Improving behavioral and clinical indicators in Asians and Pacific Islanders with diabetes: findings from a community clinic-based program.

AIMS: This project tested the six-month impact of Stanford's Diabetes Self-Management Program (DSMP), adapted for Asians and Pacific Islanders (APIs), on behavioral and clinical indicators. METHODS: Participants attended DSMP workshops at a community health center. Employing a one-group, pre-post-test design, data were collected at baseline and six-months. Ninety-six eligible API adults were enrolled. All attended four or more of the six weekly sessions, and 82 completed data collection. Measures included body mass index, blood pressure, blood lipids, blood glucose, HbA1c, as well as health behaviors. Data were analyzed by descriptive statistics and paired t-tests. RESULTS: Adaptations to DSMP were minimal, but critical to the local acceptance of the program. At six-months, significant behavioral improvements included: (1) increased minutes in stretching and aerobic exercise per week (p<0.001); (2) reduced symptoms of hypoglycemia and hyperglycemia (p<0.001); (3) increased self-efficacy (p<0.001); and (4) increased number of days and times testing blood sugar levels (p<0.001). Significant clinical improvements included: (1) lower BMI (p<0.001); (2) lower HbA1c (p<0.001); (3) lower total cholesterol, triglycerides, and LDL (p<0.001); and (4) lower blood pressure (p<0.001). CONCLUSIONS: Findings suggest that the DSMP can be successfully adapted to API populations and can improve clinical measures as well as health behaviors.

Early growth in offspring of diabetic mothers.

OBJECTIVE: By age 5 years, offspring of diabetic mothers (ODMs) are heavier and have altered glucose metabolism compared with offspring of mothers without diabetes (non-DMs). This study evaluates the growth pattern of ODMs before the age of 5 years. RESEARCH DESIGN AND METHODS: Anthropometric measures (z scores) from birth, 1.5 years, and 7.7 years in Pima Indian children were compared by maternal diabetes status. RESULTS: After adjustment for earlier gestational age at delivery (37.8 vs. 39.3 weeks, P < 0.01), ODMs were heavier at birth (z score birth weight 0.49 vs. -0.04, P < 0.01) than non-DMs. At age 1.5 years, ODMs were shorter than the non-DMs (z score = -0.24 vs. 0.12, P < 0.01) but their weight and relative weight (RW; weight adjusted for age, sex, and length or height) were similar. From birth to 1.5 years, ODMs showed significant "catch down" of weight compared with non-DMs (change in weight z score from birth to 1.5 years of ODMs and non-DMs was -0.56 and 0.12, respectively, P < 0.01). By age 7.7 years, ODMs were heavier (weight z score 0.89 vs. -0.07, P < 0.01) but had similar height as non-DMs. Differences in glucose and insulin concentrations at age 7.7 years were dependent on RW. CONCLUSIONS: ODMs had a dramatically different growth pattern from that of non-DMs. Gestational age-adjusted birth weight was higher. During the first 1.5 postnatal years, the change in weight z score and attained height were reduced. Subsequently, height caught up to that of non-DMs, while weight gain greatly exceeded that of non-DMs.

Hypothalamic-pituitary-thyroid axis and sympathetic nervous system involvement in hyperthermia induced by 3,4-methylenedioxymethamphetamine (Ecstasy).

An acute and potentially life-threatening complication associated with the recreational use of the 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) is hyperthermia. In the present study, Sprague-Dawley rats treated with MDMA (40 mg/kg s.c.) responded with a significant increase (maximal at 1 h) in rectal and skeletal muscle temperatures that lasted for at least 3 h post-treatment. Hypophysectomized (HYPO) and thyroparathyroidectomized (TX) animals treated with MDMA (40 mg/kg s.c.) did not become hyperthermic and in fact displayed a significant hypothermia. The HYPO and TX animals were also resistant to the serotonergic neurotoxic effects of MDMA assessed by serotonin measurements 4 to 7 days later in the striatum and hippocampus. MDMA (40 mg/kg s.c.) induced a significant increase in thyroxine levels 1 h post-treatment. Thyroid hormone replacement in TX animals returned the hyperthermic response seen after MDMA. Prazosin, an alpha(1)-antagonist (0.2 mg/kg i.p.), administered 30 min before MDMA significantly attenuated the MDMA-induced increase in rectal temperature, but had no effect on skeletal muscle temperature. Cyanopindolol, a beta(3)-antagonist (4 mg/kg s.c.), administered 30 min before MDMA (40 mg/kg s.c.) significantly attenuated the increase in skeletal muscle temperature, but had no effect on the rise in rectal temperature. The combination of prazosin and cyanopindolol resulted in an abolishment of MDMA-induced hyperthermia. The mechanisms of thermogenesis induced by MDMA seem to result from an interaction between the hypothalamic-pituitary-thyroid axis and the sympathetic nervous system, wherein mechanisms leading to core and skeletal muscle hyperthermia after MDMA exposure seem to be differentially regulated by alpha(1)- and beta(3)-adrenergic receptors.

An antisense oligonucleotide targeted at MAO-B attenuates rat striatal serotonergic neurotoxicity induced by MDMA.

The present study was designed to elucidate the role of dopamine (DA) metabolism in the serotonergic neurotoxicity induced by 3,4-methylenedioxymethamphetamine (MDMA). An antisense (AS) oligonucleotide (ODN) sequence targeted at monoamine oxidase-B (MAO-B) was utilized to attenuate MAO-B activity prior to MDMA administration. Sprague-Dawley rats were surgically implanted with intracerebroventricular (icv) cannulae and received a continuous infusion of MAO-B AS-ODN via an osmotic minipump. Constant AS ODN infusion for 7 days at a rate of 0.5 microl/h (total daily dose 600 pmol) resulted in a 63% knockdown of MAO-B activity. MDMA (40 mg/kg, sc) produced a rise in body temperature within 1 h of MDMA administration and a reduction in striatal serotonin (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) levels 7 days later. Pretreatment with the MAO-B AS ODN prior to MDMA attenuated this reduction in serotonergic markers, yet had no effect on MDMA-induced hyperthermia. Furthermore, in vivo microdialysis revealed that previous AS ODN treatment failed to alter the acute DA release induced by MDMA (10 mg/kg, sc) within the striatum. These results indicate that MAO-B plays an integral role in the development of MDMA-induced neurotoxicity while not affecting MDMA-induced hyperthermia or acute DA release.

Early excess weight gain of children in the Pima Indian population.

OBJECTIVE: To determine the period of childhood in which weight relative to height increases in Pima Indian children and young adults in comparison with the general US population. METHODS: Heights and weights of children in the Pima Indian population were derived from either clinical examinations conducted by the Department of Public Health Nursing (from 1-48 months of age), or from examinations in the National Institutes of Health longitudinal survey of health in the Pima population (for birth and ages 5-20 years), and compared with standards for the US population recently published by the National Center for Health Statistics. RESULTS: Weight relative to height (weight-for-length in children aged <24 months, body mass index at ages > or =2 years) was significantly higher in Pima children at all ages examined after the first month of life. Compared with reference values, the most dramatic increases in weight relative to height occurred in 2 stages of childhood: mean z scores of weight-for-length increased between 1 month (mean +/- SEM: males: -0.2 +/- 0.19; females: -0.02 +/- 0.14) and 6 months (males: 0.8 +/- 0.04; females: 0.7 +/- 0.04) of age; mean z scores for body mass index increased gradually between 2 years (males: 0.4 +/- 0.06; females: 0.4 +/- 0.08) and 11 years (males: 1.4 +/- 0.08; females: 1.4 +/- 0.08) and remained stable thereafter. CONCLUSION: Excessive weight gain occurs early in the Pima population with changes relative to reference values most marked in the first 6 months of life and between 2 and 11 years. Interventions toward primary prevention of obesity may need to be targeted at children rather than adults in this population.