A Survey of Diabetic Educators and Patients for the Revision of Korean Food Exchange Lists

BackgroundFood exchange lists are one of the main methods of nutritional education. However, Korean food exchange lists have not been revised since 1994. Therefore, we surveyed the opinions of diabetes educators and patients with diabetes regarding the need for revision of the current food exchange lists.MethodsFor two weeks beginning on 10 March 2008, a 12-item questionnaire regarding the opinion and need for revision of the current food exchange lists was e-mailed to diabetes educators nationwide. Another 15-question survey was administered to patients with diabetes in 13 hospitals located in the Seoul and Gyeonggi regions of Korea.ResultsWe obtained survey responses from 101 diabetes educators and 209 patients; 65 (64.3%) of the educators answered that the current food exchange lists should be revised. The items that needed revision were the glycemic index, addition of new foods and reaffirmation of exchange standard amounts. The patients demanded specific education about choosing appropriate foods, a balanced meal plan, proper snacks, and dining intake.ConclusionOur survey results demonstrate the need to revise the Korean food exchange lists. This process should focus on glycemic index, the addition of new foods and reconfirmation of one exchange reference unit

Selective activation of hTRPV1 by N-geranyl cyclopropylcarboxamide, an amiloride-insensitive salt taste enhancer.

TRPV1t, a variant of the transient receptor potential vanilloid-1 (TRPV1) has been proposed as a constitutively active, non-selective cation channel as a putative amiloride-insensitive salt taste receptor and shares many properties with TRPV1. Based on our previous chorda tympani taste nerve recordings in rodents and human sensory evaluations, we proposed that N-geranylcyclopropylcarboxamide (NGCC), a novel synthetic compound, acts as a salt taste enhancer by modulating the amiloride/benzamil-insensitive Na(+) entry pathways. As an extension of this work, we investigated NGCC-induced human TRPV1 (hTRPV1) activation using a Ca(2+)-flux signaling assay in cultured cells. NGCC enhanced Ca(2+) influx in hTRPV1-expressing cells in a dose-dependent manner (EC50 = 115 µM). NGCC-induced Ca(2+) influx was significantly attenuated by ruthenium red (RR; 30 µM), a non-specific blocker of TRP channels and capsazepine (CZP; 5 µM), a specific antagonist of TRPV1, implying that NGCC directly activates hTRPV1. TRPA1 is often co-expressed with TRPV1 in sensory neurons. Therefore, we also investigated the effects of NGCC on hTRPA1-expressing cells. Similar to hTRPV1, NGCC enhanced Ca(2+) influx in hTRPA1-expressing cells (EC50 = 83.65 µM). The NGCC-induced Ca(2+) influx in hTRPA1-expressing cells was blocked by RR (30 µM) and HC-030031 (100 µM), a specific antagonist of TRPA1. These results suggested that NGCC selectively activates TRPV1 and TRPA1 in cultured cells. These data may provide additional support for our previous hypothesis that NGCC interacts with TRPV1 variant cation channel, a putative amiloride/benzamil-insensitive salt taste pathway in the anterior taste receptive field

Five hTRPA1 Agonists Found in Indigenous Korean Mint, Agastache rugosa.

Transient receptor potential ankyrin1 (TRPA1) and transient receptor potential vanilloid 1 (TRPV1) are members of the TRP superfamily of structurally related, nonselective cation channels and mediators of several signaling pathways. Previously, we identified methyl syringate as an hTRPA1 agonist with efficacy against gastric emptying. The aim of this study was to find hTRPA1 and/or hTRPV1 activators in Agastache rugosa (Fisch. et Meyer) O. Kuntze (A.rugosa), commonly known as Korean mint to improve hTRPA1-related phenomena. An extract of the stem and leaves of A.rugosa (Labiatae) selectively activated hTRPA1 and hTRPV1. We next investigated the effects of commercially available compounds found in A.rugosa (acacetin, 4-allylanisole, p-anisaldehyde, apigenin 7-glucoside, L-carveol, β-caryophyllene, trans-p-methoxycinnamaldehyde, methyl eugenol, pachypodol, and rosmarinic acid) on cultured hTRPA1- and hTRPV1-expressing cells. Of the ten compounds, L-carveol, trans-p-methoxycinnamaldehyde, methyl eugenol, 4-allylanisole, and p-anisaldehyde selectively activated hTRPA1, with EC50 values of 189.1±26.8, 29.8±14.9, 160.2±21.9, 1535±315.7, and 546.5±73.0 μM, respectively. The activities of these compounds were effectively inhibited by the hTRPA1 antagonists, ruthenium red and HC-030031. Although the five active compounds showed weaker calcium responses than allyl isothiocyanate (EC50=7.2±1.4 μM), our results suggest that these compounds from the stem and leaves of A.rugosa are specific and selective agonists of hTRPA1

Activation of TRPV1 by capsaicin and NGCC.

<p>(<b>A</b>) TRPV1 current was activated by capsaicin (100 nM) and reversibly blocked by TRPV1 antagonist, CPZ (1 µM) in HEK293T cells transiently transfected with hTRPV1. NGCC (1 mM) induced an inward current in a capsaicin-sensitive cell. Neither capsaicin nor NGCC evoked the currents in non-transfected cells (n = 3). Dashed lines indicate zero current. (<b>B</b>) NGCC-induced currents were blocked by CPZ in hTRPV1-expressing HEK293T cells. (<b>C</b>) Summary of normalized current density in cells expressing hTRPV1 (n = 4). (<b>D</b>) Current density of the first pulse was normalized to 1.0. NGCC triggered inward currents in a dose-dependent manner in hTRPV1-expressing HEK293T cells (n = 3). Results are presented as the mean ± SEM.</p

Activation of hTRPA1 by AITC and NGCC.

<p>(<b>A</b>) AITC (100 µM) induced an inward current in hTRPA1-expressing cells. AITC-induced currents were partially inhibited by TRPA1 antagonist, HC-030031 (100 µM) and recovered after wash out. NGCC triggered an inward current in a AITC-sensitive cell. Neither AITC nor NGCC evoked the currents in non-transfected cells (n = 3). (<b>B</b>) NGCC-induced currents were blocked by HC-030031 in hTRPA1-expressing cells. (<b>C</b>) Summary of normalized current density in cells expressing hTRPA1 (n = 4). (<b>D</b>) NGCC triggered inward currents in a dose-dependent manner in hTRPA1-expressing cells (n = 4). Results are presented as the mean ± SEM.</p

Effects of S3969 or NGCC on αβγ hENaC-expressing cells.

<p>Cells expressing αβγ-hENaC were loaded with FMP blue-dye and the effects of S3969 or NGCC were quantitatively evaluated using membrane potential assay. S3969 depolarized membrane potential on αβγ hENaC-expressing cells and benzamil (Bz) effectively inhibited S3969 activity. NGCC showed no effect on αβγhENaC-expressing cells. Experiments were repeated in triplicate and data points represent the means ± SEM (n = 3–4).</p

Calcium responses in hTRPV1-expressing cells stimulated with capsaicin (Cap) and NGCC.

<p>(<b>A</b>) Cells expressing hTRPV1 were loaded with Fura-2 AM and Ca²⁺ images were obtained at 0 and 60 s after stimulation with Cap or NGCC. The non-specific blocker of TRP channels, RR (30 µM), and the specific TRPV1 antagonist, CPZ (5 µM), were added to test the selectivity of Cap and NGCC. Representative ratiometric images are shown after treatment with Cap and NGCC. (<b>B</b>) As a control, the Ca²⁺ response was monitored in non-hTRPV1-expressing HEK 293T cells treated with Cap or NGCC. (<b>C</b>) The effects of Cap or NGCC treatment were quantified using Calcium-4 in a cell-based assay in the presence or absence of 30 µM RR or 5 µM CPZ. Experiments were repeated in triplicate and data points represent the means ± SEM (n = 3).</p

Effects of the ten compounds from <i>A</i>.<i>rugosa</i> on hTRPA1- and hTRPV1-expressing cells.

<p>(A) The activities of the ten compounds from <i>A</i>. <i>rugosa</i> including acacetin (1 mM), 4-allylanisole (1 mM), apigenin 7-glucoside (1 mM), <i>p</i>-anisaldehyde (1 mM), <i>L</i>-carveol (0.3 mM), methyl eugenol (0.3 mM), <i>trans</i>-<i>p</i>-methoxycinnamaldehyde (0.1 mM), <i>β</i>-caryophyllene (1 mM), pachypodol (0.3 mM), and rosmarinic acid (0.1 mM) were analyzed in hTRPA1-Flp-In 293 stable cells. hTRPA1-Flp-In 293 stable cells were successfully activated by a specific agonist for hTRPA1, AITC (30 μM) and five compounds. According to quantitative analysis, the effects of five active compounds on hTRPA1-Flp-In 293 stable cells were significantly inhibited by two hTRPA1 antagonists, RR (30 μM) and HC-030031 (100 μM). (B) The effects of the ten compounds from <i>A</i>. <i>rugose</i> were monitored in HEK293T cells transiently expressing hTRPV1 by Ca²⁺ imaging and counting the responding cells (%). hTRPV1 was significantly stimulated by capsaicin (0.1 μM), a specific agonist for hTRPV1, but not by ten compounds. Statistical analysis is specifically indicated for each experiment (**p<0.001, ***p<0.0001).</p