Insulin-sensitive glucoreceptors in rat preoptic area that regulate FFA mobilization

1986 ◽  
Vol 251 (6) ◽  
pp. E703-E706 ◽  
Author(s):  
C. C. Coimbra ◽  
R. H. Migliorini
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Glucose ◽  
Direct Evidence ◽  
Preoptic Area ◽  
Sympathetic Outflow ◽  
Elevated Plasma ◽  
Plasma Ffa ◽  
Fasted Rats

Previous studies indicated that a longitudinal pathway connecting preoptic, lateral, and posterior hypothalamic areas participates in the process of free fatty acid (FFA) mobilization in the rat. In the present experiments, the presence of sensitive neurons in the preoptic area was investigated by examining the effects of topical stimulation with 2-deoxyglucose (2-DG) or insulin on the levels of plasma FFA in conscious unrestrained rats. Microinjections of minute amounts (50 micrograms and 1 microliter) of 2-DG into the preoptic area of fed animals induced rapid increases in the concentration of plasma FFA. Microinjections of insulin (5 microU and 0.5 microliter) produced sharp decreases of the elevated plasma FFA levels in fasted rats. Both 2-DG and insulin induced small increases in plasma glucose that did not differ from similar increases induced by equal volumes of 0.15 M NaCl. The results provide direct evidence for the presence within the preoptic area of insulin-sensitive glucoreceptors involved in FFA mobilization. The data suggest that activation of these receptors and increased sympathetic outflow to adipose tissue contributes to fasting lipolysis.

The Effects of Cold and Prostaglandin E1 on Lipid Mobilization in the Chicken

1971 ◽  
Vol 49 (5) ◽  
pp. 394-398 ◽  
Author(s):  
W. D. Wagner ◽  
R. A. Peterson ◽  
R. J. Cenedella
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Cold Exposure ◽  
Prostaglandin E1 ◽  
Plasma Free Fatty Acid ◽  
Prostaglandin E ◽  
Elevated Plasma ◽  
Lower Plasma ◽  
Lipid Mobilization ◽  
Plasma Ffa

Plasma free fatty acid (FFA) levels and the effects of prostaglandin E1 (PGE1) were studied in cold-acclimated and cold-exposed chickens and compared to controls. Chickens cold-acclimated at 4–7 or 8–11 °C for 4 weeks had significantly elevated plasma FFA when compared to the controls at 19–21 °C. Although PGE1 had no effect on the basal level of FFA of controls, a significantly lower plasma FFA was seen after injection of either 10 or 30 μg PGE1/kg in cold-acclimated chickens. Chickens cold-exposed to 2–3 °C for 4 h demonstrated significant elevations of plasma FFA when compared to controls. Only 30 μg PGE1/kg significantly depressed the plasma FFA in the cold-exposed birds. No inhibition of basal FFA release was seen in control animals. From these experiments, it is concluded that chickens mobilize FFA extensively under cold-exposure and that this stimulated lipolysis is inhibited by PGE1.

Influence of Free Fatty Acid Concentrations and Weight Loss on Adipose Tissue Direct Free Fatty Acid Storage Rates

2021 ◽  
Author(s):  
Qingyi Jia ◽  
B Gisella Carranza Leon ◽  
Michael D Jensen
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Subcutaneous Fat ◽  
Premenopausal Women ◽  
Tissue Level ◽  
Research Unit ◽  
Lower Body ◽  
Plasma Ffa

Abstract Context The factors that determine the recycling of free fatty acids (FFA) back into different adipose tissue depots via the direct storage pathway are not completely understood. Objective To assess the interactions between adipocyte factors and plasma FFA concentrations that determine regional FFA storage rates. Design We measured direct adipose tissue FFA storage rates before and after weight loss under high FFA (intravenous somatostatin and epinephrine) and low (intravenous insulin and glucose) FFA concentrations. Setting Mayo Clinic Clinical Research Unit. Patients Sixteen premenopausal women, BMI 30 - 37 kg/m 2. Intervention Comprehensive lifestyle weight loss program. Main Outcome Measure Direct FFA storage rates in upper and lower body subcutaneous fat. Results Over the entire range of FFA and under isolated conditions of elevated FFA concentrations the storage rates of FFA into upper and lower body subcutaneous fat per unit lipid were associated with concentrations, not adipocyte fatty acid storage factors. Under low FFA conditions, direct FFA storage rates were related to adipocyte CD36 content, not tissue level content of fatty acid storage factors. Weight loss did not change these relationships. Conclusions The regulation of direct FFA storage under low FFA concentration conditions appears to be at the level of the cell/adipocyte content of CD36, whereas under high FFA concentration conditions direct FFA storage at the tissue level is predicted by plasma FFA concentrations, independent of adipocyte size or fatty acid storage factors. These observations offer novel insights into how adipose tissue regulates direct FFA storage in humans.

Evidence for a longitudinal pathway in rat hypothalamus that controls FFA mobilization

1983 ◽  
Vol 245 (4) ◽  
pp. E332-E337 ◽  
Author(s):  
C. C. Coimbra ◽  
R. H. Migliorini
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Ventromedial Hypothalamus ◽  
Posterior Hypothalamus ◽  
Unilateral Lesion ◽  
Hypothalamic Region ◽  
Electrolytic Lesions ◽  
Plasma Ffa ◽  
Bilateral Lesions

In initial exploratory experiments, bilateral, symmetrical, relatively large electrolytic lesions were produced, injuring anterior, middle, and posterior hypothalamus but respecting the midlateral region. Only lesions in the preoptic-anterior hypothalamic region and in the posterior hypothalamus were effective in blocking free fatty acid (FFA) mobilization induced by intravenous 2-deoxyglucose. Lesions in the ventromedial hypothalamus were ineffective. In subsequent experiments, suppression of plasma FFA response to the drug was observed in rats with small, globular (0.5-1.0 mm diam), bilateral lesions either in the preoptic (PO) or in the lateral hypothalamic (LH) areas. Groups of animals were then prepared in which a unilateral lesion in the PO area was combined with a contralateral lesion in the LH area. Plasma FFA response to 2-deoxyglucose in these rats was also blocked but not in rats having only unilateral lesions. The hyperglycemic response to 2-deoxyglucose was not affected in any of the experimental groups. These data suggest that a longitudinal pathway connecting PO, LH, and posterior hypothalamic areas is involved in FFA mobilization from adipose tissue in rats.

Lack of effect of hyperglycemia on lipolysis in humans

1993 ◽  
Vol 265 (6) ◽  
pp. E821-E824 ◽  
Author(s):  
E. Cersosimo ◽  
S. Coppack ◽  
M. Jensen
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Glucose ◽  
Acid Metabolism ◽  
The Face ◽  
Study Interval ◽  
Free Fatty Acid Metabolism ◽  
Insulin Dependent ◽  
Adipose Tissue Lipolysis

To examine whether hyperglycemia is an independent regulator of adipose tissue lipolysis, we measured palmitate flux ([3H]palmitate) on two occasions in eight volunteers with insulin-dependent diabetes. On one. occasion, euglycemia was maintained for 4 h continuously; on a different occasion, hyperglycemia (plasma glucose, 12 mmol/l) was induced after 2 h of euglycemia. Palmitate flux decreased from 1.39 +/- 0.22 to 1.25 +/- 0.18 mumol.kg-1 x min-1 during sustained euglycemia and from 1.43 +/- 0.24 to 1.13 +/- 0.19 mumol.kg-1 x min-1 during the transition from the euglycemic to the hyperglycemic study intervals. There were no significant differences between the changes in palmitate flux from the first to the second study interval on the control (euglycemia-euglycemia) and experimental (euglycemia-hyperglycemia) study days and no difference between palmitate flux on different study days. Thus, in the face of euinsulinemia, euglucagonemia, and the absence of somatostatin, no effect of hyperglycemia on free fatty acid metabolism could be detected in humans.

Effects of noradrenaline and nicotinic acid on plasma free fatty acids and oxygen consumption in cold-adapted rats

1979 ◽  
Vol 57 (7) ◽  
pp. 725-730 ◽  
Author(s):  
Louise Lafrance ◽  
Danièle Routhier ◽  
Bernard Têtu ◽  
Christian Têtu
Keyword(s):  
Fatty Acids ◽  
Oxygen Consumption ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Nicotinic Acid ◽  
Free Fatty Acids ◽  
Simultaneous Increase ◽  
Elevated Plasma ◽  
Cold Adapted ◽  
Plasma Ffa

A 3-h noradrenaline (NA) infusion (1.5 μg kg−1 min−1) produced a sustained enhanced oxygen consumption (O2 cons.) in cold-adapted rats. Plama free fatty acid (FFA) levels were elevated by NA in control and in cold-adapted rats, but to a lesser extent in cold-adapted rats; the increase was maintained at a plateau in both groups during the entire period of NA infusion. A 1-h nicotinic acid (Nic A) infusion (1.5 mg kg−1 min−1) added to the NA infusion inhibited the calorigenic response to NA in cold-adapted rats and reduced the elevated plasma FFA concentration in control and in cold-adapted rats to values below basal levels. However, when the Nic A infusion was stopped, the O2 cons, was increased again in cold-adapted rats by the uninterrupted NA infusion, without the simultaneous increase of the plasma FFA concentration; the plasma FFA concentration was maintained in cold-adapted rats below basal values and merely brought back to basal levels in control rats. From these results, it is suggested that plasma FFA are not an essential substrate to the calorigenic response to NA observed in cold-adapted rats, as 85% of the response can occur when the plasma FFA concentration is very low.

Lack of effect of hyperglycemia on lipolysis in humans

1990 ◽  
Vol 259 (4) ◽  
pp. E542-E547
Author(s):  
M. Caruso ◽  
G. D. Divertie ◽  
M. D. Jensen ◽  
J. M. Miles
Keyword(s):  
Growth Hormone ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Glucose ◽  
Time Dependent ◽  
Constant Infusion ◽  
Insulin Dependent ◽  
Adipose Tissue Lipolysis ◽  
Per Se

Controversy exists regarding whether plasma glucose concentrations are independently involved in the regulation of adipose tissue lipolysis. In the present study, six subjects with insulin-dependent diabetes and six nondiabetic volunteers were studied during infusion of somatostatin, growth hormone, and insulin at rates designed to maintain basal rates of lipolysis, which was traced using a constant infusion of [1-14C]palmitate. A euglycemic (approximately 5 mmol/l) clamp was performed for 3 h, followed by 3 h of hyperglycemia (approximately 9 and approximately 11 mmol/l in nondiabetic and diabetic subjects, respectively). Ten nondiabetic subjects were studied during 6 h of euglycemia to exclude time-dependent changes in lipolysis. The results showed that palmitate concentrations did not change between euglycemia and hyperglycemia in either group [118 +/- 10 vs. 132 +/- 14 mumol/l and 145 +/- 21 vs. 134 +/- 15 mumol/l in nondiabetic and diabetic subjects, respectively; both P = not significant (NS)]. Similarly, palmitate rate of appearance (Ra) did not change during hyperglycemia (1.0 +/- 0.1 and 1.7 +/- 0.4 mumol.kg-1.min-1 in nondiabetic and diabetic subjects, respectively) compared with euglycemia (1.0 +/- 0.1 and 1.6 +/- 0.4 mumol.kg-1.min-1 in nondiabetic and diabetic subjects, respectively; P = NS). Palmitate concentrations and Ra did not change during 6 h of euglycemia in nondiabetic volunteers. Thus hyperglycemia per se has no effect on free fatty acid turnover. Changes in lipolysis that occur coincident with hyperglycemia are probably due to changes in other circulating substrates or hormones known to affect lipolysis.

scholarly journals Inhibition of adipose tissue lipolysis increases intramuscular lipid and glycogen use in vivo in humans

2005 ◽  
Vol 289 (3) ◽  
pp. E482-E493 ◽  
Author(s):  
Luc J. C. van Loon ◽  
Michaela Thomason-Hughes ◽  
Dumitru Constantin-Teodosiu ◽  
René Koopman ◽  
Paul L. Greenhaff ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Free Fatty Acid ◽  
Oxidation Rates ◽  
Acid Analog ◽  
Plasma Ffa ◽  
Intramuscular Lipid ◽  
Adipose Tissue Lipolysis

This study investigates the consequences of inhibition of adipose tissue lipolysis on skeletal muscle substrate use. Ten subjects were studied at rest and during exercise and subsequent recovery under normal, fasting conditions (control trial, CON) and following administration of a nicotinic acid analog (low plasma free fatty acid trial, LFA). Continuous [U-13C]palmitate and [6,6-2H2]glucose infusions were applied to quantify plasma free fatty acid (FFA) and glucose oxidation rates and to estimate intramuscular triacylglycerol (IMTG) and glycogen use. Muscle biopsies were collected to measure 1) fiber type-specific IMTG content; 2) allosteric regulators of hormone-sensitive lipase (HSL), glycogen phosphorylase, and pyruvate dehydrogenase; and 3) the phosphorylation status of HSL at Ser563 and Ser565. Administration of a nicotinic acid analog (acipimox) substantially reduced plasma FFA rate of appearance and subsequent plasma FFA concentrations ( P < 0.0001). At rest, this substantially reduced plasma FFA oxidation rates, which was compensated by an increase in the estimated IMTG use ( P < 0.05). During exercise, the progressive increase in FFA rate of appearance, uptake, and oxidation was prevented in the LFA trial and matched by greater IMTG and glycogen use. Differential phosphorylation of HSL or relief of its allosteric inhibition by long-chain fatty acyl-CoA could not explain the increase in muscle TG use, but there was evidence to support the contention that regulation may reside at the level of the glucose-fatty acid cycle. This study confirms the hypothesis that plasma FFA availability regulates both intramuscular lipid and glycogen use in vivo in humans.

scholarly journals Plasma Free Fatty Acid Concentration as a Modifiable Risk Factor for Metabolic Disease

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2590
Author(s):  
Gregory C. Henderson
Keyword(s):  
Metabolic Disease ◽  
Adipose Tissue ◽  
Risk Factor ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Free Fatty Acid ◽  
Modifiable Risk Factor ◽  
Alcoholic Fatty Liver ◽  
Health Lifestyle ◽  
Plasma Ffa

Plasma free fatty acid (FFA) concentration is elevated in obesity, insulin resistance (IR), non-alcoholic fatty liver disease (NAFLD), type 2 diabetes (T2D), and related comorbidities such as cardiovascular disease (CVD). Furthermore, experimentally manipulating plasma FFA in the laboratory setting modulates metabolic markers of these disease processes. In this article, evidence is presented indicating that plasma FFA is a disease risk factor. Elevations of plasma FFA can promote ectopic lipid deposition, IR, as well as vascular and cardiac dysfunction. Typically, elevated plasma FFA results from accelerated adipose tissue lipolysis, caused by a high adipose tissue mass, adrenal hormones, or other physiological stressors. Reducing an individual’s postabsorptive and postprandial plasma FFA concentration is expected to improve health. Lifestyle change could provide a significant opportunity for plasma FFA reduction. Various factors can impact plasma FFA concentration, such as chronic restriction of dietary energy intake and weight loss, as well as exercise, sleep quality and quantity, and cigarette smoking. In this review, consideration is given to multiple factors which lead to plasma FFA elevation and subsequent disruption of metabolic health. From considering a variety of medical conditions and lifestyle factors, it becomes clear that plasma FFA concentration is a modifiable risk factor for metabolic disease.

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