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PubMed1997

Linoleic acid metabolism in primary cultures of adult rat cardiomyocytes is impaired by aging.

Many of the changes that occur in the rat cardiac muscle with advancing age are related to modifications in membrane fatty acid composition, polyunsaturated fatty acids decreasing and saturated increasing as the animal develops. In the present study, using cultured adult cardiomyocytes isolated from the hearts of rats of a broad (1-24 months) age range, we demonstrated that the modifications in the fatty acid pattern of cardiomyocytes have to be related to alterations in the mechanism of desaturation/elongation of essential fatty acids. In fact, independent of the age of the animal, heart cells in culture were capable of rapidly metabolizing radiolabeled linoleic acid taken up from the surrounding medium, but to a different extent. The ability of heart cells to metabolize linoleic acid to higher and more unsaturated metabolites decreased with the animal's age. As the age of the animal increased, the pattern of fatty acids of the cultured cardiomyocytes showed a gradual but significant shift, similar to those reported in the whole heart. Data here reported confirm that the basic aging-related process in the cellular model system may also be relevant to aging in the whole animal.

Aging↗
PubMed2000

Conjugated linoleic acid supplementation reduces adipose tissue by apoptosis and develops lipodystrophy in mice.

Conjugated linoleic acid (CLA) is a naturally occurring group of dienoic derivatives of linoleic acid found in beef and dairy products. CLA has been reported to reduce body fat. To examine the mechanism(s) of CLA reduction of fat mass, female C57BL/6J mice were fed standard semipurified diets (10% fat of total energy) with or without CLA (1% wt/wt). Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick endlabeling (TUNEL) and DNA fragmentation analysis revealed that fat-mass decrease by CLA was mainly due to apoptosis. Tumor necrosis factor (TNF)-alpha and uncoupling protein (UCP)-2 mRNA levels increased 12- and 6-fold, respectively, in isolated adipocytes from CLA-fed mice compared with control mice. Because it is known that TNF-alpha induces apoptosis of adipocytes and upregulates UCP2 mRNA, a marked increase of TNF-alpha mRNA with an increase of UCP2 in adipocytes caused CLA-induced apoptosis. However, with a decrease of fat mass, CLA supplementation resulted in a state resembling lipoatrophic diabetes: ablation of brown adipose tissue, a marked reduction of white adipose tissue, marked hepatomegaly, and marked insulin resistance. CLA supplementation decreased blood leptin levels, but continuous leptin infusion reversed hyperinsulinemia, indicating that leptin depletion contributes to the development of insulin resistance. These results demonstrate that intake of CLA reduces adipose tissue by apoptosis and results in lipodystrophy, but hyperinsulinemia by CLA can be normalized by leptin administration.

Adipose Tissue↗
PubMed1975

Positional specificity of gamma-ketol formation from linoleic acid hydroperoxides by a corn germ enzyme.

We have shown unequivocally that the positional specificity of gamma-ketol formation by a corn germ enzyme was different from that observed previously by others with an alfalfa seedling enzyme. When the pure positional isomers of linoleic acid hydroperoxide served as substrates, the corn germ enzyme formed one of two gamma-ketols: 12-oxo-9-hydroxy-trans-10-octadeconoic acid from 13-hydroperoxys-10-octadecenoic acid from 13-hydroperoxy-cis-9,trans-11-octadecadienoic acid (99+% pure) and 10-oxo-13-hydroxy-trans-11-octadecenoic acid from 9-hydroperoxy-trans-10,cis-12-octadecadienoic acid (96% pure). Also isolated from these reactions was one of two alpha-ketols commonly found as a result of catalysis by linoleic acid hydroperoxide isomerase: 12-oxo-13-hydroxy-cis-9-octadecenoic acid from the 13-hydroperoxide and 10-oxo-9-hydroxy-cis-12-octadecenoic acid from the 9-hydroperoxide. Evidence is offered that gamma-ketol formation is catalyzed by linoleic acid hydroperoxide isomerase, the same enzyme responsible for alpha-ketol production.

Hydroxy Acids↗
PubMedDate not supplied

Conjugated linoleic acid isomers and their conjugated derivatives inhibit growth of human cancer cell lines.

Conjugated linoleic acid (CLA), mainly c9,t11- and t10,c12-isomers, and polyunsaturated n-3 fatty acids (n-3 PUFA) have been shown to reduce tumor growth. This study compared, on a set of human tumor cells (breast, lung, colon, prostate and melanoma), the antiproliferative effects of: i) trans monounsaturated fatty acids (MUFA) vs. cis MUFA and MUFA vs. PUFA, ii) individual isomers of CLA vs. linoleic acid, iii) CLA-conjugated derivatives vs. their non-conjugated homologues and vs. CLA isomers. Tumor cells were exposed to medium containing individual FA (100 microM) for 48 h and their proliferation was determined by measuring the cellular DNA content (fluorescent Hoechst 33342 dye). The antiproliferative effects of FA varied with the type of cells and were mainly dependent on the degree of unsaturation and on the position and configuration of their double bonds. One isomer of CLA (t9,t11-18:2) and CLA-conjugated derivatives exhibited the strongest growth-inhibitory effect against cancer cells. These results suggest that ruminant products contain active compounds against human tumor cell proliferation.

Cell Growth Processes↗
PubMed1981

Metabolism of linoleic Acid by barley lipoxygenase and hydroperoxide isomerase.

The oxidation of linoleic acid in incubation mixtures containing extracts of barley lipoxygenase and hydroperoxide isomerase, and the production of these enzymes in quiescent and germinated barley, were investigated. The ratio of 9-hydroperoxylinoleic acid to 13-hydroperoxylinoleic acid was higher for incubation mixtures containing extracts of quiescent barley than for mixtures containing extracts of germinated barley; production of 13-hydroperoxylinoleic acid from germinated barley exceeded that of quiescent barley. Hydroperoxy metabolites of linoleic acid were converted to 9-hydroxy-10-oxo-cis-12-octadecenoic acid, 13-hydroxy-10-oxo-trans-11-octadecenoic acid, and small amounts of 11-hydroxy-12,13-epoxy-cis-9-octadecenoic acid and 11-hydroxy-9,10-epoxy-cis-13-octadecenoic acid whether quiescent or germinated barley was the enzyme source; a fifth product, 13-hydroxy-12-oxo-cis-9-octadecenoic acid was formed only when germinated barley was the enzyme source.Lipoxygenase was readily extracted by buffer, but hydroperoxide isomerase was bound in a catalytically active state to the insoluble barley grist and was efficiently extracted only when Triton X-100 was included in the extraction buffer. Hydroperoxide isomerase was localized in the embryo of quiescent barley, but it was present in the embryo, acrospire, and in small but concentrated amounts in the rootlet of germinating barley. The levels of both lipoxygenase and hydroperoxide isomerase increased through the thirteenth day of germination.

Journal Article↗
PubMed1998

Dietary linoleic acid alters alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD), a key enzyme of niacin synthesis from tryptophan, in the process of protein expression in rat liver.

alpha-Amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) [EC 4.1.1.45] is a key enzyme of niacin synthesis from tryptophan. In this study, we examined whether dietary linoleic acid alters the protein expression of ACMSD in rat liver. Antibody against rat liver ACMSD was prepared by injecting mice with the purified enzyme. With the use of this polyclonal antibody and analysis by two-dimensional electrophoresis, we studied the mechanism by which the level of liver ACMSD activity was varied in rats fed a linoleic acid diet. In the rats fed a dietary linoleic acid (L), ACMSD protein levels in the liver were strongly suppressed as compared with the rats fed a fat-free diet (FF). These results suggest that the expression level of ACMSD might be modulated by linoleic acid or their metabolites.

Animals↗
PubMed1997

Linoleic acid enhances the secretion of plasminogen activator inhibitor type 1 by HepG2 cells.

This study was undertaken in order to assess whether triglycerides and/or their fatty acids directly influence the secretion of plasminogen activator inhibitor type 1 (PAI-1) in HepG2 cells. To this end, subconfluent HepG2 cells were incubated with triglyceride-rich particles (TGRP) isolated from Intralipid for 16 h, and PAI-1 levels were determined in conditioned medium using a specific ELISA. TGRP (1 to 6 mg triglycerides/ml) concentration-dependently increased PAI-1 secretion by cells, concomitantly with significant increases in intracellular triglyceride (TG) levels. Fatty acid analysis indicated that the incubation of cells with 3 mg of TG per ml of TGRP induced significant accumulation of 18:2 n-6 (linoleic acid, LA) and 18:3 n-3 (linolenic acid) reflecting the fatty acid composition at the added triglycerides. We then tested the comparative effects on PAI-1 secretion by HepG2 cells of LA and 18:1 n-9 (oleic acid, OA). LA, as a bovine serum albumin (BSA) complex, concentration-dependently (1 to 35 mumol/L) increased the secretion of PAI-1 by cells, whereas OA-BSA only minimally affected it at the highest concentration used (35 mumol/L). Incorporation of LA into cell pools, in the presence of increasing concentration of the FA in the medium, was studied by the use of a preparation containing [14C]LA. LA accumulated in all lipid classes including diacylglycerol, the incorporated LA being converted into arachidonic acid (AA) as assessed by HPLC radiochromatography of the fatty acid methyl esters. It is concluded that PAI-1 secretion in HepG2 cells is modulated by triacylglycerols and by linoleic acid and/or its metabolic products.

Animals↗
PubMed2001

Estimation of conjugated linoleic acid intake by written dietary assessment methodologies underestimates actual intake evaluated by food duplicate methodology.

Conjugated linoleic acids (CLA) are conjugated isomers of linoleic acid, which may promote health with regard to cancer, heart disease, diabetes, bone formation, growth modulation and immunity. The c9,t11 isomer of CLA, rumenic acid (RA), is the major isomer present in the diet. However, dietary intakes of CLA and RA by humans have not been examined rigorously, nor has the relationship between dietary CLA or RA and health (e.g., body composition). Three-day dietary records (DR) were collected from adult men (n = 46) and women (n = 47) and analyzed using a nutrient database modified to contain total CLA and RA. Simultaneously, 3-d food duplicates (FD) were collected to determine analytically individual fatty acid intakes, including those of total CLA and RA. Chronic total CLA and RA intakes were estimated using a semiquantitative food-frequency questionnaire (FFQ). Body composition was estimated using body mass index and percentage of body fat. Total CLA intake was estimated from FD to be 212 +/- 14 and 151 +/- 14 mg/d (mean +/- SEM) for men and women, respectively; RA intake was estimated to be 193 +/- 13 and 140 +/- 14 mg/d for men and women, respectively. In general, CLA and RA intakes estimated by DR and FFQ were significantly lower than those estimated by FD. Body composition was not significantly related to dietary total CLA or RA intake. In conclusion, results suggest that DR and FFQ methodologies are not reliable estimators of individual total CLA and RA intakes and may underestimate total CLA and RA intakes of groups. Intake of total CLA and RA was found to be significantly lower than that suggested previously by others.

Adult↗
PubMed1998

Conjugated linoleic acid decreases hepatic stearoyl-CoA desaturase mRNA expression.

Conjugated dienoic derivatives of linoleic acid (CLA) is a collective term for positional and geometric isomers of linoleic acid that occur naturally in foods. The two predominant isomers of CLA are the c9,t11 and t10,c12. One of the effects of CLA is to modify membrane fatty acid composition by decreasing the activity of stearoyl-CoA desaturase enzyme activity. We analyzed the changes of stearoyl-CoA desaturase gene 1 (scd1) mRNA to further define the mechanism for the decrease in Scd enzyme activity by CLA. Mice fed for two weeks with either a fat-free high carbohydrate diet (CHO) or a 5.0% corn oil diet (CO), supplemented with 0.5% CLA had a 45% and 75% decrease respectively, in scd1 mRNA levels in the liver. Consistent with the effects observed in mice, 150 microM CLA suppressed the expression of scd1 mRNA in the H2.35 mouse liver cells by 60%. Further studies with enzymatically prepared c9,t11 isomer showed that the inhibitory effect of CLA on scd1 mRNA expression in H2.35 liver cells was by isomers other than the c9,t11-CLA.

Animals↗
PubMed2004

Incorporation of arachidonic and linoleic acid hydroperoxides into cultured human umbilical vein endothelial cells.

The current study assessed the differential incorporation of 12-hydroperoxyeicosatetraenoic acid (12-HPETE), arachidonic acid (AA), 12-hydroxyeicosatetraenoic acid (12-HETE) and the linoleic acid (LA) oxidation products, 13-hydroxyoctadecadienoic acid (13-HODE) and 13-hydroperoxyoctadecadienoic acid (13-HPODE), into human umbilical vein endothelial cells (HUVEC). Approximately 80-90% of AA (10(-8)-10(-5)M) and 80% of LA (10(-8)-10(-5)M) were incorporated into HUVEC within 12h, while less than 50% of the hydroxy metabolites (12-HETE, 12-HPETE, 13-HODE, 13-HPODE) were incorporated into HUVEC over 48h. Further, treatment of HUVEC with either 12-HPETE or 13-HPODE (concentrations of 10(-5)M) had no effect on cell number at a 48h time point when compared with control. These results demonstrate that exogeneous hydroxy metabolites are incorporated into HUVEC to a lesser degree than were endogenous fatty acids. Further, we speculate that 12-HPETE and 13-HPODE are rapidly metabolized to substances without significant cytotoxic effects.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1989

Linoleic acid metabolism in metastatic and nonmetastatic murine mammary tumor cells.

The mechanism(s) by which dietary linoleic acid (18:2n-6) enhances mammary tumor growth and metastasis is not known. Since arachidonic acid (20:4n-6)-derived prostaglandins (PG) may play a role in the metastatic dissemination of tumor cells, the ability of two murine mammary tumor cell lines, 4526 (metastasis positive) and line 168 (spontaneous metastasis negative), to convert 18:2n-6 into prostaglandins was examined. Cells were initially incubated with [14C]18:2n-6 and after 8-24 h the [14C]fatty acids were quantitated by high-performance liquid chromatography following transesterification. [14C]18:2n-6 was metabolized primarily to [14C]dihomogammalinolenic acid (20:3n-6) in line 4526 cells and [14C]20:4n-6 in line 168 cells. Examination of cellular fatty acid levels revealed a 20:3n-6/20:4n-6 ratio of 1.79 +/- 0.36 and 0.20 +/- 0.02 in line 4526 and 168 cells, respectively. These data are consistent with an inherently lower delta 5 desaturase activity in line 4526 relative to 168. To assess the metabolism of 18:2n-6 into eicosanoid products, the cell lines were prelabeled with [14C]18:2n-6 or 0-40 microM nonradiolabeled 18:2n-6 overnight and subsequently stimulated with calcium ionophore A23187 for 1 h. Total PGE production, as determined by radioimmunoassay, was greater in 168 relative to 4526 cells at all 18:2n-6 concentrations. 14C-prostaglandins detected by high-performance liquid chromatography and argentation thin-layer chromatography were: PGF1 alpha and PGE1 (derived from 20:3n-6) and PGF2 alpha and PGE 2 (derived from 20:4n-6) from line 4526; PGE1 and PGE2 from line 168. PGE1/PGE2 ratios were 1.43 +/- 0.07 and 0.23 +/- 0.03 for 4526 and 168 lines, respectively. Neither cell line synthesized lipoxygenase products following [14C]18:2n-6 or [3H]-20:4n-6 incubations under the conditions employed. Additional studies are warranted in order to define the biological properties of 1- and 2-series cyclooxygenase products as they relate to tumor cell metastasis.

Animals↗
PubMed1999

Conjugated linoleic acid and other anticarcinogenic agents of bovine milk fat.

Prevention is an important strategy for conquering cancer. Milk fat contains a number of components, such as conjugated linoleic acid, sphingomyelin, butyric acid, ether lipids, beta-carotene, and vitamins A and D that have anticancer potential. Conjugated linoleic acid inhibits the growth of a number of human cancer cell lines and suppresses chemically-induced tumor development at a number of sites in animal models. As little as 0.1% of dietary conjugated linoleic acid inhibits the development of rat mammary tumors, independent of the amount and type of fat in the diet. Sphingomyelin, through its metabolites ceramide and sphingosine, participates in multiple antiproliferative pathways associated with suppression of carcinogenesis. Dietary sphingomyelin inhibits murine colon tumor development. Butyric acid, uniquely present in ruminant milk, is a potent antineoplastic agent and may ameliorate its potency through synergy with other milk fat components. Dietary butyric acid inhibits mammary carcinoma development in rats. In humans, ether lipids, beta-carotene, and vitamins A and D are associated with anticancer effects. Cows have the ability to extract anticarcinogenic components from pasture and feed and transfer them to milk. Use of genetic engineering and other techniques to increase the range and level of anticarcinogens in pasture and supplements may increase the anticancer potential of milk.

Animal Feed↗
PubMed1988

Effects of dose levels of autoxidized linoleic acid on the drug-metabolizing system in rat liver.

Autoxidized linoleic acid (AL) having 800 meq/kg of peroxide value and 1,700 meq/kg of carbonyl value was given in repeated oral doses at a daily dose of 0 (control)--7.5 ml/kg to male Wistar rats for 5 successive days. The effect of increasing AL dose on the drug-metabolizing system was investigated in rat liver microsomes and S-9 fractions. All the rats of a daily dose of 5.0-7.5 ml/kg died after the third day of consecutive oral doses. The cytochrome P-450 and b5 contents, enzyme activities in electron transfer system, aminopyrin-N-demethylase activity and S-9 activity (metabolic activation of 2-acetylaminofluorene) in the drug-metabolizing system changed essentially in a similar manner, that is, both the contents and the activities were increased by a small dose of AL, and were decreased by a large dose of AL. These results strongly supported the findings in a previous report wherein we observed the periodical effect of AL dose on the drug-metabolizing system.

2-Acetylaminofluorene↗
PubMed1982

Physiological effects of varying dietary linoleic acid in spontaneously hypertensive rats.

The effect of dietary variations in linoleic acid (LA) on the development of hypertension was studied in young male spontaneously hypertensive rats (SHR). All groups developed elevated systolic blood pressures, but after 7 weeks on the experimental diets the blood pressures of the rats fed the diet with a low LA content (0.17% as supplied by 8% coconut oil) were significantly lower than the group fed a high level of LA (9.5% as supplied by 17% corn oil) in the diet. Rats fed the high LA diet had increased urine output and developed a mild but persistent polydipsia. After 4 months on the experimental diets, potassium excretion was decreased in proportion to the amount of LA in the diet but sodium excretion was not altered. Serum potassium was significantly elevated in the group fed high LA after 5 months. The effects of LA on hypertension of SHR appear to be opposite to those observed during salt-induced hypertension. Since LA is the dietary precursor of the prostaglandins, the effects observed may be due to the availability of precursor for renal prostaglandin synthesis which has been reported to be altered in SHR.

Animals↗
PubMed2006

Effect of dietary conjugated linoleic acid and monounsaturated fatty acid content on pig muscle and adipose tissue lipase and esterase activity.

Three levels (0%, 1%, and 2%) of conjugated linoleic acid (CLA) were combined with two levels (low and high) of monounsaturated fatty acids (MUFA) for pig feeding. The activity of neutral lipase (NL), acid lipase (AL), phospholipase (PL), neutral esterase (NE), and acid esterase (AE) was measured in extracts from muscle and subcutaneous adipose tissues. The addition of CLA in the diet only affected the lipolytic activity in muscle, whereas differences in MUFA content of pig diets were mainly responsible for the lipolytic enzyme modifications observed in adipose tissue. Nevertheless, a significant effect of the interaction CLA x MUFA on the activity of several lipolytic enzymes was observed in both tissues. The effect of either linoleic acid (LA) or CLA on the activity of muscle and adipose lipolytic enzymes was determined by in vitro assays. Remarkable inhibitory or activation effects were detected depending on the enzyme and kind of tissue.

Adipose Tissue↗
PubMed2002

Influence of conjugated vs. conventional linoleic acid on liver metastasis and hepatic lipidperoxidation in BOP-induced pancreatic cancer in Syrian hamster.

While conjugated linoleic acid (CLA) is regarded as an essential fatty acid with anticarcinogenic effects, conventional linoleic acid (LA) is reported to promote tumour growth in various experimental studies probably caused by high sensitivity to non-enzymatic lipid peroxidation. In order to evaluate the impact of dietary LA and CLA on liver metastasis and lipidperoxidation (LPO), 60 Syrian hamsters were injected with 10 mg N -nitrosobis-2-oxopropylamine (BOP)/kg body weight s.c. for 12 weeks. Animals were fed a special diet containing LA or CLA. The experiment was terminated after 24 weeks. Incidence, number and size of liver metastases were histologically determined. Furthermore, the activities of antioxidative enzymes and concentration of hepatic lipidperoxidation were measured intra- and extrametastatically. Incidence, number and size of liver metastases did not differ between the tumour groups. Otherwise, antioxidative enzyme activity of GSH-Px was higher in non-metastatic liver, while SOD activity and lipidperoxidation were increased in liver metastases. Conclusively there was no difference between the groups fed with LA and CLA according to the impact on liver metastasis in ductal pancreatic cancer.

Animals↗
PubMed2005

Cis-9,trans-11-CLA exerts anti-inflammatory effects in human bronchial epithelial cells and eosinophils: comparison to trans-10,cis-12-CLA and to linoleic acid.

Interaction of eosinophils and bronchial epithelial cells plays a pivotal role in maintaining inflammatory airway disease. Since conjugated linoleic acids (CLA) are suggested to exert anti-inflammatory effects, one purpose of this study was to compare cis-9,trans-11-CLA and trans-10,cis-12-CLA with regard to their influence on the stimulus-induced activation of eosinophils. ECP (eosinophil cationic protein) released in co-culture of stimulated and CLA-treated eosinophils with stimulated bronchial epithelial cells (BEAS-2B) was measured and cis-9,trans-11-CLA was found to be most potent in inhibiting ECP formation. Further, expression of the activation markers CD69 and CD13 induced by various stimuli (TNF-alpha, IL-5, IL-3) was significantly reduced in the presence of cis-9,trans-11-CLA. Subsequently, various concentrations of cis-9,trans-11-CLA vs. linoleic acid (LA, cis-9,cis-12-octadecadienoic acid) were tested for the effect on proliferative response and release of the pro-inflammatory cytokine IL-8 in stimulated BEAS-2B. Addition of cis-9,trans-11-CLA attenuated cell growth and significantly reduced IL-8 production at mRNA and protein levels. In contrast, LA had a slight stimulating effect on proliferation and was less effective in reducing the cytokine release. It was demonstrated that the inhibitory effect of cis-9,trans-11-CLA on IL-8 production is mediated through activation of the nuclear receptor PPARgamma, since blocking the receptor with a selective antagonist (GW9662) restored the stimulus-induced enhancement in IL-8 mRNA expression and protein secretion. PPARgamma has previously been shown to be closely involved in the downregulation of inflammation during hyperresponsiveness related to pulmonary immune responses. Thus, targeting PPARgamma, cis-9,trans-11-CLA might be of therapeutic value in the focus of airway disease while ameliorating inflammatory processes by affecting epithelial and eosinophil functions.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1987

A high linoleic acid diet diminishes enhanced intestinal uptake of sugars in diabetic rats.

Intestinal absorption is altered in rats by diabetes and by dietary manipulation. For 5 wk rats were fed chow (C) or semisynthetic diets containing isocaloric amounts of a high content of either polyunsaturated (P) or saturated (S) fatty acids; then half were rendered hyperglycemic with streptozotocin while the remaining half served as nondiabetic controls. Studies were performed after a total of 8 wk on C, P, or S. Jejunal villous surface area was greater in diabetic rats than in control rats fed C or S, whereas the jejunal mucosal surface area was significantly greater in diabetic animals than in control animals only when they were fed S. Ileal mucosal surface area was similar in diabetic and in control rats fed C, S, or P; although ileal villous surface area was greater in diabetic than in control rats only when they were fed C. The jejunal and ileal uptake of varying concentrations of glucose and galactose was higher in diabetic rats than controls fed C or S. In contrast, the enhanced uptake of these sugars was reduced or normalized in diabetic rats fed P. The jejunal brush-border membrane (BBM) content of phospholipids was higher in diabetic than in control rats fed chow, but there was no difference in diabetic vs. control animals fed P or S in BBM total free fatty acids, phospholipids, or cholesterol. Thus feeding a high linoleic acid diet diminishes the enhanced intestinal uptake of glucose and galactose in diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗