Effects of starvation on thyroid function were studied in 5- to 6-week-old (R× U) F₁ rats. Starvation lowered plasma TSH in female, but not in male rats. Plasma T₄ and T₃ levels decreased, whereas the dialysable T₄ fraction increased during starvation. Free T₄ (FT₄) levels decreased rapidly in females, but only after prolonged fasting in male rats. Glucose decreased, and free fatty acid levels increased during starvation. Peripheral TRH levels did not change during food deprivation. Since effects of starvation were most apparent in young female rats, such rats were used to study hypothalamic TRH release during starvation and subsequent refeeding. Basal in vitro hypothalamic TRH secretion was less in starved rats than in control or refed animals. In vitro hypothalamic TRH release in medium with 56 ml KC1 increased 3-fold compared to basal release, and in these depolarization conditions TRH release was similar between hypothalami from control, starved and refed rats. In rats starved for 2 days, TRH level in hypophysial portal blood was lower than that of controls. Thus, diminished thyroid function during starvation may at least in part be caused by a reduced hypothalamic TRH release.

Diabetes mellitus is frequently associated with reduced levels of TSH, PRL, GH, and gonadotropins. In this study we have wanted to determine whether chemically induced diabetes mellitus is associated with a decreased hypothalamic release of TRH. Male rats were made diabetic with streptozotocin (STZ; 65 mg/kg), whereas controls received vehicle. After 2 weeks, STZ diabetic rats had 25% lower body weights, 3.5-fold higher blood glucose, and 40-60% lower plasma TSH, T3, and T4 levels than controls. The plasma T4 dialyzable fraction had increased 2.5-fold in STZ diabetic rats, and the plasma free T4 concentration was similar to that in controls. Thus, treatment with STZ results in decreased plasma TSH and T4 levels, but does not reduce free T4 concentrations. The content of TRH in hypothalami of 2-week STZ diabetic rats was similar to that in controls, but in vitro these hypothalami released less TRH than those of control rats. In 2-week STZ diabetic rats, TRH in hypophysial stalk blood was 30% lower than that in control rats. The in vitro TRH secretion from hypothalami of untreated rats was dependent on the glucose concentrations in the incubation medium; increasing the glucose concentration from 10 to 30 mM did not alter TRH secretion, but basal TRH release increased in the absence of glucose. In conclusion, STZ-induced diabetes in the rat is associated with reduced hypothalamic secretion of TRH, which, in turn, may be responsible for the reduced plasma TSH and thyroid hormone levels. Furthermore, it is suggested that the inhibitory effect of STZ-induced diabetes on TRH secretion is probably not due to hyperglycemia.

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The cross-sectional association of systolic blood pressure with dietary sodium, calcium, and potassium, as estimated from dietary histories, was investigated by multiple regression analysis of data gathered in the Netherlands in the early 1950s in a general health examination of 2,291 middle-aged civil servants and spouses of civil servants. A statistically significant negative trend with systolic blood pressure was seen for calcium intake in both males and females, even after adjustments for covariates. For sodium and potassium intake, the observed negative trends were not significant after multivariate analyses. In addition, no consistent associations were found between diastolic blood pressure and the micronutrients after multivariate analyses, except for a significant negative association with calcium intake in females. In this study population, blood pressure was a strong independent risk factor of total mortality: 15- and 25-year mortality was about twice as high for hypertensives (greater than or equal to 160 mmHg) as for normotensives (less than 160 mmHg). These findings support the conclusion in recent epidemiologic studies that higher intakes of calcium are associated with lower systolic blood pressure, and they extend the evidence to an earlier time period.

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