Cinnamon extract regulates plasma levels of adipose-derived factors and expression of multiple genes related to carbohydrate metabolism and lipogenesis in adipose tissue of fructose-fed rats.

We reported earlier that dietary cinnamon extract (CE) improves systemic insulin sensitivity and dyslipidemia by enhancing insulin signaling. In the present study, we have examined the effects of CE on several biomarkers including plasma levels of adipose-derived adipokines, and the potential molecular mechanisms of CE in epididymal adipose tissue (EAT). In Wistar rats fed a high-fructose diet (HFD) to induce insulin resistance, supplementation with a CE (Cinnulin PF, 50 mg/kg daily) for 8 weeks reduced blood glucose, plasma insulin, triglycerides, total cholesterol, chylomicron-apoB48, VLDL-apoB100, and soluble CD36. CE also inhibited plasma retinol binding protein 4 (RBP4) and fatty acid binding protein 4 (FABP4) levels. CE-induced increases in plasma adiponectin were not significant. CE did not affect food intake, bodyweight, and EAT weight. In EAT, there were increases in the insulin receptor ( IR) and IR substrate 2 ( IRS2) mRNA, but CE-induced increases in mRNA expression of IRS1, phosphoinositide-3-kinase, AKT1, glucose transporters 1 and 4 , and glycogen synthase 1 expression and decreased trends in mRNA expression of glycogen synthase kinase 3beta were not statistically significant. CE also enhanced the mRNA levels of ADIPOQ, and inhibited sterol regulatory element binding protein-1c mRNA levels. mRNA and protein levels of fatty acid synthase and FABP4 were inhibited by CE and RBP4, and CD36 protein levels were also decreased by CE. These results suggest that CE effectively ameliorates circulating levels of adipokines partially mediated via regulation of the expression of multiple genes involved in insulin sensitivity and lipogenesis in the EAT.

Cinnamon extract attenuates TNF-alpha-induced intestinal lipoprotein ApoB48 overproduction by regulating inflammatory, insulin, and lipoprotein pathways in enterocytes.

We have previously reported that the obesity-associated proinflammatory cytokine, TNF-alpha, stimulates the overproduction of intestinal apolipoprotein (apo) B48 containing lipoproteins. In the current study, we have evaluated whether a water-soluble cinnamon extract [CE (Cinnulin PF)] attenuates the dyslipidemia induced by TNF-alpha in Triton WR-1339 treated hamsters, and whether CE inhibits the oversecrection of apoB48-induced by TNF-alpha in enterocytes in a 35S labeling study. In vivo, oral treatment of Cinnulin PF (50 mg per kg BW), inhibited the postprandial overproduction of apoB48-containing lipoproteins and serum triglyceride levels. In ex vivo 35S labeling studies, CE (10 and 20 microg/ml) inhibited the oversecretion of apoB48 induced by TNF-alpha treated enterocytes into the media. To determine the molecular mechanisms, TNF-alpha treated primary enterocytes isolated from chow-fed hamsters, were incubated with CE (10 microg/ml), and the expression of the inflammatory factor genes, IL1-beta, IL-6, and TNF-alpha, insulin signaling pathway genes, insulin receptor (IR), IRS1, IRS2, phosphatidylinositol 3-kinase (PI3-K), Akt1 and phosphatase and tensin homology (PTEN), as well as the key regulators of lipid metabolism, cluster of differentiation (CD)36, microsomal triglyceride transfer protein (MTTP), and sterol regulatory element binding protein (SREBP)-1c were evaluated. Quantitative real-time PCR assays showed that CE treatment decreased the mRNA expression of IL-1beta, IL-6 and TNF-alpha, improved the mRNA expression of IR, IRS1, IRS2, PI3K and Akt1, inhibited CD36, MTTP, and PTEN, and enhanced the impaired SREBP-1c expression in TNF-alpha treated enterocytes. These data suggest that a water extract of cinnamon reverses TNF-alpha-induced overproduction of intestinal apoB48 by regulating gene expression involving inflammatory, insulin, and lipoprotein signaling pathways. In conclusion, Cinulin PF improves inflammation related intestinal dyslipidemia.

Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes.

Chromium is an essential nutrient involved in normal carbohydrate and lipid metabolism. The chromium requirement is postulated to increase with increased glucose intolerance and diabetes. The objective of this study was to test the hypothesis that the elevated intake of supplemental chromium is involved in the control of type 2 diabetes. Individuals being treated for type 2 diabetes (180 men and women) were divided randomly into three groups and supplemented with: 1) placebo, 2) 1.92 micromol (100 microg) Cr as chromium picolinate two times per day, or 3) 9.6 micromol (500 microg) Cr two times per day. Subjects continued to take their normal medications and were instructed not to change their normal eating and living habits. HbA1c values improved significantly after 2 months in the group receiving 19.2 pmol (1,000 microg) Cr per day and was lower in both chromium groups after 4 months (placebo, 8.5 +/- 0.2%; 3.85 micromol Cr, 7.5 +/- 0.2%; 19.2 micromol Cr, 6.6 +/- 0.1%). Fasting glucose was lower in the 19.2-micromol group after 2 and 4 months (4-month values: placebo, 8.8 +/- 0.3 mmol/l; 19.2 micromol Cr, 7.1 +/- 0.2 mmol/l). Two-hour glucose values were also significantly lower for the subjects consuming 19.2 micromol supplemental Cr after both 2 and 4 months (4-month values: placebo, 12.3 +/- 0.4 mmo/l; 19.2 micromol Cr, 10.5 +/- 0.2 mmol/l). Fasting and 2-h insulin values decreased significantly in both groups receiving supplemental chromium after 2 and 4 months. Plasma total cholesterol also decreased after 4 months in the subjects receiving 19.2 micromol/day Cr. These data demonstrate that supplemental chromium had significant beneficial effects on HbA1c, glucose, insulin, and cholesterol variables in subjects with type 2 diabetes. The beneficial effects of chromium in individuals with diabetes were observed at levels higher than the upper limit of the Estimated Safe and Adequate Daily Dietary Intake.

Effect of exercise (running) on serum glucose, insulin, glucagon, and chromium excretion.

Chromium is involved in normal glucose metabolism. To test whether chromium is also associated with the exercise-induced increases in glucose utilization, urinary chromium excretion, serum glucose, insulin, and glucagon of nine male runners (23-46 yr) were evaluated. Blood samples were taken prior to, immediately following, and 2 h after a strenuous 6-mile run. Urine samples were also taken at these times, and total daily urine collections were made the day of the run and the following day. Mean serum glucose for all runners immediately after running was 185 +/- 19 mg/dl compared with 90 +/- 1 mg/dl (mean +/- SE) prior to running. Mean serum glucagon immediately after running was significantly elevated compared with that observed prior to or 2 h after running; serum insulin levels were not altered significantly. Mean urinary chromium concentration was increased nearly five-fold 2 h after running; similar results were obtained when chromium concentration was expressed per mg of creatinine. Total daily urinary Cr excretion was approximately two times higher the day of running compared with the following nonrun day. Daily urinary excretion of sodium, potassium, and calcium were measured to determine if exercise had a general nonspecific effect on renal function; daily urinary excretion of these was not changed by exercise. These data demonstrate that accompanying the exercise-induced changes associated with increased glucose utilization, there is a significant increase in chromium excretion.

Serum chromium of human subjects: effects of chromium supplementation and glucose.

Seventy-six adult subjects, 48 males and 28 females, were given placebo or 200 micrograms Cr in the form of chromic chloride in a double-blind crossover study, with 3-month experimental periods, to determine basal serum Cr levels and the effects of Cr supplementation on serum Cr and related variables. Basal serum Cr determined by graphite furnace atomic absorption for all subjects was 0.13 +/- 0.02 ng/ml (mean +/- SEM), and increased significantly to 0.38 +/- 0.02 ng/ml following 3 months of Cr supplementation. There were no significant differences in the serum Cr values for males and females. Serum Cr 90 min following a glucose load (1 g per kg body wt) was not significantly different from fasting during either the placebo or Cr supplementation periods. These data demonstrate that serum Cr increased significantly following Cr supplementation and is a reflection of Cr intake, but serum Cr concentration, even that following a glucose load, does not appear to be a meaningful indicator of Cr status.

Urinary chromium excretion and insulinogenic properties of carbohydrates.

Eleven male and nine female adult subjects were given one of the following five carbohydrate-drink combinations (per kg body wt) on five mornings separated by greater than or equal to 2 wk: 1) 1.0 g glucose, 2) 0.9 g uncooked cornstarch, 3) 1.0 g glucose followed 20 min later by 1.75 g fructose, 4) 0.9 g uncooked cornstarch followed 20 min later by 1.75 g fructose, and 5) water followed 20 min later by 1.75 g fructose. Glucose plus fructose was the most insulinogenic followed by glucose alone, starch plus fructose, starch alone, and water plus fructose. The urinary losses of chromium followed a similar pattern. Subjects with the highest concentrations of circulating insulin displayed decreased ability to mobilize chromium on the basis of urinary chromium excretion. Therefore, urinary chromium losses are related to the insulinogenic properties of carbohydrates.

Supplemental-chromium effects on glucose, insulin, glucagon, and urinary chromium losses in subjects consuming controlled low-chromium diets.

The effects of low-chromium diets containing chromium in the lowest quartile of normal intake on glucose tolerance and related variables in 11 females and 6 male subjects were evaluated. Subjects with glucose concentration greater than 5.56 mmol/L but less than 11.1 mmol/L 90 min after an oral-glucose challenge were designated as the hyperglycemic group and the remainder, the control group. Glucose tolerance and circulating insulin and glucagon of the hyperglycemic group all improved during chromium supplementation (200 micrograms/d) whereas those of the control group were unchanged. Glucose and insulin concentrations 60 min after the oral-glucose challenge and the sum of the 0-90 min and 0-240 min glucose values were all significantly lower after chromium supplementation in the hyperglycemic group. These data demonstrate that consumption of diets in the lowest 25% of normal chromium intake lead to detrimental effects on glucose tolerance, insulin, and glucagon in subjects with mildly impaired glucose tolerance.

Urinary chromium excretion of human subjects: effects of chromium supplementation and glucose loading.

The utilization of inorganic chromium by free-living human subjects was studied in 76 volunteers (male, 48; female, 28) who were supplemented with 200 micrograms of inorganic chromium as chromic chloride or a placebo tablet for 3 months in a double-blind, cross-over experiment. For all subjects, initial mean +/- SEM urinary chromium (Cr) level was 0.20 +/- 0.01 (range, 0.05 to 0.58) ng/ml and did not differ by sex. Initial chromium/creatinine ratio (Cr/Ct) was 0.15 +/- 0.01 (range 0.03 to 0.36) ng Cr/mg creatinine for females and was significantly lower, 0.10 +/- 0.01 (range 0.03 to 0.36) for males. Mean urinary Cr level increased to 1.0 +/- 0.12 after 2 and to 1.13 +/- 0.08 ng/ml after 3 months' supplementation. The Cr/Ct ratio increased to 0.69 +/- 0.10 for females and to 0.50 +/- 0.04 for males after 2 months' supplementation; values were similar after 3 months. An increase in urinary Cr excretion in response to a glucose load was demonstrated for nonsupplemented normal free-living subjects but not for subjects supplemented daily with trivalent chromium. Urinary Cr excretion after a glucose challenge was not predictable and did not depend on Cr status.

Dietary chromium decreases insulin resistance in rats fed a high-fat, mineral-imbalanced diet.

The effects of chromium (Cr) supplementation on diet-induced insulin resistance produced by feeding a high-fat, low-Cr diet were studied in rats to ascertain the role of Cr in insulin resistance. Wistar male rats were maintained for 16 weeks after weaning on a basal diet containing 40% lard, 30% sucrose, and 25% casein by weight and adequate vitamins and minerals without added Cr (-Cr). Fasting levels of insulin, glucose, and triglycerides and the responses during an intravenous glucose tolerance test (IVGTT) were compared as indices of insulin resistance and the effectiveness of dietary Cr. IVGTTs and blood sampling for data analyses were performed over a 40-minute period after IV glucose injection (1.25 g/kg body weight) in overnight-fasted animals under pentobarbital anesthesia (40 mg/kg body weight). All animals were normoglycemic (-Cr, 109 +/- 3 mg/dL; +Cr, 119 +/- 5), with fasting insulin levels elevated in the -Cr group (65 +/- 10 microU/mL) versus the +Cr group (31 +/- 4 microU/mL). Increases in plasma triglycerides in the -Cr group were not significant. Following glucose injection, the rate of glucose clearance was lower in the -Cr group (1.74 +/- 0.22 v2.39 +/- 0.11%/min), and 40-minute glucose areas in the -Cr group tended to be higher than in the +Cr group. The insulin response to glucose injection was 20% higher in the -Cr group. Forty-minute plasma triglyceride areas were lower in +Cr rats (875 +/- 62 v 1,143 +/- 97 mg/dL.min in -Cr rats). These data demonstrate that the insulin resistance induced by feeding a high-fat, nutrient-stressed diet is improved by Cr.

Overproduction of insulin in the chromium-deficient rat.

The hypothesis that the insulin secretory hyperresponsiveness observed in rats with diet-induced insulin resistance may be a basic characteristic of dietary chromium (Cr) deficiency was evaluated. Two groups of weanling rats were fed ad libitum a purified diet containing 64% sucrose, 20% casein, 5% corn oil, and the recommended levels of vitamins and minerals without added Cr. Cr-deficient (-Cr) rats were provided with distilled drinking water only, while Cr-supplemented (+Cr) rats received water containing 5 ppm Cr as CrCl3. A third group of rats fed a commercial chow diet served as sucrose controls. Effects of Cr deficiency were assessed by comparing fasting levels of glucose, insulin, and plasma lipids in blood samples collected biweekly from the -Cr and +Cr groups over a 3-month period. Both groups of rats fed the low-Cr sucrose diet developed a transient hyperinsulinemia and hyperlipidemia relative to the chow-fed control rats. There were significant effects of Cr supplementation on plasma triglycerides during the initial 2 weeks of dietary adaptation. Effects of the low-Cr diet were evaluated after the 12-week period by comparing the insulin response area and glucose clearance during a 40-minute intravenous glucose tolerance test (IVGTT). The rates of glucose clearance (KG) in -Cr and +Cr rats were similar (4.2 +/- 1.0 and 4.3 +/- 0.8%/min, respectively) and were comparable to the K(G) in chow-fed rats (4.6 +/- 0.8). In contrast, insulin secretory responses in -Cr rats were exaggerated (area, 14,083 +/- 3,399 microU/mL x min), being twofold greater (P < .05) relative to the +Cr group (6,183 +/- 864). The insulin secretory response area in chow-fed rats (7,081 +/- 408 microU/mL x min) was similar to the value in the +Cr group. These observations provide support for the hypothesis that Cr deficiency can lead to elevated insulin secretory responses to glucose.

Chromium improves insulin response to glucose in rats.

The effects of chromium (Cr) supplementation on insulin secretion and glucose clearance (KG) during intravenous glucose tolerance tests (IVGTTS) were assessed in rats with impaired glucose tolerance due to dietary Cr deficiency. Male Wistar rats were maintained after weaning on a basal low-Cr diet containing 55% sucrose, 15% lard, 25% casein. American Institute of Nutrition (AIN)-recommended levels of vitamins, no added Cr, and an altered mineral content as required to produce Cr deficiency and impaired glucose tolerance. The Cr-supplemented group ([+Cr] n = 6) were provided with 5 ppm Cr as CrCl3 in the drinking water, and the Cr-deficient group ([-Cr]n = 5) received purified drinking water. At 12 weeks on the diet, both groups of rats were hyperinsulinemic (+Cr, 103 +/- 13; -Cr, 59 +/- 12 microU/mL) and normoglycemic (+Cr, 127 +/- 7; -Cr, 130 +/- 4 mg/dL), indicating insulin resistance. After 24 weeks, insulin levels were normal (+Cr, 19 +/- 5; -Cr, 21 +/- 3 microU/mL) and all rats remained normoglycemic (+Cr, 124 +/- 8; -Cr, 131 +/- 6 mg/dL). KG values during IVGTTS were lower in -Cr rats (KG = 3.58%/min) than in +Cr rats (KG = 5.29%/min), correlating with significantly greater 40-minute glucose areas in the -Cr group (P < .01). Comparisons of 40-minute insulin areas indicated marked insulin hyperresponsiveness in the -Cr group, with insulin-secretory responses increased nearly twofold in -Cr animals (P < .05). Chromium deficiency also led to significant decreases in cyclic adenosine monophosphate (cAMP)-dependent phosphodiesterase (PDE) activity in spleen and testis (P < .01). In these studies, Cr deficiency was characterized by both beta-cell hypersecretion of insulin and tissue insulin resistance that were associated with decreased tissue levels of cAMP PDE activity.

Chromium supplementation of human subjects: effects on glucose, insulin, and lipid variables.

Seventy-six normal, free-living subjects were given supplements of 200 micrograms chromium (Cr) in the form of chromic chloride or a placebo in a double-blind crossover study with 3-month experimental periods. Twenty of the 76 subjects had serum glucose concentrations greater than or equal to 100 mg/dL 90 minutes after a glucose challenge (1 g glucose per kilogram of body weight). Chromium supplementation significantly decreased (P less than 0.05) the 90-minute glucose concentration of these subjects from 135 +/- 9 to 116 +/- 11 mg/dL; fasting glucose concentrations also decreased significantly. The 90-minute serum glucose levels of the 35 subjects with glucose concentrations less than the fasting serum glucose level were increased significantly by Cr supplementation, from 71 +/- 1 to 81 +/- 4 mg/dL. Fasting and 90-minute serum glucose concentrations of the remaining subjects who displayed 90-minute glucose concentrations greater than fasting levels but less than 100 mg/dL were not affected by Cr supplementation. In this study, immunoreactive serum insulin concentration, body weight, lipids, and other selected clinical variables did not change significantly during Cr supplementation. These data demonstrate that Cr supplementation decreases the serum glucose levels of subjects with 90-minute glucose concentrations greater than or equal to 100 mg/dL following a glucose challenge, increases serum glucose levels of subjects with 90-minute glucose concentrations less than fasting levels, and has no effect on the serum glucose levels of subjects with 90-minute glucose values similar to but greater than fasting levels.

Effects of supplemental chromium on patients with symptoms of reactive hypoglycemia.

To determine if chromium (Cr) is involved in hypoglycemia, eight female patients with symptoms of hypoglycemia were supplemented with 200 micrograms of Cr as chromic chloride for three months in a double-blind crossover experimental design study. Chromium supplementation alleviated the hypoglycemic symptoms and significantly raised the minimum serum glucose values observed two to four hours following a glucose load. Insulin binding to red blood cells and insulin receptor number also improved significantly during Cr supplementation. These data suggest that impaired Cr nutrition and/or metabolism may be a factor in the etiology of hypoglycemia.

Exercise effects on chromium excretion of trained and untrained men consuming a constant diet.

Chromium excretion of eight trained and five sedentary men was determined on rest days and after exercise to exhaustion at 90% of maximum O2 consumption (VO2max) to determine if degree of physical fitness affects urinary Cr losses. Subjects were fed a constant daily diet containing approximately 9 micrograms Cr/1,000 kcal. VO2max of the trained runners was in the good or above range based on their age and that of the sedentary subjects was average or below. While consuming the control diet, basal urinary Cr excretion of subjects who exercise regularly was significantly lower than that of the sedentary control subjects, 0.09 +/- 0.01 and 0.21 +/- 0.03 microgram/day (mean +/- SE), respectively. When subjects consumed self-chosen diets, basal urinary Cr excretion of the trained subjects was also significantly lower than that of the untrained subjects. Daily urinary Cr excretion of trained subjects was significantly higher on the day of a single exercise bout at 90% VO2max compared with nonexercise days, 0.12 +/- 0.02 and 0.09 +/- 0.01 microgram/day, respectively. Urinary Cr excretion of sedentary subjects was not altered after controlled exercise. These data demonstrate that basal urinary Cr excretion and excretion in response to exercise are related to VO2max and therefore degree of physical fitness.

Effects of chromium and guar on sugar-induced hypertension in rats.

Ingestion of sugars (sucrose, fructose, glucose) by various rat strains is associated with perturbations in the glucose/insulin system and higher systolic blood pressure (SBP). The association suggests causality, because alterations in insulin metabolism have been found in essential hypertension and many experimental forms of hypertension. To test the hypothesis that sugar-induced SBP elevation is secondary to perturbed insulin metabolism, we examined in 2 experiments effects of chromium and guar, substances known to affect insulin metabolism, on SBP of Spontaneously Hypertensive Rats (SHR). In both studies, sucrose compared to starch ingestion caused significant elevation of SBP; but addition of 2 chromium nicotinate complexes and guar prevented development of sugar-induced SBP elevations. The basal, genetic hypertension of the SHR was not affected by either nutrient. An additional finding in the first study was that sugar-consuming SHR supplemented with chromium had greater BW and increased organ weight (kidney, spleen, and liver) than nonsupplemented SHR. Accordingly, we have shown that two different mechanisms known to ameliorate insulin perturbations, use of chromium and guar, prevent sugar-induced SBP elevations. Since essential hypertension may be due to insulin perturbations and high dose chromium supplementation seems nontoxic, this may prove to be a useful means to lower blood pressure (BP) in some essential hypertensives, as well as diabetic hypertensives. Soluble fiber in the form of guar is also quite effective in favorably influencing sugar-induced SBP elevations.

Insulin-like biological activity of culinary and medicinal plant aqueous extracts in vitro.

To evaluate the possible effects on insulin function, 49 herb, spice, and medicinal plant extracts were tested in the insulin-dependent utilization of glucose using a rat epididymal adipocyte assay. Cinnamon was the most bioactive product followed by witch hazel, green and black teas, allspice, bay leaves, nutmeg, cloves, mushrooms, and brewer's yeast. The glucose oxidation enhancing bioactivity was lost from cinnamon, tea, witch hazel, cloves, bay leaf and allspice by poly(vinylpyrrolidone) (PVP) treatment, indicating that the active phytochemicals are likely to be phenolic in nature. The activity of sage, mushrooms, and brewers's yeast was not removed by PVP. Some products such as Korean ginseng, flaxseed meal, and basil have been reported to be effective antidiabetic agents; however, they were only marginally active in our assay. Our technique measures direct stimulation of cellular glucose metabolism, so it may be that the active phytochemicals in these plants improve glucose metabolism via other mechanisms or that this in vitro screening is not a reliable predictor of hypoglycemic effects in vivo for some products. In summary, the positive effects of specific plant extracts on insulin activity suggest a possible role of these plants in improving glucose and insulin metabolism.

Dietary chromium deficiency effect on sperm count and fertility in rats.

Male rats raised on a low chromium diet containing less than 100 ppb chromium had decreased sperm counts and decreased fertility at age 8 months compared to the Cr-supplemented controls. Decreased sperm cell production and fertility were not apparent at age 4 months. At age 7-8 months the frequency of conception was 25 percent or less and the sperm count of the low chromium males was approximately 50 percent of that of the Cr-supplemented rats.

Dietary and metabolite effects on trivalent chromium retention and distribution in rats.

The purpose of this study was to determine if diet or various metabolites alter chromium (Cr) uptake and distribution in rats. Radioactively labeled Cr was detected within 15 min of oral administration to rats, and the total amount retained remained relatively constant from 1 to 24 h. Dietary Cr intake did not alter Cr retention or distribution. The majority of the Cr was retained in the carcass. However, when the amount of labeled Cr was expressed per gram of tissue, the highest amounts of Cr were found in the kidneys, spleen, and pancreas. Pharmacological doses of insulin, epinephrine, glucagon, and dibutyryladenosine-3'-5'cyclic monophosphate, prostaglandins A1, A2, B1, B2, E1, E2, F1 alpha, and F2 alpha did not significantly influence Cr retention. Glucose, sucrose, nicotinic acid, glutathione, and other metabolites administered orally in conjunction with labeled Cr also did not significantly alter Cr retention. These data indicate that most nutrients and metabolites do not alter Cr retention and distribution. The regulation of Cr homeostasis appears to be at the level of excretion.

Dietary chromium intake. Freely chosen diets, institutional diet, and individual foods.

Chromium content of 22 daily diets, designed by nutritionists to be well-balanced, ranged from 8.4 to 23.7 micrograms/1000 cal with a mean +/- SEM chromium content of 13.4 +/- 1.1 micrograms/1000 cal. Most diary products are low in chromium and provide less than 0.6 micrograms/serving. Meats, poultry, and fish are also low in chromium, providing 2 micrograms of chromium or less per serving. Chromium contents of grain products, fruits, and vegetables vary widely, with some foods providing greater than 20 micrograms/serving. In summary, chromium content of individual foods varies, and is dependent upon chromium introduced in the growing, transport, processing, and fortification of the food. Even well-balanced diets may contain suboptimal levels of dietary chromium.

Insulin potentiating factor and chromium content of selected foods and spices.

An unidentified factor that potentiates the action of insulin in glucose metabolism was investigated in selected foods and spices. Chromium content of these foods and spices was also determined. Foods and spices were extracted with 0.1N NH4OH (1:20, w/v) and the supernatants assayed for insulin potentiation activity in the rat epididymal fat cell assay. Among the selected foods, tuna fish, peanut butter, and vanilla ice cream had some insulin potentiating activity. Among the spices, apple pie spice, cinnamon, cloves, bay leaves, and turmeric potentiated insulin activity more than three-fold. Chromium concentration of foods ranged from 1 to 145 ng/g, and spices ranged from 4 to 1818 ng/g. Insulin potentiating activity of foods and spices did not correlate with total chromium. Spices are generally used for flavor and taste in food preparations, but cinnamon, cloves, bay leaves, and turmeric may have an additional role in glucose metabolism.