used a drug called acipimox to reduce FFA. Acipimox is a nicotinic acid analogue. Nicotinic acid = Niacin = Vitamin B3. This means that niacin will have many of the same effects as acipimox. Other evidence shows that niacin does indeed have the expected effects. Niacin is very inexpensive and available anywhere vitamins are sold. (niacinamide is related but not identical and probably does not have the same effects)

FFA is a powerful mediator of GH feedback which seems to work at the pituitary gland. High serum GH causes high serum FFA, which directly or indirectly inhibits further secretion of endogenous GH. Niacin or any other drug or supplement that reduces FFA should therefore have the effect of reducing the negative feedback.

Niacin is a water soluble B vitamin. It is considered reasonably safe in doses up to approximately one gram in non-sustained release form. However megadoses of niacin do present some risks to the liver, especially in multiple gram doses in sustained release form.

Doses in the 500 to 1000 mg range are safe for most people and should still have some FFA reducing effects, so niacin appears to be a promising supplement for people who supplement GH. For example if one normally injects GH in the morning then it might be a good idea to take niacin at bed time. In theory the reduction of FFA during sleep would enhance the release of endogenous GH. I do not however think this strategy should be used in place of cycling. The purpose would be to further reduce the risks that the practice of cycling is designed to reduce, while also enhancing total GH and IGF-1.

Another benefit might be a reduction of the risk of insulin resistance, which is a possible side-effect of GH therapy. In a recent study diabetics and non-diabetics taking acipimox at night realized significant improvements in insulin resistance and glucose tolerace. Niacin can also be effective in reducing cholesterol levels.

Ideally one would take several grams of niacin to gain the full FFA-reducing effects but I think doses in excess of about one gram should be taken only under the supervision of a physician. From the evidence I have seen I would avoid multiple gram doses of sustained release niacin completely, but doses of two to three grams of the non-sustained release form might be an acceptable risk for some people if under doctor's supervision.

Niacin can cause a harmless but sometimes annoying "flushing" effect on the skin. The flushing disappears in most people after a few days as the body becomes accustomed to the niacin. People who want to take niacin might want to start with smaller doses in the 50 mg range and then increase the dosage gradually. Talk to your doctor before moving up to higher doses.


Title
Long-term administration of acipimox potentiates growth hormone response to growth hormone-releasing hormone by decreasing serum free fatty acid in obesity.
Author
Nam SY ; Lee ; Kim KR ; Lee HC ; Nam MS ; Cho JH ; Huh KB
Address
Division of Endocrinology, Department of internal Medicine, Yong Dong Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Source
Metabolism, 45(5):594-7 1996 May
Abstract
Obesity is associated with an impairment of normal growth hormone (GH) secretion and blunted responses to all stimuli. A high plasma free fatty acid (FFA) level is frequently observed in obesity. FFA participates in the regulation of pituitary GH secretion. To determine whether the derangement of GH secretion in obesity is associated with high plasma FFA levels, tests with GH-releasing hormone (GHRH) and acipimox (ACX), an antilipolytic agent able to decrease FFA, were undertaken in six obese subjects and seven normal control subjects. In addition, the effect of prolonged suppression of FFA level on GH response to GHRH after administration of ACX for 1 month was also examined in each of the obese subjects. The GH response in obese subjects (median, 9.1 microg/L) to GHRH (1-29) (1 microg/kg intravenously [IV]) was significantly blunted as compared with normal control subjects (23.5 microg / L, P < .05). Basal FFA levels were higher in obese subjects (855.2 microEq / L than in normal control subjects (514.6 microEq / L, P < .05). One-dose ACX (500 mg) decreased FFA levels in both obese and normal subjects: the lowest FFA levels in obese subjects (158.3 microEq/L 2 to 2.5 hours after ACX were similar to those of normal control subjects (108.7 microEq/L). One-dose ACX potentiated GHRH-stimulated GH response in both obese and normal subjects. GH responses potentiated by ACX in obese subjects (27.1 microg/L) were similar to GH responses to GHRH in normal control subjects, but lower than in normal subjects treated with ACX plus GHRH (58.5 microg / L, P < .05). Thereafter, all of the obese subjects were treated with ACX for 1 month, after which the ACX plus GHRH tests were repeated. After 1 month of acipimox administration in the obese subjects, GH responses (38.8 microg/L) were significantly higher than those of obese subjects treated with GHRH and one-dose ACX plus GHRH (P < .05). They were similar to GH responses of normal control subjects receiving the one-dose ACX plus GHRH test. In conclusion, in obesity the prolonged suppression of FFA levels induced by long-term administration of ACX potentiated somatotrope responsiveness, likely acting at the pituitary level, suggesting that the duration of FFA suppression had an important relation to the magnitude of GH response.
Language
Eng
Unique Identifier
96202745
 

Title
Overnight lowering of free fatty acids with Acipimox improves insulin resistance and glucose tolerance in obese diabetic and nondiabetic subjects.
Author
Santomauro AT; Boden G; Silva ME; Rocha DM; Santos RF; Ursich MJ; Strassmann PG; Wajchenberg BL
Address
Endocrine Service, Hospital das Clinicas, S~ao Paulo, Brazil.
Source
Diabetes, 48(9):1836-41 1999 Sep
Abstract
Obesity is commonly associated with elevated plasma free fatty acid (FFA) levels, as well as with insulin resistance and hyperinsulinemia, two important cardiovascular risk factors. What causes insulin resistance and hyperinsulinemia in obesity remains uncertain. Here, we have tested the hypothesis that FFAs are the link between obesity and insulin resistance/hyperinsulinemia and that, therefore, lowering of chronically elevated plasma FFA levels would improve insulin resistance/hyperinsulinemia and glucose tolerance in obese nondiabetic and diabetic subjects. Acipimox (250 mg), a long-acting antilipolytic drug, or placebo was given overnight (at 7:00 P.M., 1:00 A.M., 7:00 A.M.) to 9 lean control subjects, 13 obese nondiabetic subjects, 10 obese subjects with impaired glucose tolerance, and 11 patients with type 2 diabetes. Euglycemic-hyperinsulinemic clamps and oral glucose tolerance tests (75 g) were performed on separate mornings after overnight Acipimox or placebo treatment. In the three obese study groups, Acipimox lowered fasting levels of plasma FFAs (by 60-70%) and plasma insulin (by approximately 50%). Insulin-stimulated glucose uptake during euglycemic-hyperinsulinemic clamping was more than twofold higher after Acipimox than after placebo. Areas under the glucose and insulin curves during oral glucose tolerance testing were both approximately 30% lower after Acipimox administration than after placebo. We conclude that lowering of elevated plasma FFA levels can reduce insulin resistance/hyperinsulinemia and improve oral glucose tolerance in lean and obese nondiabetic subjects and in obese patients with type 2 diabetes.
Language
Eng
Unique Identifier
99408493

Title
Acute inhibition of somatotroph response to human growth hormone-releasing hormone 1-44 occurs following three hours but not one hour of growth hormone infusion.
Author
Rosenbaum M; Leibel RL; Gertner JM
Address
Division of Pediatric Endocrinology, New York Hospital-Cornell Medical College, New York 10021.
Source
Metabolism, 38(6):590-3 1989 Jun
Abstract
Our previous studies have demonstrated that a short-term (three hour) infusion of methionyl human growth hormone (met-hGH, 2 micrograms/kg/h) is associated with a rise in serum concentrations of free fatty acids and glycerol, and a blunting of somatotroph response to human growth hormone releasing hormone 1-44 (GRH) in normal volunteers. To gain more information on the time course of this blunting, and to determine whether it could be temporally dissociated from the GH-induced rise in serum concentrations of lipolytic products, the response to GRH (0.3 micrograms/kg) was measured in five normal adult volunteers from hours 1.0 to 3.5 of a 3.5-hour infusion of saline or met-hGH 2 micrograms/kg/h. Somatotroph response to the same dose of GRH from hours 3.0 to 5.5 of a longer (5.5-hour) infusion of saline or met-hGH (2 micrograms/kg/h) in five other volunteers was used for comparison. There was a significant blunting of somatotroph response following three hours, but not one hour of met-hGH infusion. The longer infusion was associated with a significant rise in serum concentrations of free fatty acids, and the shorter met-hGH infusion was too brief to provoke such a rise. Neither met-hGH infusion was associated with a significant rise in serum concentrations of glycerol, insulin, glucose, or insulin-like growth factors (IGF). This study provides further evidence that there is an association between circulating FFA and somatotroph function and suggests that FFA may act as messengers, which provide information to central systems regarding the energy balance of the organism.
Language
Eng
Unique Identifier
89261133
 

Title
Acipimox-mediated plasma free fatty acid depression per se stimulates growth hormone (GH) secretion in normal subjects and potentiates the response to other GH-releasing stimuli.
Author
Peino R; Cordido F; Pe~nalva A; Alvarez CV; Dieguez C; Casanueva FF
Address
Department of Medicine, School of Medicine, Santiago de Compostela University, Spain.
Source
J Clin Endocrinol Metab, 81(3):909-13 1996 Mar
Abstract
Increases in plasma free fatty acids (FFA) inhibit the GH response to a variety of stimuli; however, the role of FFA depression in GH control is far from understood. In the present work, FFA reduction was obtained by the administration to normal subjects of acipimox, a lipid-lowering drug devoid of side-effects. Each subject tested underwent two paired tests. In one, acipimox was administered orally at a dose of 250 mg at -270 min and at a dose of 250 mg at -60 min; in the matched test, placebo was given at similar intervals. To induce GH release, four stimuli acting through different mechanisms were used: pyridostigmine (120 mg, orally) at -60 min, GHRH (1 microgram/kg, iv) at 0 min, GH-releasing peptide (GHRP-6; His-D-Trp-Ala-Trp-D-Phe-Lys-NH2; 1 microgram/kg, iv) at 0 min, and finally, GHRH plus GHRP-6 at the same doses at 0 min. GH secretion was analyzed as the area under the secretory curve (AUC; mean +/- SE, micrograms per L/120 min). Acipimox pretreatment alone (n = 6) induced a reduction in FFA levels compared with placebo treatment. The FFA reduction led to a sustained GH secretion that increased from 2.4 +/- 1.8 micrograms/L at -120 min to 14.2 +/- 4.0 at 120 min. The GH AUC for placebo was 266 +/- 100, and that for acipimox was 1781 +/- 408 (P < 0.05). In the pyridostigmine-treated group (n = 6), the acipimox-pyridostigmine AUC (2046 +/- 323) was higher (P < 0.05) than the placebo-pyridostigmine AUC (764 +/- 101), but was not different from the AUC of acipimox alone. Previous FFA reduction nearly doubled the GHRH-mediated GH secretion (n = 6; placebo-GHRH AUC, 1817 +/- 365; acipimox-GHRH test, 3228 +/- 876; P < 0.05). A similar enhancement was observed when the stimulus employed was GHRP-6 (n = 6; placebo-GHRP-6 AUC, 2034 +/- 295; acipimox-GHRP-6, 4827 +/- 703; P < 0.05). Furthermore, even the most potent GH stimulus known to date, i.e. GHRH plus GHRP-6, was enhanced by the FFA suppression (placebo-GHRH-GHRP-6 AUC, 2034 +/- 277; acipimox-GHRH-GHRP-6, 5809 +/- 758; P < 0.05). The enhancing effect of lowering FFA levels was additive regardless of the stimulus employed. These results indicate that 1) FFA reduction per se stimulates GH secretion with a delayed time of action; 2) FFA reduction enhanced in an additive manner the GH secretion elicited by such different stimuli as pyridostigmine, GHRH, and GHRP-6; and 3) the observation that FFA reduction enhanced the response to the most potent GH stimulus, GHRH plus GHRP-6, suggests that FFA suppression acts by a separate mechanism. FFA reduction may have value in the clinical setting for assessing GH reserve.
Language
Eng
Unique Identifier
96368541
 

Title
Restoration of growth hormone (GH) response to GH-releasing hormone in elderly and obese subjects by acute pharmacological reduction of plasma free fatty acids.
Author
Pontiroli AE; Manzoni MF; Malighetti ME; Lanzi R
Address
Istituto Scientifico San Raffaele, Divisione di Medicina Interna, Universit`a degli Studi di Milano, Italy.
Source
J Clin Endocrinol Metab, 81(11):3998-4001 1996 Nov
Abstract
GH induces lipolysis in vivo, increasing plasma free fatty acid (FFA) levels; in turn, FFA are able to reduce GH release, and acipimox, a nicotinic acid analog able to block lipolysis, enhances in normal subjects the GH response to GHRH. Obesity and old age are characterized by a blunted GH response to several stimuli, including GHRH; reports also indicate high plasma FFA levels in obesity and sometimes in the elderly. The aim of this study was to evaluate the possible role of FFA in GH release in obese and elderly subjects. According to a randomized, single blind, cross-over protocol, six healthy subjects, six obese subjects, and six elderly subjects received on 2 different days, with a 1-week interval, placebo or acipimox (250 mg, orally) at 0700 and 1100 h; GHRH [GHRH-(1-44)NH2; 50 micrograms in healthy subjects and in elderly subjects, 100 micrograms in obese subjects] was injected iv at 1300 h, and blood samples for evaluation of plasma FFA, blood glucose, serum insulin (IRI), and serum GH levels were taken from 1200 to 1500 h. Plasma FFA levels were always lower (P < 0.05) after acipimox than after placebo (0.03 +/- 0.01 vs. 0.13 +/- 0.02 g/L in healthy subjects, 0.09 +/- 0.01 vs. 0.27 +/- 0.02 g/L in obese, 0.02 +/- 0.005 vs. 0.17 +/- 0.01 g/L in elderly subjects); serum IRI levels were also lower (P < 0.05) after acipimox than after placebo in the three groups of subjects (16 +/- 3 vs. 30 +/- 5, 120 +/- 30 vs. 181 +/- 32, and 21 +/- 3 vs. 49 +/- 9 pmol/L); both FFA (P < 0.05) and IRI levels (P < 0.05) were higher in obese than in healthy or elderly subjects after placebo and acipimox. Blood glucose levels were not different in the three groups of subjects after either placebo or acipimox. The integrated GH response to GHRH-(GH delta area) was always greater (P < 0.05) after acipimox than after placebo (4677 +/- 633 vs. 1599 +/- 373 in healthy, 1469 +/- 230 vs. 343 +/- 114 in obese, 2304 +/- 759 vs. 325 +/- 133 micrograms/L.120 min in elderly subjects); after both placebo and acipimox, the GH delta area was greater (P < 0.05) in healthy subjects than in obese or elderly subjects. The GH delta area of elderly and obese subjects after acipimox was not different from the GH delta area of healthy subjects after placebo. Changes in GH delta areas were not significantly related to changes in FFA or IRI induced by acipimox; in contrast, absolute values of FFA and IRI as well as basal GH levels were all significantly related to the GH delta area. At multiple regression analysis, FFA was the only significant predictor of GH delta area. These data indicate that acute pharmacological reduction of plasma FFA levels restores the blunted GH response to GHRH commonly observed in obese and elderly subjects: however, when lipolysis is blocked to a similar extent, healthy subjects still show a higher GH delta area than obese or elderly subjects. As FFA are the best predictor of the GH delta area, we suggest that in obesity, the blunted GH release is due to high FFA levels, whereas in the elderly there might be an abnormal sensitivity to normal FFA levels.
Language
Eng
Unique Identifier
97082614
 

Niacin is not without some risks, however, especially if taken in very large doses in excess of one gram, and in sustained release form.

This material is from http://www.pharminfo.com/pubs/msb/niacin.html

The Toxicity of Niacin

Reprinted from the April 1994 issue of Medical Sciences Bulletin , published by Pharmaceutical Information Associates, Ltd.


Niacin (nicotinic acid) is widely used for reducing serum cholesterol levels, in part because it is effective, and in part because it is available and cheap. In doses of 2 to 3 g daily, it reduces levels of total and high-density lipoprotein cholesterol (LDL-C) by an average of 20% to 30%, reduces triglyceride levels 35% to 55%, increases high-density lipoprotein cholesterol (HDL-C) 20% to 35%, and reduces Lp(a) lipoprotein. In primary prevention, niacin reduces total mortality as well as mortality from coronary artery disease; used in secondary prevention along with bile acid resins, it slows or reverses the progression of atherosclerosis. And it costs only about $2.00 for a 10-day supply. Does all this sound too good to be true? Results from a recent study by McKenney et al. (Medical College of Virginia School of Pharmacy) indicate that not all the news about niacin is good news. In therapeutic doses, niacin can be dangerous, particularly sustained-release niacin.

The Virginia researchers conducted a randomized, double-blind, parallel-group comparison of sustained-release (SR) and immediate-release (IR) niacin in 46 patients with hypercholesterolemia. The 36-week trial included a 6-week evaluation and instruction period followed by five 6-week treatment periods during which niacin was given in escalating doses (500 mg/day initially, increasing up to 3Êg/day). Both the IR niacin product (Rugby Laboratories, division of Marion Merrell Dow) and the SR niacin (Goldline Laboratories) were effective for improving the lipid profile. At the highest (3-g) dose, SR niacin reduced total cholesterol by about 40% and LDL-C by 50%, while IR niacin reduced total cholesterol by about 16% and LDL- C by about 22%. Both formulations at the 3-g dose reduced triglycerides by about 41%. IR niacin elevated HDL-C by 35% at the 3-g dose, while SR niacin elevated HDL-C by only 9.4%, a significant difference.

Both formulations were associated with considerable side effects. Nine of the 23 patients assigned to IR niacin withdrew from the trial before completing the 3-g dose phase because of adverse reactions, including vasodilation (flushing, itching, rash), fatigue, and acanthosis nigricans (a wart-like skin eruption). Eighteen of the 23 patients in the SR niacin group withdrew before completing the 3-g dose phase because of gastrointestinal effects, fatigue, and hepatotoxicity. Thus, 39% of patients on IR niacin and 78% of those on SR niacin withdrew because of side effects.

More than half the patients in the SR niacin group showed evidence of hepatotoxicity. Liver aminotransferase levels were three times the upper limit in 12 of the 18 who withdrew, and 3 patients had symptoms of hepatic dysfunction (fatigue, nausea, anorexia). Toxicity appeared dose related; changes in liver function test results reached statistical significance by the time the dosage reached 1500 mg/day, and 9 of the 12 with substantial hepatotoxicity were taking 2 to 3 g/day. Hepato-toxicity did not develop in any patients taking IR niacin.

In recent years, numerous case reports have described hepatotoxicity linked to high-dose niacin therapy; almost all the patients were taking SR niacin. Toxicity was noted in some cases in as little as 1 week after initiating therapy, and in others as late as 48 months. Usually, toxicity resolved after drug discontinuation, but in some cases liver dysfunction progressed to stage 3 and 4 encephalopathy, and one patient required liver transplantation. Perhaps even more hepatotoxi- city would have developed in patients in the McKenney study if the trial had continued beyond 5 weeks. Other major side effects reported in the literature include activation of peptic ulcers, hyperuricemia and gout, and impaired glucose tolerance. While McKenney et al. noted no change in uric acid levels, they did see elevations in fasting glucose levels with increasing doses. The elevations were significant in the SR niacin group at doses of 2 g and over. By the end of the trial, six patients with normal glucose levels at baseline (three in each group) had fasting glucose levels above 7.8Êmmol/L (140 mg/dL). One patient taking IR niacin had a bleeding pep-tic ulcer, apparently from activation of peptic ulcer disease.

A number of products have been implicated in niacin-induced hepatotoxicity, including two prescription products: Nicobid from Rhone-Poulenc Rorer (Collegeville, PA) and Slo-Niacin from Upsher- Smith (Minneapolis). Other implicated products include Nature's Plus, Niatrol, Endur-Acin, and generic products from Rugby Laboratories (Rockville Center, NY), Major Pharmaceuticals (San Diego), and Goldline Laboratories (Ft. Lauderdale, FL). According to Goldline, their SR niacin is a generic version of Rhone-Poulenc's Nicobid. Neither Goldline nor Rhone-Poulenc promote their SR niacin for cholesterol reduction. Only two prescription products (both of them IR niacin) are approved for cholesterol reduction: Upsher-Smith's Niacor and Rhone-Poulenc's Nicolar. "All other IR dosage forms and all SR dosage forms are available as nonprescription drugs for the treatment of nicotinic acid deficiencies and are not regulated by the FDA," said McKenney et al. In many published cases, a patient went to the health food store for IR niacin because of the health claims and the price, switched to SR niacin because of side effects associated with IR niacin, and then had to visit the doctor because of symptoms that turned out to be caused by hepatotoxicity. "Given the degree of toxic effects we encountered," said the investigators, "we believe that allowing niacin to remain on the nonprescription market, where it may be used in high doses for cholesterol lowering without proper monitoring by trained health care professionals, presents a potentially serious public health problem."

This study poses some interesting questions. Why was SR niacin more effective than IR niacin in reducing LDL-C? Why was IR niacin more effective for increasing HDL-C? Do phar-macokinetic differences explain the efficacy and toxicity differences? Slower absorption of SR niacin may mean lower peak serum levels, but fewer side effects may mean higher total ingested dose. Increased hepatotoxicity with SR niacin may be due to steadier bathing of liver cells, and the hepato-toxicity may explain the cholesterol reductions.

According to editorialist Louis Lasagna, the FDA has approved niacin for treating hypercholesterolemia, and the National Cholesterol Education Program recommends it for primary prevention. Niacin still has a role in managing dyslipidemia, said Lasagna, "but not on the basis of self-diagnosis and self- treatment." The Medical College of Virgin-ia cholesterol research center routinely evaluates the efficacy and safety of drugs for hypercholesterolemia. "The incidence and severity of adverse reactions experienced with both niacin dosage forms in the present study, but particularly with SR niacin, were much greater than any investigational drug we have evaluated for hypercholesterolemia," concluded McKen-ney et al. "If niacin were being evaluated for efficacy and safety and our experiences were replicated by others, we do not believe that it would be approved by the FDA for use in the management of hypercholesterolemia." (McKenney JM et al. JAMA. 1994;271:672-677. Lasagna L. JAMA. 1994;271:709-710)

Score Document Title

100 [Pharmacologic treatment of lipid metabolism disorders] (Gmi´nski J; Wiad Lek, 1996)
95 The control on growth hormone release by free fatty acids is maintained in acromegaly. (Lanzi R; J Clin Endocrinol Metab, 1999 Apr)
94 Effect of decreasing plasma free fatty acids by acipimox on hepatic glucose metabolism in normal rats. (Lee KU; Metabolism, 1996 Nov)
94 The additional effects of acipimox to simvastatin in the treatment of combined hyperlipidaemia [corrected and republished article originally printed in J Intern Med 1997 Feb;241(2):151-5] (Hoogerbrugge N; J Intern Med, 1998 May)
94 The additional effects of acipimox to simvastatin in the treatment of combined hyperlipidaemia [corrected and republished in J Intern Med 1998 May;243(5):151-6] (Hoogerbrugge N; J Intern Med, 1997 Feb)
94 Optimal metabolic conditions during fluorine-18 fluorodeoxyglucose imaging; a comparative study using different protocols. (Bax JJ; Eur J Nucl Med, 1997 Jan)
93 Effect of acute acipimox administration on the rates of lipid and glycogen synthesis in cachectic tumor-bearing rats. (Obeid OA; Nutr Cancer, 1997)
91 Effects of acipimox on haemorheology and plasma lipoproteins in patients with mixed hyperlipoproteinaemia. (Otto C; Br J Clin Pharmacol, 1998 Nov)
91 Tolerability and effects of high doses acipimox as additional lipid-lowering therapy in familial hypercholesterolemia. (Stuyt PM; Neth J Med, 1998 Nov)
79 Restoration of growth hormone (GH) response to GH-releasing hormone in elderly and obese subjects by acute pharmacological reduction of plasma free fatty acids. (Pontiroli AE; J Clin Endocrinol Metab, 1996 Nov)
76 Uncoupling of fatty acid and glucose metabolism in malignant lymphoma: a PET study. (Nuutinen J; Br J Cancer, 1999 May)
74 [Pharmacology of hypolipidemic agents] (F´ery F; Rev Med Brux, 1997 Feb)
55 Evidence for an inhibitory effect of physiological levels of insulin on the growth hormone (GH) response to GH-releasing hormone in healthy subjects. (Lanzi R; J Clin Endocrinol Metab, 1997 Jul)
54 Acipimox-mediated plasma free fatty acid depression per se stimulates growth hormone (GH) secretion in normal subjects and potentiates the response to other GH-releasing stimuli. (Peino R; J Clin Endocrinol Metab, 1996 Mar)
54 Impaired growth hormone secretion in obese subjects is partially reversed by acipimox-mediated plasma free fatty acid depression. (Cordido F; J Clin Endocrinol Metab, 1996 Mar)
53 Effect of acute pharmacological reduction of plasma free fatty acids on growth hormone (GH) releasing hormone-induced GH secretion in obese adults with and without hypopituitarism. (Cordido F; J Clin Endocrinol Metab, 1998 Dec)
53 Lowering fatty acids potentiates acute insulin response in first degree relatives of people with type II diabetes. (Paolisso G; Diabetologia, 1998 Oct)
53 The reduction in postprandial lipemia after exercise is independent of the relative contributions of fat and carbohydrate to energy metabolism during exercise. (Malkova D; Metabolism, 1999 Feb)
53 Effects of an acute decrease in non-esterified fatty acid levels on muscle glucose utilization and forearm indirect calorimetry in lean NIDDM patients. (Piatti PM; Diabetologia, 1996 Jan)
52 Overnight lowering of free fatty acids with Acipimox improves insulin resistance and glucose tolerance in obese diabetic and nondiabetic subjects. (Santomauro AT; Diabetes, 1999 Sep)
52 Long-term administration of acipimox potentiates growth hormone response to growth hormone-releasing hormone by decreasing serum free fatty acid in obesity. (Nam SY; Metabolism, 1996 May)
52 Acute pharmacological reduction of plasma free fatty acids enhances the growth hormone (GH)-releasing hormone-mediated GH secretion in patients with Cushing's syndrome. (Leal-Cerro A; J Clin Endocrinol Metab, 1997 Sep)
51 Long-term effects of a sustained-release preparation of acipimox on dyslipidemia and glucose metabolism in non-insulin-dependent diabetes mellitus. (Davoren PM; Metabolism, 1998 Mar)
51 Treatment possibility of hypercholesterolaemia associated with hypertriglyceridaemia. (Paragh G; Acta Biol Hung, 1997)
51 The effect of circulating non-esterified fatty acids on the entero-insular axis. (Ranganath L; Eur J Clin Invest, 1999 Jan)

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