Brief food restriction increases FA oxidation and glycogen synthesis under insulin-stimulated conditions

2002 ◽  
Vol 282 (4) ◽  
pp. R1210-R1218 ◽  
Author(s):  
Michelle Z. Tucker ◽  
Lorraine P. Turcotte
Keyword(s):  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Food Intake ◽  
Glucose Uptake ◽  
Food Restriction ◽  
Glycogen Synthesis ◽  
Palmitate Uptake ◽  
Ad Libitum ◽  
Muscle Triglyceride ◽  
White Gastrocnemius

To determine the effects of brief food restriction on fatty acid (FA) metabolism, hindlimbs of F344/BN rats fed either ad libitum (AL) or food restricted (FR) to 60% of baseline food intake for 28 days were perfused under hyperglycemic-hyperinsulinemic conditions (20 mM glucose, 1 mM palmitate, 1,000 μU/ml insulin, [3-3H]glucose, and [1-14C]palmitate). Basal glucose and insulin levels were significantly lower ( P < 0.05) in FR vs. AL rats. Palmitate uptake (34.3 ± 2.7 vs. 24.5 ± 3.1 nmol/g/min) and oxidation (3.8 ± 0.2 vs. 2.7 ± 0.3 nmol · g−1 · min−1) were significantly higher ( P < 0.05) in FR vs. AL rats, respectively. Glucose uptake was increased in FR rats and was accompanied by significant increases in red and white gastrocnemius glycogen synthesis, indicating an improvement in insulin sensitivity. Although muscle triglyceride (TG) levels were not significantly different between groups, glucose uptake and total preperfusion TG concentration were negatively correlated ( r 2 = 0.27, P < 0.05). In conclusion, our results show that under hyperglycemic-hyperinsulinemic conditions, brief FR resulted in an increase in FA oxidative disposal that may contribute to the improvement in insulin sensitivity.

Insulin fails to alter plasma LCFA metabolism in muscle perfused at similar glucose uptake

2002 ◽  
Vol 283 (1) ◽  
pp. E73-E77 ◽  
Author(s):  
Alice J. Yee ◽  
Lorraine P. Turcotte
Keyword(s):  
Fatty Acid ◽  
Glucose Uptake ◽  
Chain Fatty Acid ◽  
Cellular Mechanisms ◽  
Long Chain Fatty Acid ◽  
Malonyl Coa ◽  
Palmitate Uptake ◽  
Induced Changes ◽  
Muscle Triglyceride ◽  
Long Chain

Insulin has been shown to alter long-chain fatty acid (LCFA) metabolism and malonyl-CoA production in muscle. However, these alterations may have been induced, in part, by the accompanying insulin-induced changes in glucose uptake. Thus, to determine the effects of insulin on LCFA metabolism independently of changes in glucose uptake, rat hindquarters were perfused with 600 μM palmitate and [1-14C]palmitate and with either 20 mM glucose and no insulin (G) or 6 mM glucose and 250 μU/ml of insulin (I). As dictated by our protocol, glucose uptake was not significantly different between the G and I groups (10.3 ± 0.6 vs. 11.0 ± 0.5 μmol · g−1 · h−1; P > 0.05). Total palmitate uptake and oxidation were not significantly different ( P > 0.05) between the G (10.1 ± 1.0 and 0.8 ± 0.1 nmol · min−1 · g−1) and I (10.2 ± 0.6 and 1.1 ± 0.2 nmol · min−1 · g−1) groups. Preperfusion muscle triglyceride and malonyl-CoA levels were not significantly different between the G and I groups and did not change significantly during the perfusion ( P > 0.05). Similarly, muscle triglyceride synthesis was not significantly different between groups ( P > 0.05). These results demonstrate that the presence of insulin under conditions of similar glucose uptake does not alter LCFA metabolism and suggest that cellular mechanisms induced by carbohydrate availability, but independent of insulin, may be important in the regulation of muscle LCFA metabolism.

Nonnutritive flow impairs uptake of fatty acid by white muscles of the perfused rat hindlimb

2003 ◽  
Vol 284 (3) ◽  
pp. E611-E617 ◽  
Author(s):  
L. H. Clerk ◽  
M. E. Smith ◽  
S. Rattigan ◽  
M. G. Clark
Keyword(s):  
Fatty Acid ◽  
Connective Tissue ◽  
Glucose Uptake ◽  
Tibialis Anterior ◽  
Extensor Digitorum Longus ◽  
Insulin Infusion ◽  
Fat Cells ◽  
Triglyceride Hydrolysis ◽  
Palmitate Uptake ◽  
White Gastrocnemius

Triglyceride hydrolysis by the perfused rat hindlimb is enhanced with serotonin-induced nonnutritive flow (NNF) and may be due to the presence of nonnutritive route-associated connective tissue fat cells. Here, we assess whether NNF influences muscle uptake of 0.55 mM palmitate in the perfused hindlimb. Comparisons were made with insulin-mediated glucose uptake. NNF induced during 60 nM insulin infusion inhibited hindlimb oxygen uptake from 22.0 ± 0.5 to 9.7 ± 0.8 μmol · g−1 · h−1( P < 0.001), 1-methylxanthine metabolism (indicator of nutritive flow) from 5.8 ± 0.4 to 3.8 ± 0.4 nmol · min−1 · g−1( P = 0.004), glucose uptake from 29.2 ± 1.7 to 23.1 ± 1.8 μmol · g−1 · h−1( P = 0.005) and muscle 2-deoxyglucose uptake from 82.1 ± 4.6 to 41.6 ± 6.7 μmol · g−1 · h−1( P < 0.001). Palmitate uptake, unaffected by insulin alone, was inhibited by NNF in extensor digitorum longus, white gastrocnemius, and tibialis anterior muscles; average inhibition was from 13.9 ± 1.2 to 6.9 ± 1.4 μmol · g−1 · h−1( P = 0.02). Thus NNF impairs both fatty acid and glucose uptake by muscle by restricting flow to myocytes but, as shown previously, favors triglyceride hydrolysis and uptake into nearby connective tissue fat cells. The findings have implications for lipid partitioning in limb muscles between myocytes and attendant adipocytes.

Impaired plasma FFA oxidation imposed by extreme CHO deficiency in contracting rat skeletal muscle

1994 ◽  
Vol 77 (2) ◽  
pp. 517-525 ◽  
Author(s):  
L. P. Turcotte ◽  
P. J. Hespel ◽  
T. E. Graham ◽  
E. A. Richter
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Glucose Uptake ◽  
Swimming Exercise ◽  
Rat Skeletal Muscle ◽  
Palmitate Oxidation ◽  
Plasma Ffa ◽  
Ffa Metabolism ◽  
Palmitate Uptake

The extent to which carbohydrate (CHO) availability affects free fatty acid (FFA) metabolism in contracting skeletal muscle is not well characterized. To study this question, rats were depleted of glycogen by swimming exercise and lard feeding 24 h before perfusion of their isolated hindquarters. After 20 min of preperfusion with a medium containing no glucose, palmitate (600 or 2,000 microM), and [1–14C]palmitate, flow was restricted to one hindlimb, which was electrically stimulated for 2 min to further deplete muscles of glycogen. After 2 min of recovery, glucose was added to the perfusate at final concentrations of 0, 6, or 20 mM, and after another 3 min muscles were stimulated for 30 min. At 6 and 2,000 microM palmitate, glucose uptake after 30 min of stimulation averaged 23.5 +/- 9.3 and 45.9 +/- 10.6 mumol.g-1.h-1 with 6 and 20 mM glucose, respectively. At 6 and 2,000 microM palmitate, palmitate uptake was lower (30–37%, P < 0.05) with 0 than with 6 or 20 mM glucose. At 600 microM palmitate, percent palmitate oxidation was higher (27%, P < 0.05) with 0 than with 6 or 20 mM glucose, resulting in similar total palmitate oxidation with the three glucose concentrations (0.28 +/- 0.01 mumol.g-1.h-1). At 2,000 microM palmitate, percent palmitate oxidation was not significantly different among glucose concentrations, resulting in a significantly lower rate of palmitate oxidation with 0 (0.62 +/- 0.18 mumol.g-1.h-1) than with 6 or 20 mM glucose (0.77 +/- 0.25 and 0.78 +/- 0.20 mumol.g-1.h-1, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Glucose metabolism in epitrochlearis muscle of acutely exercised and trained rats

1986 ◽  
Vol 250 (2) ◽  
pp. E137-E143 ◽  
Author(s):  
T. A. Davis ◽  
S. Klahr ◽  
E. D. Tegtmeyer ◽  
D. F. Osborne ◽  
T. L. Howard ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Acute Exercise ◽  
Glycogen Synthesis ◽  
Prior Training ◽  
Glycogen Stores

Effects of insulin on glycogen synthesis (GS), glycolytic utilization (GU), and glucose uptake (GT) were studied in isolated epitrochlearis muscles from exercise-trained or sedentary rats during recovery from acute exercise or at rest. During the 1st h after acute exercise, the enhanced basal and insulin-stimulated GT was directed mainly toward replenishment of glycogen but basal GU was also increased. During the second through third hours after exercise, basal GS decreased but remained greater than rest and basal GU and GT returned to normal. Insulin sensitivity of these parameters was enhanced. Training alone reduced basal GS but enhanced insulin sensitivity of GT and GU. Training reduced the acute exercise-stimulated increase in basal and insulin sensitivity of GS during recovery from acute exercise, probably due to elevated glycogen stores. Thus recovery from acute exercise or training, either alone or in combination, enhances insulin stimulated GT in muscle; however, the increased glucose is primarily channeled toward GS after acute exercise, which is reduced by prior training and is directed to GU in trained animals either at rest or after acute exercise.

scholarly journals Distinct glucose lowering and beta cell protective effects of vanadium and food restriction in streptozotocin-diabetes

1999 ◽  
pp. 546-554 ◽  
Author(s):  
MC Cam ◽  
B Rodrigues ◽  
JH McNeill
Keyword(s):  
Insulin Sensitivity ◽  
Food Intake ◽  
Beta Cell ◽  
Beta Cells ◽  
Food Restriction ◽  
Plasma Insulin ◽  
Protective Effects ◽  
Glucose Lowering ◽  
Insulin Levels ◽  
Pancreatic Insulin

Vanadium is an oral insulin-mimetic agent that diminishes hyperglycemia, improves beta-cell insulin store and secretory function, and can reverse the diabetic state chronically after withdrawal from treatment. As food restriction has been reported to enhance insulin sensitivity and reduce insulin demand, we assessed the contribution of a reduced food intake to the glucose lowering and beta-cell protective effects of vanadium. Streptozotocin (STZ)-diabetic rats were untreated (D) or administered vanadyl sulfate in the drinking water (DT) at one week prior to and for 5 weeks following the administration of STZ. An additional group was pair-fed (DP) with an equal amount of food as that consumed by the DT group. Shortly after the induction of diabetes, hyperglycemic D rats demonstrated a significant rise in plasma insulin to levels that initially exceeded that of the controls. This was followed by a steady reduction over several weeks, suggesting a gradual depletion of functional beta-cells. Both vanadium treatment and pair-feeding abolished the insulin hypersecretory response following STZ administration. Glucose lowering was enhanced in DT animals when administered higher concentrations of vanadium, despite no further reduction in food intake, and all DT animals (10/10) were normoglycemic by 5 weeks. Mean pancreatic insulin content in DT rats was improved fourfold and was associated with a greater number of granulated beta-cells. Conversely, food restriction only modestly improved glycemia and the pancreatic insulin store and, unlike DT, DP rats remained highly glucose-intolerant. At 5 weeks of diabetes, fed circulating glucose and insulin levels were strongly correlated (P=0.0002) in the D and DP groups, supporting the notion that glucose lowering with food restriction is dependent on improved plasma insulin levels. A separate correlation was observed in DT animals within a lower range of plasma insulin, suggesting that vanadium, unlike food restriction, reduced plasma glucose by enhancing insulin sensitivity. Thus, vanadium preserves beta-cells in STZ-diabetes at least partially by abolishing the insulin hypersecretory response and the eventual exhaustion of residual insulin stores following a moderate dose of STZ. This property of vanadium would appear to be useful in the treatment of prediabetic and newly diagnosed insulin-dependent diabetes mellitus.

scholarly journals The disposition of carbohydrate between glycogenesis, lipogenesis and oxidation in liver during the starved-to-fed transition

1988 ◽  
Vol 252 (2) ◽  
pp. 325-330 ◽  
Author(s):  
M J Holness ◽  
P A MacLennan ◽  
T N Palmer ◽  
M C Sugden
Keyword(s):  
Glucose Uptake ◽  
Pyruvate Dehydrogenase ◽  
Temporal Relationship ◽  
Glycogen Synthesis ◽  
Glucose Flux ◽  
Hepatic Glucose ◽  
Ad Libitum ◽  
Time Courses

A comparison was made between the time courses of restoration of pyruvate dehydrogenase activities, fructose 2,6-bisphosphate concentrations and lipogenic rates, together with net hepatic glucose flux and glycogen synthesis/deposition in livers of 48 h-starved rats provided with laboratory chow ad libitum for up to 24 h. Increased glycogenesis, lipogenesis and net glucose uptake were observed after 1 h of re-feeding, preceding re-activation of pyruvate dehydrogenase, which occurred after 3-4 h. Increased concentrations of fructose 2,6-bisphosphate were only observed after 5-6 h. The implication of the temporal relationship between these parameters is discussed.

scholarly journals CD36 inhibition prevents lipid accumulation and contractile dysfunction in rat cardiomyocytes

2012 ◽  
Vol 448 (1) ◽  
pp. 43-53 ◽  
Author(s):  
Yeliz Angin ◽  
Laura K. M. Steinbusch ◽  
Peter J. Simons ◽  
Sabrina Greulich ◽  
Nicole T. H. Hoebers ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Glucose Uptake ◽  
Lipid Accumulation ◽  
Insulin Signalling ◽  
Culture Conditions ◽  
Contractile Dysfunction ◽  
Rat Cardiomyocytes ◽  
Akt Phosphorylation ◽  
Palmitate Uptake

An increased cardiac fatty acid supply and increased sarcolemmal presence of the long-chain fatty acid transporter CD36 are associated with and contribute to impaired cardiac insulin sensitivity and function. In the present study we aimed at preventing the development of insulin resistance and contractile dysfunction in cardiomyocytes by blocking CD36-mediated palmitate uptake. Insulin resistance and contractile dysfunction were induced in primary cardiomyocytes by 48 h incubation in media containing either 100 nM insulin (high insulin; HI) or 200 μM palmitate (high palmitate; HP). Under both culture conditions, insulin-stimulated glucose uptake and Akt phosphorylation were abrogated or markedly reduced. Furthermore, cardiomyocytes cultured in each medium displayed elevated sarcolemmal CD36 content, increased basal palmitate uptake, lipid accumulation and decreased sarcomere shortening. Immunochemical CD36 inhibition enhanced basal glucose uptake and prevented elevated basal palmitate uptake, triacylglycerol accumulation and contractile dysfunction in cardiomyocytes cultured in either medium. Additionally, CD36 inhibition prevented loss of insulin signalling in cells cultured in HP, but not in HI medium. In conclusion, CD36 inhibition prevents lipid accumulation and lipid-induced contractile dysfunction in cardiomyocytes, but probably independently of effects on insulin signalling. Nonetheless, pharmacological CD36 inhibition may be considered as a treatment strategy to counteract impaired functioning of the lipid-loaded heart.

The effect of housing and food restriction during winter on growth of male red deer calves

1997 ◽  
Vol 64 (1) ◽  
pp. 171-176 ◽  
Author(s):  
J. R. Webster ◽  
I. D. Corson ◽  
J. M. Suttie
Keyword(s):  
Growth Rate ◽  
Food Intake ◽  
Energy Expenditure ◽  
Food Restriction ◽  
Red Deer ◽  
Management Practice ◽  
Live Weight ◽  
Normal Growth ◽  
Cold Weather ◽  
Ad Libitum

AbstractLow winter growth is a characteristic of male red deer and is caused, in part by a combination of reduced appetite and higher energy expenditure due to cold weather. This study aimed to determine whether housing during winter would reduce energy expenditure and increase the growth rate of male red deer calves. An additional aim was to investigate whether food restriction in winter would be compensated for by increased spring growth. In each of two consecutive years, 80 calves were randomly allocated to eight groups (no. = 10) comprising two replicates of four treatments during winter. Groups were housed inside (I) or outside (O) and given food either ad libitum (AL) or restricted (R) to maintain live weight. Winter treatments (southern hemisphere) ran from 22 May to 25 August (year 1) and from 5 June to 5 September (year 2). During these periods, animals were weighed weekly and group food intake recorded daily. At the end of winter animals were moved outside onto pasture and weighed monthly until the end of spring (27 November, year 1 and 7 December, year 2). In year 2 weighing continued during summer, until 4 April. The animals were slaughtered on 28 November and 18 January (year 1) and 5 April (year 2). The effect of housing on live-weight gain (LWG) and dry-matter intake (DM1) in AL groups was not significant in either year. However in R groups, O had a higher DMI than I in both years (P < 0·05) and a higher LWG than I in year 1 (P < 0·05). LWG was loiver in R than in AL groups in winter in year 1 (P < 0·05) and year 2 (P < 0·001) and live weight was lower in R than in AL groups at the end of winter in both years. Live weight was still lower in R than in AL groups at the end of spring in both years (P < 0·01). In year 2, this live-weight difference was not significant by the end of summer. Hot carcass weight (HCW) was greater in AL animals than R animals (P < 0·05) and dressing proportion was higher in R than in AL (P < 0·05) in year 1. GR (an index of body fatness) was greater (P < 0·05) in O than I in year 1 and was greater (P < 0·05) in AL than in R animals in year 2. Differences in GR between treatments were not significant in either year, with HCW as a covariate.In conclusion, housing calves given food ad libitum during winter did not reduce DMI or increase growth rate. When normal growth rates were prevented by restricting food intake, housing lowered DMI requirement, although such a situation is unlikely to be a useful farm management practice as recovery from the growth check was slow. Annual variations in climate may determine both the food savings made by housing and the extent of compensatory growth of food-restricted animals in spring.

scholarly journals Gonadotropin-Releasing Hormone-II Messenger Ribonucleic Acid and Protein Content in the Mammalian Brain Are Modulated by Food Intake

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5069-5077 ◽  
Author(s):  
Alexander S. Kauffman ◽  
Karolina Bojkowska ◽  
Aileen Wills ◽  
Emilie F. Rissman
Keyword(s):  
Food Intake ◽  
Food Restriction ◽  
Mammalian Brain ◽  
Mrna Levels ◽  
Female Reproduction ◽  
Messenger Ribonucleic Acid ◽  
Medial Habenula ◽  
Sufficient Energy ◽  
Peptide Family ◽  
Ad Libitum

GnRH-II is the most evolutionarily conserved member of the GnRH peptide family. In mammals, GnRH-II has been shown to regulate reproductive and feeding behaviors. In female musk shrews, GnRH-II treatment increases mating behaviors and decreases food intake. Although GnRH-II-containing neurons are known to reside in the midbrain, the neural sites of GnRH-II action are undetermined, as is the degree to which GnRH-II is regulated by energy availability. To determine whether GnRH-II function is affected by changes in food intake, we analyzed the levels of GnRH-II mRNA in the midbrain and GnRH-II protein in numerous target regions. Adult musk shrews were ad libitum fed, food restricted, or food restricted and refed for varying durations. Compared with ad libitum levels, food restriction decreased, and 90 min of refeeding reinstated, GnRH-II mRNA levels in midbrain and GnRH-II peptide in several target areas including the medial habenula and ventromedial nucleus. Refeeding for 90 min also reinstated female sexual behavior in underfed shrews. In male shrews, abundant GnRH-II peptide was present in all sites assayed, including the preoptic area, a region with only low GnRH-II in females. In contrast to females, food restriction did not affect GnRH-II protein in male brains or inhibit their mating behavior. Our results further define the relationship between GnRH-II, energy balance, and reproduction, and suggest that food restriction may inhibit female reproduction by reducing GnRH-II output to several brain nuclei. We postulate that this highly conserved neuropeptide functions similarly in other mammals, including humans, to fine-tune reproductive efforts with periods of sufficient energy resources.

Effects of food restriction on body mass, energy metabolism and thermogenesis in a tree shrew (Tupaia belangeri)

2018 ◽  
Author(s):  
Xue-na Gong ◽  
Hao Zhang ◽  
Di Zhang ◽  
Wan-long Zhu
Keyword(s):  
Food Intake ◽  
Metabolic Rate ◽  
Body Mass ◽  
Food Restriction ◽  
Tree Shrew ◽  
Tree Shrews ◽  
Tupaia Belangeri ◽  
Brown Adipose ◽  
Food Shortages ◽  
Ad Libitum

AbstractThis study investigates the energy strategies of a small mammal in response to food shortages as a function of food restriction (FR), metabolic rate and ambient temperature. We subjected tree shrews (Tupaia belangeri) to FR and measured body mass, survival rate, resting metabolic rate (RMR), nonshivering thermogenesis (NST) and cytochrome c oxidase (COX) activity of brown adipose tissue (BAT). Cold-exposed animals restricted to 80% of ad libitum food intake had significantly increased RMR and NST and decreased body mass and survival rates compared with those kept at room temperature on the same FR level. Animals classified has having a high RMR consumed 30.69% more food than those classified as having a low RMR, but showed no differences in body mass or survival when restricted to 80% of ad libitum food intake. These results indicate that tree shrews, known for their relatively high metabolic rates, are sensitive to periods of FR, which supports the metabolic switch hypothesis. Our findings are also consistent with the prediction that small mammals with food hoarding behaviors, like tree shrews, may have a lower tolerance for food shortages than non-hoarding species.

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