THE ADRENAL CORTEX OF THE PANTOTHENIC ACID-DEFICIENT RAT: CARBOHYDRATE METABOLISM1,2

Winters, Robert W.; Schultz, Robert B.; Krehl, Willard A.

doi:10.1210/endo-50-4-388

Cited by 31 publications

(15 citation statements)

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“…There is, however, a condition in which lipid loss is likely to be indicative of inhibition of hormone synthesis, and that is pantothenic acid deficiency. This has been suggested by Winters, Schultz & Krehl (1952), who also produced evidence of functional failure of the adrenal in the deficient rat. Disturbance of extra-adrenal lipid metabolism by lack in pantothenic acid was found by Deane & McKibbin (1946); they observed that fatty livers developed in their control rats but not in their deficient rats.…”

Section: Discussionmentioning

confidence: 68%

Inhibition by hexoestrol of adrenocortical secretion in the rat

Vogt¹

1955

The Journal of Physiology

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It has been known for a long time (Korenchevsky & Dennison, 1935; Selye, Collp & Thomsen, 1935) that oestrogens cause hypertrophy and hyperplasia of the rat adrenal cortex. Selye & Collip (1936) have shown that this effect is absent in the hypophysectomized rat, even when the adrenal cortex is maintained by adrenocorticotrophic hormone (ACTH). The inference is that oestrogens cause an increase in secretion of ACTH and thus produce adrenal hypertrophy indirectly. During hexoestrol administration the pituitary hypertrophies and goes on growing for at least 6 weeks (Somers, 1948). Gemzell (1952) was able to demonstrate an increase in the amount of circulating ACTH in rats injected with oestradiol. The release of ACTH by oestrogens is considered to be an example of an unspecific response to stress (Tepperman, Engel & Long, 1943). Loeser (1939) observed the disappearance of lipids from the adrenals of rats injected with stilboestrol. A detailed examination of the effect of hexoestrol (Vogt, 1945) showed that sudanophilic lipids disappeared almost completely from the zonae fasciculata and reticularis in the course of 5 days, and from all three layers if the treatment lasted 10 days or more. These effects, too, were absent in hypophysectomized rats not given ACTH: experiments with ACTHmaintained rats were not performed.The functional state of lipid-depleted adrenals has been a matter of conjecture. Many histologists consider them to be hyperactive glands (Dosne & Dalton, 1941;Sarason, 1943), whereas others (Zwemer, 1936;Deane & McKibbin, 1946; Flexner & Groilman, 1939) suggest that they are in a state of exhaustion following initial hyperactivity. Both these interpretations are prompted by the observation that the early response to any stress or to an injection of ACTH is a diminution of adrenal lipids, more especially of cholesterol esters. However, this diminution is followed by recovery to normal or even by deposition of abnormally high amounts of lipids whenever treatment

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Section: Discussionmentioning

confidence: 68%

Inhibition by hexoestrol of adrenocortical secretion in the rat

Vogt¹

1955

The Journal of Physiology

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“…Fasted rats on a pantothenate-deficient diet are hypoglycemic compared to either ad libitum or pair fed controls [51], [52]. Fasted pantothenate-deficient rats are also impaired in gluconeogenesis [53], while ketogenesis is not affected [54].…”

Section: Discussionmentioning

confidence: 99%

Pantothenate Kinase 1 Is Required to Support the Metabolic Transition from the Fed to the Fasted State

et al. 2010

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Coenzyme A (CoA) biosynthesis is regulated by the pantothenate kinases (PanK), of which there are four active isoforms. The PanK1 isoform is selectively expressed in liver and accounted for 40% of the total PanK activity in this organ. CoA synthesis was limited using a Pank1 −/− knockout mouse model to determine whether the regulation of CoA levels was critical to liver function. The elimination of PanK1 reduced hepatic CoA levels, and fasting triggered a substantial increase in total hepatic CoA in both Pank1 −/− and wild-type mice. The increase in hepatic CoA during fasting was blunted in the Pank1 −/− mouse, and resulted in reduced fatty acid oxidation as evidenced by abnormally high accumulation of long-chain acyl-CoAs, acyl-carnitines, and triglycerides in the form of lipid droplets. The Pank1 −/− mice became hypoglycemic during a fast due to impaired gluconeogenesis, although ketogenesis was normal. These data illustrate the importance of PanK1 and elevated liver CoA levels during fasting to support the metabolic transition from glucose utilization and fatty acid synthesis to gluconeogenesis and fatty acid oxidation. The findings also suggest that PanK1 may be a suitable target for therapeutic intervention in metabolic disorders that feature hyperglycemia and hypertriglyceridemia.

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“…Acetylation is retarded, as indicated by a decrease in the portion of para-aminobenzoic acid or sulfonamide excreted in the urine in the acetylated form. Adrenal cortical function is impaired as shown by depletion of sudanophilic and ketosteroid substances from the adrenals of rats, disappearance of the eosinopenic response to adrenocorticotrophic hormone (ACTH), fall in the blood level of glucose accompanied by increased sensitivity to insulin, and defective regeneration of adrenal cholesterol in rats forced to swim for a long time in cold water (18)(19)(20)(21).…”

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confidence: 99%