Favorable glycemic response of type 2 diabetics to low-calorie cranberry juice.

Fruit and vegetable intake is typically low for type 2 diabetics, possibly due to a perceived adverse effect on glycemic control. Cranberry juice (CBJ) may represent an attractive means for increasing fruit intake and simultaneously affording positive health benefits. This single cross-over design compared metabolic responses of type 2 diabetics (n= 12) to unsweetened low-calorie CBJ (LCCBJ; 19 Cal/240 mL), carbohydrate sweetened normal calorie CBJ (NCCBJ; 120 Cal/240 mL), isocaloric low-calorie sugar water control (LCC), and isocaloric normal calorie sugar water control (NCC) interventions. CBJ flavonols and anthocyanins, and proanthocyanidins were quantified with HPLC, LC-MS, and MALDI-TOF that includes an original characterization of several large oligomeric proanthocyanidins. Blood glucose peaked 30 min postingestion after NCCBJ and NCC at 13.3 +/- 0.5 and 12.8 +/- 0.9 (mmol/L), and these responses were significantly greater than the LCCBJ and LCC peaks of 8.1 +/- 0.5 and 8.7 +/- 0.5, respectively. Differences in glycemic response remained significant 60 min, but not 120 min postingestion. Plasma insulin values 60 min postingestion for NCCBJ and NCC interventions were 140 +/- 19 and 151 +/- 18 (pmol/L), respectively, and significantly greater than the LCCBJ and LCC values of 56 +/- 10 and 54 +/- 10; differences were not significant 120 min postingestion. Metabolic responses within the 2 high and 2 low-calorie beverages were virtually identical; however, exposure to potentially beneficial nutrients was greater with CBJ. Relative to conventionally sweetened preparation, LCCBJ provides a favorable metabolic response and should be useful for promoting increased fruit consumption among type 2 diabetics or others wishing to limit carbohydrate intake.

Sequence analysis of the int-2/fgf-3 gene in aggressive human breast carcinomas.

A number of primary human breast carcinomas exhibit amplification of the chromosome 11 region containing the int-2/fgf-3 proto-oncogene, and progression of breast cancer has been correlated with int-2 amplification or with certain restriction fragment length polymorphisms (RFLPs) of the int-2 gene. Using the polymerase chain reaction (PCR), we obtained the int-2 coding sequences from six primary tumors, four of which exhibited amplification of the int-2 gene and one of which exhibited amplification of the neu gene. The majority of these tumors (five of six) were aggressive, as judged by their early recurrence, metastasis, or both. Nucleotide sequencing of PCR products revealed that previously described BamHI and PstI RFLPs of the int-2 gene, as well as a new polymorphism at position 9154, were located within the intron between the second and third exons. A seventh tumor was used to localize one of the PstI RFLPs 5 bp from the splice-acceptor site of the third exon. However, none of the tumor DNAs analyzed showed differences in the int-2 protein coding regions when compared with normal placenta DNA. These results imply that aggressive human breast cancers encode an unaltered form of the int-2 protein.

Analysis of the int-1, int-2, c-myc, and neu oncogenes in human breast carcinomas.

We have examined the DNA obtained from 100 primary breast carcinomas for oncogene markers which might have predictive value for poor prognosis. Ninety-six of the tumors were analyzed for the presence of restriction fragment length polymorphisms (RFLPs) previously identified in the int-2 gene. An 8.4-kilobase BamHI fragment and a 3.9-kilobase PstI fragment specific for the int-2 gene, in the absence of other restriction fragments, was found in 17 of 50 (34%) lymph node-negative patients and in 27 of 44 (61%) lymph node-positive patients. This combination of int-2 RFLPs (8.4/3.9) was found in a significantly different proportion (P = 0.02) of patients with greater than 3 positive lymph nodes compared to patients with fewer positive lymph nodes, suggesting that these RFLPs may be valuable for distinguishing among node-negative patients for chemotherapy. In contrast, the observed low frequency of int-1, int-2, neu, and c-myc amplification limited their usefulness as clinical predictors of disease recurrence.