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PubMed2006

Chronic palmitate but not oleate exposure induces endoplasmic reticulum stress, which may contribute to INS-1 pancreatic beta-cell apoptosis.

Chronic free fatty acid (FFA) exposure induces pancreatic beta-cell death, which may contribute to the development of type 2 diabetes. The mechanisms involved in FFA-induced cell death are not completely understood. Here we have investigated the effect of FFA on endoplasmic reticulum (ER) stress pathways in INS-1 pancreatic beta-cells. INS-1 cells exposed to palmitate for 16-24 h under serum-free conditions showed marked apoptosis and increased protein levels of phosphorylated eukaryotic translation initiation factor 2alpha (eIF2alpha), activating transcription factor 4 (ATF4), X box-binding protein 1 (XBP-1), and C/EBP homologous transcription factor (CHOP) compared with control cells. The CHOP transcription factor has been implicated in mediating ER stress-induced apoptosis. Unexpectedly, the levels of the ER chaperone proteins Grp78/BiP and PDI were not affected by palmitate treatment, suggesting that the cell protective aspects of the unfolded protein response (UPR) are not up-regulated by palmitate. Palmitate-treated cells had markedly altered distribution of ER chaperones and altered ER morphology, suggesting that accumulation of misfolded proteins might trigger the ER stress response. In contrast, oleate treatment did not significantly induce the UPR pathways, nor was it as detrimental to INS-1 beta-cells. The results suggest that activation of the UPR may significantly contribute to palmitate- but not oleate-induced pancreatic beta-cell death.

Animals↗
PubMed1999

Sodium palmitate induces partial mitochondrial uncoupling and reactive oxygen species in rat pancreatic islets in vitro.

The aim of the present investigation was to study whether prolonged exposure of isolated rat islets to the long chain fatty acid sodium palmitate leads to uncoupling of respiration. It was found that culture of islets in the presence of palmitate abolished glucose-sensitive insulin release and decreased insulin contents. This was paralleled by decreased ATP contents, increased respiration, and decreased islet cell mitochondrial membrane potential. Using electron microscopy, an increase in the beta-cell mitochondrial volume in islets exposed to palmitate was observed. The addition of the uncoupler carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone, at a concentration that decreased mitochondrial membrane potential to a similar extent as palmitate, diminished the glucose-induced insulin release. In addition, islet generation of reactive oxygen species, but not of nitric oxide, was increased in response to a long-term palmitate exposure. It is concluded that long-term exposure to a long chain fatty acid induces partial uncoupling of beta-cell oxidative phosphorylation and that this may contribute to the loss of glucose-sensitive insulin release.

Adenosine Triphosphate↗
PubMed2004

Evidence that protein kinase Cdelta is not required for palmitate-induced cytotoxicity in BRIN-BD11 beta-cells.

Chronic exposure of pancreatic beta-cells to saturated fatty acids leads to loss of viability, an effect that has been implicated in the process of beta-cell 'lipotoxicity' associated with the progression of type 2 diabetes. The mechanisms involved are unknown but recent evidence has implicated the delta isoform of protein kinase C (PKCdelta) in mediating fatty acid toxicity. We have investigated this proposition in the clonal insulin-secreting cell line, BRIN-BD11. BRIN-BD11 cells were found to undergo apoptosis when exposed to palmitate and this response was attenuated by the purportedly selective inhibitor of PKCdelta, rottlerin. However, activation of PKCdelta with the phorbol ester, phorbol-12-myristate-13-acetate (PMA), failed to promote cell death and down-regulation of PKCdelta did not prevent the cytotoxic effects of palmitate. Moreover, rottlerin remained effective as a blocker of the palmitate response in cells depleted of PKCdelta. Since rottlerin can inhibit various other kinases in addition to PKCdelta, a range of additional kinase inhibitors was also tested. Of these, only the putative Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) inhibitor, KN-62, was found to inhibit palmitate-induced cell death. However, this effect was not reproduced by a more selective pseudo-substrate inhibitor of CaM kinase II. Therefore, the present results reveal that palmitate induces cell death in BRIN-BD11 cells and suggest that this may involve the activation of a rottlerin (and KN-62)-sensitive kinase. However, it is clear that PKCdelta is not required for this response.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2003

Palmitate-induced activation of the hexosamine pathway in human myotubes: increased expression of glutamine:fructose-6-phosphate aminotransferase.

The nutrient sensing capacity of the hexosamine biosynthetic pathway (HBP) has been implicated in the development of insulin resistance of skeletal muscle. To study the molecular mechanism of the free fatty acid (FFA)-induced activation of the HBP myotubes obtained from muscle biopsies of metabolically characterized, subjects were stimulated with different fatty acids for 20 h. Incubation with the saturated fatty acids palmitate and stearate (0.5 mmol/l) resulted in a three- to fourfold increase in mRNA expression of glutamine:fructose-6-phosphate aminotransferase (GFAT), the key and rate-limiting enzyme of the hexosamine pathway. Unsaturated fatty acids or 30 mmol/l glucose had little or no effect. Palmitate increased the amount of GFAT protein nearly two-fold, and subsequently, the concentration of UDP-N-acetylglucosamine, the end product of the HBP, was 1.3-fold enhanced in the palmitate-stimulated myotubes. The nonmetabolized fatty acid bromopalmitate had no effect. The DNA binding activity of the transcription factor Sp1, a target downstream of the HBP, was increased by palmitate and completely lost after enzymatic removal of O-GlcNAc. No correlation was found between the palmitate-induced increase in GFAT protein and the insulin resistance in the respective subjects. The findings reveal a new mechanism for how FFAs induce the activation of the HBP.

Cells, Cultured↗
PubMed1997

Comparison of a carbohydrate-rich diet and diets rich in stearic or palmitic acid in NIDDM patients. Effects on lipids, glycemic control, and diurnal blood pressure.

OBJECTIVE: To compare the effects on lipid levels, glycemic control, and diurnal blood pressure of two diets rich in one of the two quantitatively most important saturated fatty acids, stearic and palmitic acid, with a carbohydrate-rich diet in NIDDM patients. RESEARCH DESIGN AND METHODS: A total of 15 NIDDM patients participated in a randomized crossover study with three 3-week diet interventions separated by 2-week washout periods. Patients started with a diet rich in stearic acid (44 E% [percent of total energy] fat [13 E% stearic acid], 40 E% carbohydrate, 15 E% protein), palmitic acid (45 E% fat [16 E% palmitic acid], 40 E% carbohydrate, 15 E% protein), or carbohydrate (29 E% fat, 51 E% carbohydrate, and 18 E% protein), then were shifted to the other two diets in a randomized block design. At the start and end of each intervention period, fasting blood samples were drawn for analysis of lipids and blood glucose. In addition, diurnal blood pressure was measured. RESULTS: At the end of the 3-week interventions, total cholesterol was significantly higher after the palmitic acid-rich diet than after the stearic acid-rich or carbohydrate-rich diets (5.3 +/- 1.3 vs. 5.0 +/- 1.2 and 4.9 +/- 1.2 mmol/l, respectively; P = 0.03). No significant differences in triglyceride, LDL, or HDL cholesterol levels were seen after the three intervention diets. No difference in effects between the diet periods were seen for fructosamine, HbA1c, fasting blood glucose, or diurnal blood pressure. CONCLUSIONS: For the first time, it has been demonstrated that a diet rich in palmitic acid was not as effective in lowering cholesterol levels as carbohydrate-rich and stearic acid-rich diets in NIDDM patients. No deleterious effects were seen on diurnal blood pressure, triglyceride levels, and glycemic control. Development of foods containing stearic acid rather than the more atherogenic saturated fatty acids may allow a wider choice of acceptable foods to NIDDM patients.

Adult↗
PubMed1996

The effects of palmitate on human erythrocyte membrane potential and osmotic stability.

To evaluate the mechanism(s) of erythrocyte stabilization in hypotonic medium by free fatty acids, we have studied the effect of palmitic acid and its derivatives on human erythrocyte membrane electrochemical properties, osmotic stability and fluidity. Palmitic acid increased the membrane potential to the highest extent as compared with its derivatives. The membrane potential was equal to -11.0 +/- 1.7 mV in the absence and -23.3 +/- 3.2 mV in the presence of 400 mumol 1(-1) of palmitic acid, -15.3 +/- 2.2 mV in the presence of 400 mumol 1(-1) of methyl ester of palmitic acid and -14.2 +/- 1.8 mV in the presence of 400 mumol 1(-1) of lauric aldehyde. We propose that free fatty acids, containing the charged carboxylic end group, in contrast to the corresponding esters or aldehydes, can act as ionophores. At the same time, the osmotic stabilization of erythrocytes by palmitic acid and its derivatives was higher in sodium-containing as compared with potassium-containing media and did not correlate with the effect of these compounds on the membrane potential. We suggest that protective potassium leakage does not play a main role in erythrocyte osmotic stabilization by free fatty acids. Possibly this stabilization is due to the structural rearrangement of the whole membrane.

Erythrocyte Membrane↗
PubMed1975

Structure and synthesis of milk fat XI. Effects of heparin on paths of incorporation of glucose and palmitic acid into milk fat.

Intravenous injection of heparin increases lipoprotein lipase activity of circulating serum presumably by removing the enzyme from its location on the capillary endothelium. The incorporation of carbon-14 uniformly labeled glucose and carbon-14 1-labeled palmitic acid into fractionated milk fat triglycerides was studied in both normal and heparin treated lactating goats. The objective was to remove lipoprotein lipase from the mammary gland capillaries and to contrast normal milk fat synthesis with a situation presumed to cause the gland to be solely dependent on the phosphatidic acid pathway. The studies with labeled glucose indicated that under normal conditions there are two sources of milk glyceride glycerol; while following heparin injections, there is a single glycerol pool providing most of the glyceride glycerol. The investigations with labeled palmitic acid indicated that under normal conditions there are two sources of palmitic acid coming from the blood which enter nonequilibrating cellular pools. Palmitic acid from both pools is available for triglyceride synthesis. Following heparin injections there appears to be a common intracellular pool of pre-formed palmitic acid derived from the blood. The data indicate that lipoprotein lipase operating on blood triglycerides yields a 2-mono-glyceride which subsequently enters the gland and is utilized for milk fat synthesis.

Animals↗
PubMed1999

Protein-mediated palmitate uptake and expression of fatty acid transport proteins in heart giant vesicles.

Giant sarcolemmal vesicles were isolated from rat heart and hindlimb muscles for a) characterization of long-chain fatty acid transport in the absence of metabolism and b) comparison of fatty acid transport protein expression with fatty acid transport. Giant vesicles contained cytosolic fatty acid binding protein. Palmitate uptake was completely divorced from its metabolism. All palmitate taken up was recovered in the intravesicular cytosol as unesterified FA. Palmitate uptake by heart vesicles exhibited a K m of 9.7 nm, similar to that of muscle (K m = 9.7 nm). Vmax (2.7 pmol/mg protein/s) in heart was 8-fold higher than in muscle (0.34 pmol/mg protein/s). Palmitate uptake was inhibited in heart (55-80%) and muscle (31-50%) by trypsin, phloretin, sulfo-N-succinimidyloleate (SSO), or a polyclonal antiserum against the 40 kDa plasma membrane fatty acid binding protein (FABPpm). Palmitate uptake by heart and by red and white muscle vesicles correlated well with the expression of fatty acid translocase (FAT/CD36) and fatty acid binding protein FABPpm, which may act in concert. The expression of fatty acid transport protein (FATP), was 10-fold lower in heart vesicles than in white muscle vesicles. It is concluded that long-chain fatty acid uptake by heart and muscle vesicles is largely protein-mediated, involving FAT/CD36 and FABPpm. The role of FATP in muscle and heart remains uncertain.

Animals↗
PubMed2002

Palmitate-induced apoptosis of microvascular endothelial cells and pericytes.

BACKGROUND: Recent observations in the EURODIAB Complications Study demonstrated that markers of insulin resistance are strong risk factors for retinopathy incidence in patients with diabetes. However, the molecular mechanism underlying this remains to be elucidated. In this study, we investigated the influence of palmitate, a major saturated free fatty acid in plasma, on the apoptotic cell death of cultured microvascular endothelial cells (EC) and retinal pericytes. MATERIALS AND METHODS: The intracellular formation of reactive oxygen species (ROS) was detected using the fluorescent probe CM-H(2)DCFDA. DNA synthesis was determined by measuring [(3) H]-thymidine incorporation into cells. DNA fragmentations of EC were quantitatively analyzed in an enzyme-linked immunosorbent assay, and DNA laddering was evaluated on agarose gel electrophoresis. RESULTS: Palmitate increased ROS generation in microvascular EC. Furthermore, palmitate significantly inhibited DNA synthesis and induced apoptotic cell death in EC, which were completely prevented by an antioxidant, N-acetylcysteine. Palmitate up-regulated pericyte mRNA levels of a receptor for advanced glycation end products (AGE), and thereby potentiated the apoptotic effects of AGE on pericytes. CONCLUSIONS: The results suggest that palmitate could induce apoptotic cell death in microvascular EC and pericytes through the overgeneration of intracellular ROS, and thus be involved in the development of diabetic retinopathy.

Apoptosis↗
PubMedDate not supplied

[Effect of thyroxine and hydrocortisone on the content of retinol and retinyl palmitate in liver tissue, kidney and blood of rats, loaded with high doses of retinyl acetate].

Administration of hight doses of retinyl acetate into rats caused an increase in content of retinol in liver tissue and kidney and retinyl palmitate in liver tissue, kidney and blood. The simultaneous administration of thyroxine decreased the accumulation of retinol and retinyl palmitate in liver tissue. At the same time, in kidney content of retinol was increased but content of retinol and retinyl palmitate in blood and retinyl palmitate in kidney did not differ from the values estimated in the control group. The simultaneous administration of retinyl acetate and hydrocortisone decreased the accumulation of retinol and retinyl palmitate in liver tissue, increased the content of vitamin A in blood and did not influence its content in kidney.

Animals↗
PubMed1976

Glucose and palmitate uptake in the myocardium of isolated hearts from adrenalectomized cats.

Hearts from chronically adrenalectomized (ADX) cats deprived of any steroid support for 9-12 days were isolated and perfused in a Langendorff apparatus at a constant pressure of 95 mm Hg. The perfusion medium was Krebs-Henseleit buffer with either 10 mM glucose or 0.4 mM palmitate complexed to 3 percent albumin. Labeled 14C substrate was used and the transient rate of glucose and palmitate uptake was measured. Oxygen consumption and [14C] palmitate incorporation into CO2, and heart lipids were also measured. ADX hearts showed an enhanced glucose uptake rate compared with controls, 65 +/- 11.3 mumoles/gm to 16.2 +/- 6. However, the qO2 was not significantly different from control hearts. Palmitate uptake, O2 consumption, and 14CO2 were significantly lower in ADX hearts perfused with fatty acid as the energy substrate. Fatty acid uptake decreased from 9.7 +/- 1.0 to 3.6 +/- 1.1 and lipid fractions in the heart showed significant decreases in [14C] palmitate incorporated into triglycerides (p less than 0.001) and monoglycerides (p less than 0.01). The ADX heart does not appear to have any impairment to glucose uptake but does show an impairment to fatty acid uptake. Because the heart uses lipid as the primary energy source, the impairment probably is not the primary factor responsible for cardiac failure in adrenal insufficiency because of its capability of using other available substrates for energy.

Adrenalectomy↗
PubMed2003

[Apoptosis-inducing effect of palmitic acids on rat pancreatic islet cells in primary culture: a preliminary study].

OBJECTIVE: To investigate the in vitro apoptosis-inducing effect of palmitic acid on pancreatic islet cells in primary culture, thereby to understand the role of palmitic acid in the pathogenesis of type 2 diabetes mellitus. METHOD: SD rat pancreatic islet cells were isolated and cultured in monolayer in vitro followed by incubation with stepwise diluted palmitic acid (0, 0.125, 0.25 mmol/L and 0.5 mmol/L respectively), and the insulin concentrations in the culture medium were determined by radio immunological methods. Morphological observation with a fluorescence microscope was conducted after double staining of the cells with PI/Hoechst 33342. RESULTS: The glucose-stimulated insulin secretion was inhibited by palmitic acid at the concentration of 0.25 and 0.5 mmol/L, which also induced obvious cell apoptosis. CONCLUSION: Palmitic acid is capable of inducing islet cell apoptosis in a dose-dependent manner.

Animals↗
PubMed2003

High levels of palmitic acid lead to insulin resistance due to changes in the level of phosphorylation of the insulin receptor and insulin receptor substrate-1.

Insulin resistance is defined as the decrease in the glucose disposal in response to insulin by the target tissues. High concentrations of nonesterified fatty acids (NEFA) in plasma have been implicated with many insulin resistance states. We evaluated several aspects of the insulin resistance induced by palmitic acid in rats and found that after treatment with 0.09 g/kg of palmitic acid there is a delay in the curve of tolerance to glucose. We measured the changes in protein phosphorylation in samples from abdominus rectus muscle and there was a decrease of 64 and 75% in the levels of phosphorylation in tyrosine of the insulin receptor and insulin receptor substrate-1, respectively. This diminution in the tyrosine phosphorylation is consistent with a decrease in the main pathway known to be activated after insulin treatment, the mitogen activated protein kinases (MAPKs). If the animals were treated with inhibitors of PKC, like sphingosine, there was a prevention of the effect of palmitic acid determined at the level of tyrosine phosphorylation. According with this result, we found an increase in the phosphorylations in serine of the insulin receptor after the treatment with palmitate. These results suggest that PKC has a role as negative regulator (by phosphorylation in serine) of the insulin receptors activation in the insulin resistance induced by palmitic acid.

Animals↗
PubMed2005

A novel long-acting analgesic: buprenorphine palmitate in rats.

BACKGROUND: A long-acting analgesic may be particularly desirable in patients with long-lasting pain. In order to provide a long-acting analgesic effect, a novel buprenorphine ester, buprenorphine palmitate, was synthesized in our laboratory. The aim of the study was to evaluate whether the ester had a long-lasting effect. METHODS: The antinociceptive effects (dose-range studies) of buprenorphine HCl and buprenorphine palmitate were evaluated using the plantar test in Sprague-Dawley rats. RESULTS: We found that intramuscular injection of buprenorphine HCl 0.05, 0.1 and 1 micromol/kg in rats produced dose-related antinociceptive effects of 2, 3, and 4 h, respectively. Intramuscular injection of buprenorphine palmitate 1, 5, and 10 micromol/kg also produced dose-related antinociceptive effects of 72, 76 and 78 h, respectively. On an equimolar basis of 1 micromol/kg, the durations of action of intramuscular buprenorphine HCl and buprenorphine palmitate were 4 and 72 h, respectively. CONCLUSIONS: Intramuscular injection of buprenorphine palmitate in rats produced a long-lasting antinociceptive effect which was much longer (18-fold) than did intramuscular buprenorphine HCl.

Analgesics, Opioid↗
PubMed1992

Transport of fatty acids into human and rat peroxisomes. Differential transport of palmitic and lignoceric acids and its implication to X-adrenoleukodystrophy.

The different topology of palmitoyl-CoA ligase (on the cytoplasmic surface) and of lignoceroyl-CoA ligase (on the luminal surface) in peroxisomal membranes suggests that these fatty acids may be transported in different form through the peroxisomal membrane (Lazo, O., Contreras, M., and Singh, I. (1990) Biochemistry 29, 3981-3986), and this differential transport may account for deficient oxidation of lignoceric acid in X-adrenoleukodystrophy (X-ALD) (Singh, I., Moser, A. B., Goldfisher, S., and Moser, H. W. (1984) Proc. Natl. Acad. Sci. U.S.A. 81, 4203-4207). To define the transport mechanism for these fatty acids through the peroxisomal membrane and its possible implication to lignoceric acid metabolism in X-ALD, we examined cofactors and energy requirements for the transport of palmitic and lignoceric acids in isolated peroxisomes from rat liver and peroxisomes isolated from X-ALD and control fibroblasts. The similar rates of transport of palmitoyl-CoA (87.6 +/- 6.3 nmol/h/mg protein) and palmitic acid in the fatty acid activating conditions (83.4 +/- 5.1 nmol/h/mg protein) and lack of transport of palmitic acid (4% of palmitoyl-CoA transport) when ATP and/or CoASH were removed or substituted by alpha,beta-methyleneadenosine-5'-triphosphate (AMPCPOP) and/or desulfoCoA-agarose from assay medium clearly demonstrate that transport of palmitic acid requires prior synthesis of palmitoyl-CoA by palmitoyl-CoA ligase on the cytoplasmic surface of peroxisomes. The 10-fold higher rate of transport of lignoceric acid (5.3 +/- 0.6 nmol/h/mg protein) as compared with lignoceroyl-CoA (0.41 +/- 0.11 nmol/h/mg protein) and lack of inhibition of transport of lignoceric acid when ATP and/or CoASH were removed or substituted with AMPCPOP or desulfoCoA-agarose suggest that lignoceric acid is transported through the peroxisomal membrane as such. Moreover, the lack of effect of removal of ATP or substitution with AMPOPCP (a nonhydrolyzable substrate) demonstrates that the translocation of palmitoyl-CoA and lignoceric acid across peroxisomal membrane does not require energy. The transport, activation, and oxidation of palmitic acid are normal in peroxisomes from X-ALD. The deficient lignoceroyl-CoA ligase (13% of control) and oxidation of lignoceric acid (10% of control) as compared with normal transport of lignoceric acid into peroxisomes from X-ALD clearly demonstrates that pathogenomonic accumulation of very long chain fatty acids (greater than C22) in X-ALD is due to the deficiency of peroxisomal lignoceroyl-CoA ligase activity.

Acyl Coenzyme A↗
PubMed1989

Multiple classes of binding sites for palmitic acid on the fatty acid-binding protein molecule.

Binding characteristics of fatty acid-binding protein (FABP) toward palmitic acid were studied. On the analysis of the interaction between FABP and [3H]palmitic acid over a wide range of concentrations of the fatty acid, at least three saturation plateaux were observed. By Scatchard-plot analysis, it appeared that FABP possesses three classes of binding sites for palmitic acid with different affinities [Kd1 = 1 x 10(-6) M (N = 1), Kd2 = 4 x 10(-6) M (N = 2), Kd3 = 2 x 10(-5) M (N = 10)]. Results of both sedimentation analyses and chromatofocusing of FABPs labeled with various concentrations of [3H]palmitic acid suggested that the FABP used was homogeneous. These results indicate that several classes of binding sites for palmitic acid with different affinities are present on the FABP molecule.

Animals↗
PubMed1979

[Is the intake of palm oil (palmitic acid) in meals associated with the low incidence of respiratory distress syndrome in Nigeria? (author's transl)].

Comparative gaschromatographic assays of different domestic oils used in West Germany and the domestic oil (palm oil) used in Nigeria and other West African countries were performed. It was discovered that the palm oil contains extremely high amounts of palmitic acid and linoleic acid compared to the other oils used in Germany. In view of the fact that previous studies have shown that palmitic acid is required for the biosynthesis of lung lecithin, which is closely related to fetal maturation, we performed animal experiments with rabbits to determine the incorporation rate of 3H-marked palmitic acid into various fetal organs: (fetal lung, placenta, fetal liver, fetal intestine etc.) after a previous intravenous injection of the 3H-marked palmitic acid to the mother rabbit. The radiochromatogram showed high incorporation rates of palmitate into the lecithin by fetal lung and placenta. These results seem to document that the high content of palm oil in Nigerian meals can partly be related to the low incidence of respiratory distress syndrom in Nigerian premature infants.

Animals↗
PubMed1968

Placental transport of free palmitic and linoleic acids in the guinea pig.

Radioisotopic tracers were used to measure the unidirectional transfer rates of free fatty acids across the placenta of fed and fasted pregnant guinea pigs. Free (14)C-labeled palmitic and linoleic acids (in serum) were injected simultaneously into a jugular vein of an anesthetized pregnant guinea pig. Serial samples of maternal blood were collected from a carotid artery; fetal blood was collected from the umbilical vein of an exposed fetus. Analysis of maternal and fetal plasma revealed that: (a) the half-lives of free palmitic and linoleic acid in maternal plasma are approximately 1.3 min and 0.7 min, both in fed animals with low plasma concentrations of these acids and in fasted animals with high concentrations; (b) free linoleic and palmitic acids cross the placenta from maternal to fetal plasma in a ratio of approximately 2.0, a value which appears not to change as the transfer rates of these acids from maternal to fetal plasma are increased by fasting the mother. It is suggested that the ratio in which free linoleic and palmitic acids cross the placenta from maternal to fetal plasma is determined by the ratio of the unbound free linoleic and palmitic acid concentrations in maternal plasma. A comparison of several species indicates that a much greater proportion of fetal fatty acids comes from the mother in the guinea pig and rabbit than in the rat, the sheep, or man.

Adipose Tissue↗